Overview

Also Known As:Cav-1 KO

These Caveolin 1 knock-out mice show hyperproliferative and vascular abnormalities. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Young mutant mice exhibit characteristics of Alzheimer's disease. This mutant mouse strain may be useful in studies of vesicular and cholesterol trafficking, signal transduction, neurodegeneration and tumorigenesis.

Note that this allele is also available on a C57BL/6J congenic background (Stock No. 007083).

Donating Investigator

Michael P. Lisanti, The Albert Einstein College of Medicine

Genetic overview

Genetic Background	Generation
	F?+39 (2020-09-03 00:00:00)

Cav1^tm1Mls

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Cav1	caveolin 1, caveolae protein

View Genetics

Research Applications

Developmental Biology Research
Internal/Organ Research
Metabolism Research
Diabetes and Obesity Research
Mouse/Human Gene Homologs
Neurobiology Research
Cardiovascular Research

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Base Price

Starting at:

$278.00 Domestic price for female

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Details

Detailed Description

Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction response to the alpha-1-adrenergic receptor agonist, phenylephrine, and an enhanced vasorelaxation response to acetylcholine. Histological examination of lung tissue from mutant mice shows thickened alveolar septa, hypercellularity, reduced alveolar spaces and increased density of basement membranes and reticulin fibers. Further immunohistochemical examination of lung tissue shows an increased number of endothelial cells. Mutant derived MEF cells proliferate two times faster and are denser at confluence as indicated by growth curves and cell cycle analysis. Electron microscopy analysis reveals a complete absence of caveolae (plasmalemmal vesicles) in endothelial cells. In vitro studies measuring uptake of fluorescently-labeled albumin and in vivo studies following uptake of gold-conjugated albumin demonstrate caveolar endocytosis impairment.

Young (3-6 month old) mutant mice exhibit multiple characteristics of Alzheimer's disease pathologies including increased amyloid beta and tau deposits, neurodegeneration, astrogliosis and decreased cerebrovascular volume. The neuronal aging found in the hippocampi of young mutant mice resembles that found in aged (> 18 months of age) wild-type mice. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed.

Development

A targeting vector containing a neomycin resistance gene was used to disrupt 2.2 Kb of sequence containing exons 1 and 2. The construct was electroporated into WW6 embryonic stem (ES) cells(75% 129/Sv, 20% C57BL/6J, 5% SJL). Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6J mice for approximately 5 generations. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed and backcrossed to a 129S6/SvEv background for 1 generation. The mice are now maintained as homozygotes and are primarily a mix of 129 and C57BL/6, but a minor contribution from the SJL background (contributed from the originating ES cell line) should not be discounted.

Control Suggestions

Approximate Controls

101045 B6129SF2/J

Additional Information

Considerations for Choosing Controls

Selected References

Razani B; Engelman JA; Wang XB; Schubert W; Zhang XL; Marks CB; Macaluso F; Russell RG; Li M; Pestell RG; Di Vizio D; Hou H Jr; Kneitz B; Lagaud G; Christ GJ; Edelmann W; Lisanti MP. 2001. Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities. J Biol Chem 276(41):38121-38PubMed: 11457855 MGI: J:75193

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Genetics

Cav1^tm1Mls

Allele Symbol: Cav1^tm1Mls

Allele Name	targeted mutation 1, Michael P Lisanti
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	cav^-; Cav^tm1Mls; Cav-1-; Cav-1 KO; Caveolin-1 KO
Gene Symbol and Name	Cav1, caveolin 1, caveolae protein
Gene Synonym(s)
Strain of Origin	STOCK 129/Sv and C57BL/6J and SJL
Chromosome	6
Molecular Note	A 2.2 kb region of the gene including exons 1 and 2 and part of the promoter region was replaced with a neo resistance cassette via homologous recombination. Absence of gene expression in homozygous mutant animals was verified by Western blot analysis of heart, adipose, and lung tissue, and also of mouse embryonic fibroblasts cultured from E13.5 homozygous mutant embryos.
Mutations Made By	Michael Lisanti, The Albert Einstein College of Medicine

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

hypertrophic cardiomyopathy

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Cav1^tm1Mls related

Developmental Biology Research
- Growth Defects
Internal/Organ Research
- Adipose Defects
Metabolism Research
- Lipid Metabolism
Diabetes and Obesity Research
- Obesity Without Diabetes
  - diet-induced, resistant
Mouse/Human Gene Homologs
- Alzheimer's
Neurobiology Research
- Alzheimer's Disease
Cardiovascular Research
- Hypertriglyceridemia
- Vascular Defects

Mouse/Human Gene Homologs
- Alzheimer's
Neurobiology Research
- Alzheimer's Disease

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6J * SJL

adipose tissue phenotype

abnormal fat cell morphology
- perigonadal adipocytes completely lack an electron-dense thick band of material that surrounds the normal lipid droplet

cardiovascular system phenotype

abnormal vascular endothelial cell morphology
- lung capillaries exhibit smaller tight junctions and abnormalities in capillary endothelial cell adhesion to the basement membrane

abnormal vascular wound healing
- ligation of the common carotid artery causes a significant increase in neointimal lesion formation compared to wild-type mice

decreased vasoconstriction
- at pressures between 30 and 70 mmHg, cerebral arteries develop less myogenic tone than wild-type, indicating attenuated pressure-induced constriction
- membrane depolarization induced by 60 mM potassium results in attenuated arterial wall intracellular calcium elevation and constriction in cerebral arteries
- N-omega-nitro-L-arginine, a nitric oxide synthase inhibitor, does not restore myogenic tone in cerebral arteries, indicating that NOS activation and nitric oxide generation do not significantly contribute to the attenuated myogenic response
- pressure induces a smaller depolarization and smaller arterial wall intracellular calcium elevation in mutant cerebral arteries than in wild-type, resulting in reduced myogenic constriction

increased vascular permeability
- large increase in microvascular permeability as indicated by an increased rate of clearance for iodinated serum albumin from the circulatory system and lower levels of endogenous serum albumin
- paracellular movement of Ruthenium Red is increased in lung endothelial cells indicating hyperpermeable tight junctions/capillaries
- treatment with L-NAME, a nitric-oxide synthasae inhibitor, restores normal microvascular permeability

cellular phenotype

abnormal actin cytoskeleton morphology
- mouse embryonic fibroblasts (MEFs) lose polarity when plated on fibronectin, exhibiting a round shape with aberrant actin cytoskeleton architecture

abnormal cell morphology
- protrusive and retractile activities at cell edges are higher in MEFs and protrusions and retractions occurs throughout the cell perimeter instead of protrusions in the direction of movement and retractions in the rear end as in wild-type MEFs

abnormal cellular cholesterol metabolism
- cellular cholesterol efflux not affected although ABCA1-mediated cholesterol efflux is more sensitive to the inhibitory effects of glyburide in macrophages
- however, when cholesterol loaded, macrophages show an increase in total cellular cholesterol content
- mouse embryonic fibroblasts (MEFs) and macrophages under normal conditions or loaded with cholesterol contain reduced free cholesterol but increased esterified-cholesterol content

abnormal fibroblast chemotaxis
- MEFs plated on fibronectin move faster and exhibit impaired directional migration compared to wild-type MEFs

abnormal microtubule organizing center morphology
- microtubule organizing center reorientation toward the leading edge of a wound is reduced in MEFs

absent caveolae
- absence of caveolae in vascular smooth muscle cells
- caveolae are absent in the longitudinal muscles of the intestine
- chondrocytes lack caveolae

decreased fibroblast chemotaxis
- wound closure and chemotactic response of MEFs in a transwell assay are impaired

behavior/neurological phenotype

abnormal gait
- wider overlap (distance between superimposed hindpaw and forepaw) that coincides with stride abnormalities

abnormal involuntary movement
- mutants exhibit spinning upon tail suspension; frequency and intensity of spinning increases progressively with age such that by 50 weeks, it is seen in 50% of mutants and in all mutants by 80-90 weeks of age

abnormal locomotor behavior
- mutants tend to stop and/or change direction of movement while traversing a tunnel more often than controls

decreased exploration in new environment
- exploratory behavior in a new environment is reduced as early as 13 weeks of age

decreased grip strength
- mutants exhibit impaired ability to hold and maneuver on a bar

hypoactivity
- mutants are less active than their wild-type littermates

limb grasping
- exhibit clasping as early as 20 weeks of age and the number of mutants that clasp increases with age

short stride length
- evident by 10 weeks of age

digestive/alimentary phenotype

abnormal digestive system physiology
- mutants exhibit impaired small intestinal nitric oxide function

growth/size/body region phenotype

decreased body weight
- a defect in insulin-regulated lipogenesis contributes to the lean phenotype

homeostasis/metabolism phenotype

abnormal cellular cholesterol metabolism
- cellular cholesterol efflux not affected although ABCA1-mediated cholesterol efflux is more sensitive to the inhibitory effects of glyburide in macrophages
- however, when cholesterol loaded, macrophages show an increase in total cellular cholesterol content
- mouse embryonic fibroblasts (MEFs) and macrophages under normal conditions or loaded with cholesterol contain reduced free cholesterol but increased esterified-cholesterol content

abnormal nitric oxide homeostasis
- apamin significantly reduces small intestinal tissue relaxation to electrical field stimulation in nonadrenergic noncholinergic conditions in mutants but not controls indicating that the normal spontaneous contraction of intestinal muscle is probably maintained by increased activity of apamin-sensitive mediators
- interstitial cells of Cajal and smooth muscles of the intestine (longitudinal muscles) show reduced responsiveness to endogenous and exogenous nitric oxide
- N-omega-nitro-L-arginine is ineffective to inhibit intestinal relaxation and exogenous nitric oxide donor sodium nitroprusside relaxes longitudinal muscle less than in controls
- tained by increased activity of apamin-sensitive mediators

abnormal vascular wound healing
- ligation of the common carotid artery causes a significant increase in neointimal lesion formation compared to wild-type mice

impaired lipolysis
- mutants exhibit a 5-fold reduction in their lipolytic response to a beta3-specific adrenergic receptor agonist
- serum nonesterified fatty acid levels fail to rise in mutants in response to prolonged fasting

impaired wound healing
- mutants show a slower wound healing rate when circular punch biopsies are done on the back skin compared to wild-type

increased circulating insulin level
- post-prandial serum levels of insulin were increased in mice that had been on a high fat diet for 9 months

insulin resistance
- mutants show a blunted decline in glucose levels upon insulin injection

muscle phenotype

decreased vasoconstriction
- at pressures between 30 and 70 mmHg, cerebral arteries develop less myogenic tone than wild-type, indicating attenuated pressure-induced constriction
- membrane depolarization induced by 60 mM potassium results in attenuated arterial wall intracellular calcium elevation and constriction in cerebral arteries
- N-omega-nitro-L-arginine, a nitric oxide synthase inhibitor, does not restore myogenic tone in cerebral arteries, indicating that NOS activation and nitric oxide generation do not significantly contribute to the attenuated myogenic response
- pressure induces a smaller depolarization and smaller arterial wall intracellular calcium elevation in mutant cerebral arteries than in wild-type, resulting in reduced myogenic constriction

nervous system phenotype

abnormal brain internal capsule morphology
- the internal capsule fiber bundles are smaller in size in the striatum

decreased brain size
- brains are smaller at 60 weeks of age but not at 11 weeks of age

decreased brain weight

skeleton phenotype

abnormal chondrocyte physiology
- growth zone chondrocytes fail to exhibit a response to 1,25-dihydroxyvitaminD3

abnormal costochondral joint morphology
- cartilage of the costochondral junction is more cellular

abnormal hyaline cartilage morphology
- hyaline cartilage is more cellular, extending distally from the rib

abnormal long bone epiphyseal plate morphology
- at 8 weeks of age, cartilage extends into the epiphyseal bone and metaphyseal marrow

abnormal long bone epiphyseal plate proliferative zone
- increase in the number of columns of cells in the proliferating cell zone

abnormal long bone hypertrophic chondrocyte zone
- increase in the number of columns of cells in the hypertrophic cell zone of growth plates
- number of hypertrophic cells is increased for each column of cells

abnormal long bone metaphysis morphology
- at 8 weeks of age, in the metaphysis the trabeculae are coated with a thin layer of bone
- increase in number of trabeculae in metaphyseal bone
- metaphyseal bone volume is greater

abnormal trabecular bone morphology
- at 8 weeks of age, in the metaphysis the trabeculae are coated with a thin layer of bone
- increase in number of trabeculae in metaphyseal bone

increased long bone epiphyseal plate size
- costochondral growth plates are longer
- growth plates of femoral chondyles are extended, both vertically and in cross-section
- tibial growth plates are 12.3% longer than in wild-type

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6 * FVB/N * SJL

endocrine/exocrine gland phenotype

abnormal mammary gland morphology
- estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice
- female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter
- ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice

increased mammary gland tumor incidence
- ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis
- ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
- estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
- estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice

neoplasm

increased mammary gland tumor incidence
- ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis
- ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
- estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
- estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice

integument phenotype

abnormal mammary gland morphology
- estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice
- female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter
- ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice

increased mammary gland tumor incidence
- ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis
- ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
- estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
- estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
B6.Cg-Cav1

adipose tissue phenotype

abnormal brown fat cell morphology
- mitochodria of brown adipocytes are larger and dilated and much less electron dense than mitochondria of wild-type mice

abnormal fat cell morphology
- adipocytes lack caveolae

increased brown fat cell lipid droplet size
- adipocytes of brown adipose tissue contain larger lipid droplets than in wild-type mice

homeostasis/metabolism phenotype

abnormal triglyceride level
- n BAT
- the reduction of triglyceride content of brown adipose tissue (BAT) induced after fasting/cold treatment is much lower than in controls (3-fold reduction in mutants vs. 10-fold reduction in controls), indicating defective release of stored triglycerides in BAT

decreased core body temperature
- mild, but significant, decrease in resting core body temperature

decreased fatty acid level
- mutants fail to exhibit the normal increase in serum nonesterifited fatty acids induced by fasting or fasting/cold treatment

impaired adaptive thermogenesis
- mutants show a decrease in body temperature in response to fasting or fasting/cold treatment, however cold treatment alone has no further effect on temperature

impaired lipolysis
- after fasting/cold treatments, BAT adipocytes of wild-type mice are devoid of lipid droplets while those of mutants still contain lipid droplets, indicating decreased lipid utilization after fasting/cold treatment
- lipolysis fails to occur when mice are fasted or fasted/cold treated

integument phenotype

abnormal lactation
- premature lactation; at day 18 of pregnancy, mammary glands of mutants are engorged with milk whereas wild-type glands are just beginning milk production and exhibit accelerated milk protein production

abnormal mammary gland growth during pregnancy
- Normal - however, serum prolactin levels are normal
- premature development of the lobuloalveolar compartment of the mammary gland during pregnancy

reproductive system phenotype

abnormal mammary gland growth during pregnancy
- Normal - however, serum prolactin levels are normal
- premature development of the lobuloalveolar compartment of the mammary gland during pregnancy

respiratory system phenotype

abnormal lung vasculature morphology
- gaps in the lung capillary

cardiovascular system phenotype

abnormal lung vasculature morphology
- gaps in the lung capillary

abnormal vascular endothelial cell morphology
- absence of caveolae in microvascular endothelia (lung, heart and fat)

cellular phenotype

absent caveolae
- absence of caveolae in microvascular endothelia (lung, heart and fat) and fat adipocyte

endocrine/exocrine gland phenotype

abnormal lactation
- premature lactation; at day 18 of pregnancy, mammary glands of mutants are engorged with milk whereas wild-type glands are just beginning milk production and exhibit accelerated milk protein production

abnormal mammary gland growth during pregnancy
- Normal - however, serum prolactin levels are normal
- premature development of the lobuloalveolar compartment of the mammary gland during pregnancy

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
B6.Cg-Cav1/J

cardiovascular system phenotype

increased vascular permeability
- increase in permeability of the pulmonary endothelial barrier to plasma proteins as indicated by an accumulation of proteins, especially albumin, in bronchoalveolar lavage from 1-9 months of age and leakage of Evans blue in pulmonary tissues

cellular phenotype

absent caveolae

homeostasis/metabolism phenotype

pulmonary edema
- presence of vascular-derived fluid in pulmonary tissues

reproductive system phenotype

reduced fertility
- Background Sensitivity - decrease in fertility on a C57BL/6J background

respiratory system phenotype

abnormal lung morphology
- 60% increase in elastic fiber deposits in the lungs, with thicker layers of elastic fibers primarily around airways and arteries
- Normal - however, mutants do not exhibit emphysema
- increase in collagen deposition in the lung parenchyma and the periphery of airways

abnormal pulmonary elastic fiber morphology
- 60% increase in elastic fiber deposits in the lungs, with thicker layers of elastic fibers primarily around airways and arteries

abnormal respiratory mechanics
- from 3 months on, mutants exhibit altered respiratory mechanics, suggesting stiffening of the lung tissue

decreased lung compliance
- from 3 months on, mutants exhibit a decrease in lung compliance

increased airway resistance
- from 3 months on, mutants exhibit an increase in airway resistance

increased lung elastance
- from 3 months on, mutants exhibit a a sustained increase in lung elastance

pulmonary edema
- presence of vascular-derived fluid in pulmonary tissues

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
Not Specified

cardiovascular system phenotype

abnormal brain vasculature morphology
- 20-25% reduction in cerebrovascular volume is observed in the hippocampi from young mice

cellular phenotype

abnormal cell cytoskeleton morphology

homeostasis/metabolism phenotype

amyloid beta deposits
- amyloid beta production is increased in the hippocampus of young mice

nervous system phenotype

abnormal astrocyte morphology
- astrocytes in young mice are disorganized as compared to young wild-type mice

abnormal brain vasculature morphology
- 20-25% reduction in cerebrovascular volume is observed in the hippocampi from young mice

abnormal CNS glial cell morphology
- increase in glia and glial scar formation within the dentate gyrus

abnormal dendrite morphology
- cytoskeletal architecture within dendrites is unorganized

abnormal dentate gyrus morphology
- increase in glia and glial scar formation within the dentate gyrus
- young (3-6 months) mice exhibit a reduction in the number of neurons within the dentate gyrus

abnormal hippocampus CA1 region morphology
- Fluoro-Jade B and Nissl staining of the CA1 region from 12 month old mice indicates increased neuronal degeneration as compared to age-matched controls
- young (3-6 months) mice exhibit a reduction in the number of neurons in the CA1 region
- young mice exhibit areas of potential plaque development and disorganized astrocytes

amyloid beta deposits
- amyloid beta production is increased in the hippocampus of young mice

astrocytosis

brain ischemia
- young mice subjected to ischemic preconditioning prior to lethal ischemia lack the ability to protect CA1 neurons, a phenomenon observed in aged wild-type mice

decreased CNS synapse formation
- young mice exhibit a significant reduction in hippocampal synapses in comparison to age-matched wild-type mice, but similar to aged wild-type mice

hippocampal neuron degeneration
- Fluoro-Jade B and Nissl staining of the CA1 region from 12 month old mice indicates increased neuronal degeneration as compared to age-matched controls

tau protein deposits
- tau deposits are elevated in hippocampal homogenates from young mice

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
FVB.Cg-Cav1

adipose tissue phenotype

abnormal adipose tissue physiology
- enhanced uptake of leucine in mildly fasted mice

decreased total body fat amount
- reduced fat mass

homeostasis/metabolism phenotype

abnormal circulating amino acid level
- elevated circulating branched-chain amino acid levels

abnormal free fatty acids level
- delay in suppression of free fatty acid levels following refeeding
- impaired beta3-AR agonist induced release of free fatty acids

abnormal glucose homeostasis
- exposure to 3-mercaptopicolinic acid causes a larger drop in glucose levels compared to wild-type mice
- maintain glucose levels better in the fasted state better than wild-type controls

abnormal homeostasis
- elevated circulating peroxide levels and a small decrease in circulating pyruvate levels
- increase in lactate levels following 3-mercaptopicolinic acid treatment

abnormal respiratory quotient
- variability in the respiratory exchange ratio over a 24 hour period is reduced

decreased circulating adiponectin level
- reduced total circulating levels and a decrease in the proportion of the HMW form

decreased liver glycogen level
- in the fed state

decreased susceptibility to diet-induced obesity
- when placed on a high fat diet

enhanced gluconeogenesis
- enhanced hepatic gluconeogenesis
- following a glycerol bolus, glycerol induced glucose production is enhanced but glycerol clearance is delayed
- treatment with enoximone, a phospodiesterase inhibitor, potently increases glucose levels

enhanced lipolysis

hyperglycemia
- upon refeeding display fairly severe hyperglycemia

increased blood urea nitrogen level

increased circulating glycerol level
- following 3-mercaptopicolinic acid treatment

increased circulating insulin level

increased liver glycogen level
- in moderately fasted mice

increased oxygen consumption

increased respiratory quotient

increased triglyceride level
- in fed and fasted mice

insulin resistance

behavior/neurological phenotype

increased food intake

liver/biliary system phenotype

abnormal liver physiology
- alternate day fasting has no effect of hepatic lipid content unlike in wild-type mice
- hepatic triglyceride synthesis appears to be reduced

decreased liver glycogen level
- in the fed state

decreased susceptibility to hepatic steatosis
- fasting induced and high fat diet induced hepatic steatosis are reduced

increased liver glycogen level
- in moderately fasted mice

increased liver weight
- under all conditions tested

cellular phenotype

abnormal cellular respiration
- MEFs display a preference for glycolysis in glucose-deprived media

abnormal respiratory electron transport chain
- expression analysis indicates altered mitochondrial function
- Normal - however, mitochondria isolated from liver and lung tissue display similar function compared to wild-type controls
- mitochondria in MEFs display dramatically increased membrane potential

muscle phenotype

abnormal skeletal muscle morphology
- skeletal muscle tissue has a darker appearance indicating an increased mitochondrial content

growth/size/body region phenotype

decreased susceptibility to diet-induced obesity
- when placed on a high fat diet

increased liver weight
- under all conditions tested

weight loss
- lose more weight when fasted

The following phenotype relates to a compound genotype created using this strain

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6 * SJL

adipose tissue phenotype

abnormal fat cell morphology
- at 12 weeks of age, female mammary gland 4/subcutaneous adipocytes contain reduced lipid droplets
- lipid droplet size in adipoctyes is about 2-3-fold smaller than in wild-type

abnormal gonadal fat pad morphology
- underdeveloped peri-gonadal fat pads

abnormal mammary fat pad morphology
- at 36 weeks of age on a high fat diet, mammary gland 4 fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity

absent subcutaneous adipose tissue
- the hypodermal fat layer is absent in both males and females at 12 weeks of age

decreased subcutaneous adipose tissue amount
- at 36 weeks of age on a high fat diet, subcutaneous fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity
- underdeveloped subcutaneous fat pads

decreased total body fat amount
- 2-fold reduction in the fat-to-water ratio
- at 35 weeks of age on a high fat diet, mutants only show minor gains in fat mass compared to wild-type and have dramatically reduced adiposity in all fat pads compared to wild-type

decreased white adipose tissue amount
- at 12 weeks of age on a high fat diet, mutants exhibit a 2-fold reduction in female mammary gland/subcutaneous WAT

decreased white fat cell lipid droplet size
- lipid droplet size in adipoctyes is about 2-3-fold smaller than in wild-type

increased brown adipose tissue amount
- mutants on a high fat diet exhibit hyperplastic brown adipose tissue, putatively secondary to elevated triglyceride levels

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - mutants do not exhibit significant changes in paremeters of energy expenditure such as VO2, VCO2, respiratory quotient, heat release, or movement, indicating that leanness is not due to increased energy expenditure
- Normal - plasma glucose, insulin, and cholesterol levels were similar to wild-type in both fasting and post-prandial states at 12 weeks of age, standard chow diet

liver/biliary system phenotype
- Normal - livers show no increase in weight or steatosis

neoplasm
- Normal - mice fail to spontaneously develop mammary tumors, even at up to 9 months of age, although mammary glands at this age show pronounced lobular development with numerous acini per terminal ductal lobular unit, hyperplasia of the mammary epithelial lining, and fibrosis
- Normal - nd fibrosis

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- mutants exhibit a decrease in survival (7 days vs. 13 days in wild-type) when challenged with Salmonella enterica serovar Typhimurium

premature death
- 50% reduction in life span, with viability declining between 27 and 65 weeks of age
- mice that die within this time frame, die suddenly, without any visible signs of disease

muscle phenotype

abnormal myocardial fiber morphology
- myocyte hypertrophy and disorganization

abnormal myocardium layer morphology
- myocardium is thickened in both the left and right ventricles at 12 months of age

abnormal skeletal muscle fiber morphology
- sarcoplasmic reticulum is dilated in skeletal muscle of males
- skeletal muscle fibers of males exhibit and increase in tubular aggregate formation with age

abnormal vasoconstriction
- impaired response to phenylephrine (PE) due to increased Nos3 activity

abnormal vasodilation
- impaired acetylcholine induced relaxation of the aortic rings

decreased cardiac muscle contractility
- 29% decrease in fractional shortening at 12 months of age, indicating reduction in left ventricular systolic fraction

heart left ventricle hypertrophy
- 12 month old mutants exhibit concentric left ventricular hypertrophy

neoplasm

increased incidence of tumors by chemical induction
- 100% of mice develop tumors at 12 weeks of age compared to 10% of wild-type mice
- mutants are more susceptible to DMBA (7,12-dimethylbenzanthracene)-induced skin carcinogenesis
- tumor multiplicity is greatly increased

nervous system phenotype

increased cerebral infarction size
- mutants exhibit an increase of cerebral volume of infarction compared to wild-type, with fewer numbers of proliferating endothelial cells and increased numbers of cells undergoing apoptotic cell death in ischemic brains

respiratory system phenotype

abnormal pulmonary alveolar parenchyma morphology
- parenchymal hypercellularity

abnormal pulmonary endothelial cell surface
- reactive endothelial cell proliferation

lung inflammation
- increase in inflammatory infiltrates in the lung

pulmonary hyperemia
- alveolar spaces are filled with extravasated red blood cells
- hyperemic lungs

thick pulmonary interalveolar septum

skeleton phenotype

abnormal bone mineralization
- mineral apposition rate is increased at both metaphyseal and cortical sites at 5 weeks of age and regresses by 8 weeks of age

abnormal bone trabecula morphology
- metaphyseal trabeculae are greater in number and show reduced spacing, however trabecular thickness is not different from wild-typ

abnormal compact bone morphology
- 33% increase in stiffness and 33% decrease in postyield deflection of cortical bone

abnormal long bone epiphysis morphology
- 58.4% increase in ephiphyseal bone volume at 5 weeks

abnormal long bone metaphysis morphology
- 77.4 % increase in metaphyseal bone volume at 8 weeks but not at 5 weeks of age

abnormal osteoclast morphology
- marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures

increased bone strength
- 25% increase in maximum force
- stiffer bone capable of bearing a greater load before failure

increased bone trabecula number
- increase in trabecular number in the distal femoral epiphysis

increased compact bone area
- at the femoral mid-diaphysis, the total cortical area is increased by 19.7% and 13.8%, at 5 and 8 weeks of age, respectively, with expanded periosteal and endocortical surfaces at 8 weeks

increased trabecular bone thickness
- increase in thickness of the distal femoral epiphysis

premature bone ossification
- increase in bone formation rate at the trabecular and cortical sites at 5 weeks of age

behavior/neurological phenotype

impaired exercise endurance
- exercise intolerance when compared to wild-type in a swimming test

increased food intake
- daily food intake is higher in females

cardiovascular system phenotype

abnormal myocardial fiber morphology
- myocyte hypertrophy and disorganization

abnormal myocardium layer morphology
- myocardium is thickened in both the left and right ventricles at 12 months of age

abnormal pulmonary endothelial cell surface
- reactive endothelial cell proliferation

abnormal vasoconstriction
- impaired response to phenylephrine (PE) due to increased Nos3 activity

abnormal vasodilation
- impaired acetylcholine induced relaxation of the aortic rings

cardiac fibrosis
- increase in fibrosis at 12 months of age

cardiac hypertrophy
- 12 month old mice show thickening of the myocardium in both ventricles and generalized myoycte hypertrophy

congestive heart failure
- severe right-sided heart failure

decreased cardiac muscle contractility
- 29% decrease in fractional shortening at 12 months of age, indicating reduction in left ventricular systolic fraction

dilated heart right ventricle
- the right ventricular chamber is about 70% and 25% larger than in wild-type at 4 and 12 months of age, respectively

heart left ventricle hypertrophy
- 12 month old mutants exhibit concentric left ventricular hypertrophy

pulmonary hyperemia
- alveolar spaces are filled with extravasated red blood cells
- hyperemic lungs

pulmonary hypertension

thick interventricular septum
- increase in intraventricular septal thickness during diastole

thick ventricular wall
- about 18% and 36% increase in left ventricular wall thickness at 4 and 12 months of age, respectively

cellular phenotype

abnormal vesicle-mediated transport
- uptake and transport of albumin from the blood to the interstitium by endothelial cells is defective due to absence of caveolae

absent caveolae
- adipocytes from peri-gonadal white adipose tissue show barren membrane architecture indicating a loss of caveolae
- endothelial cells lack caveolae membranes

endocrine/exocrine gland phenotype

abnormal mammary gland duct morphology
- the mammary ductal epithelia exhibits hyperproliferation
- the number of mammary ducts per field is increased

abnormal mammary gland epithelium morphology
- mammary epithelial cell hyperplasia, even in 6 week old virgin mice

abnormal mammary gland morphology
- size of mammary glands is reduced, however overall architecture is intact

mammary gland duct hyperplasia
- intraductal hyperplasia, with the epithelial cell layer 3-4 cells thick

mammary gland hyperplasia
- mammary epithelial cell hyperplasia, even in 6 week old virgin mice

growth/size/body region phenotype

cardiac hypertrophy
- 12 month old mice show thickening of the myocardium in both ventricles and generalized myoycte hypertrophy

decreased body weight
- mice are leaner than wild-type mice on a chow diet
- relative decrease in weight is exacerbated on a high fat diet
- resistance to diet-induced obesity due to an inability to convert lipoprotein triglycerides into the fat droplet storage form

decreased susceptibility to diet-induced obesity
- mutants are resistant to obesity when challenged with a high fat diet for 36 weeks

heart left ventricle hypertrophy
- 12 month old mutants exhibit concentric left ventricular hypertrophy

slow postnatal weight gain
- lack of weight gain

hematopoietic system phenotype

abnormal macrophage physiology
- macrophages exhibit increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS
- Normal - macrophages show no differences in the uptake of opsonized bacteria from wild-type

abnormal neutrophil physiology
- polymorphonuclear neutrophil (PMN) sequestration in lungs is reduced in mutants compared to wild-type after LPS challenge

abnormal osteoclast morphology
- marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures

impaired neutrophil recruitment
- mutants lack infiltration of white pulp by neutrophils when infected with Salmonella

homeostasis/metabolism phenotype

abnormal blood homeostasis
- plasma ACRP30 (an adipoctye secreted factor) levels are reduced by 8-10 fold

abnormal chemokine level
- increased production of the chemokines CCL3, CXCL10 and CXCL10 at 3 days post Salmonella infection

abnormal circulating free fatty acids level
- free fatty acids levels fail to undergo the expected post-eating reduction seen in wild-type

abnormal cytokine level

abnormal homeostasis
- transvascular protein transport is increased, with mutants showing higher albumin and IgM clearance from the plasma to peritoneium, and increased clearance of high molecular weight Ficoll

abnormal lipid homeostasis
- mutants show kinetically delayed clearance of triglycerides in an oral fat tolerance test

abnormal nitric oxide homeostasis
- lungs exhibit increased NOS3 (eNOS)-derived nitric oxide production and impaired NOS2 (iNOS)-derived nitric oxide production after LPS challenge

decreased circulating leptin level
- plasma leptin levels are reduced more than 2-fold

decreased susceptibility to diet-induced obesity
- mutants are resistant to obesity when challenged with a high fat diet for 36 weeks

impaired exercise endurance
- exercise intolerance when compared to wild-type in a swimming test

increased cerebral infarction size
- mutants exhibit an increase of cerebral volume of infarction compared to wild-type, with fewer numbers of proliferating endothelial cells and increased numbers of cells undergoing apoptotic cell death in ischemic brains

increased circulating interferon-gamma level
- increased production of interferon-gamma at 3 days post Salmonella infection

increased circulating interleukin-6 level
- increased production of IL-6 at 3 days post Salmonella infection

increased circulating triglyceride level
- triglyceride levels are elevated in the fasted state and increased even more post-prandially, due to perturbed lipoprotein lipase activity

increased circulating tumor necrosis factor level
- increased production of TNF-alpha at 3 days post Salmonella infection

increased circulating VLDL triglyceride level
- the chylomicron/VLDL fraction of triglycerides is increased during fasting and increases dramatically above wild-type mice in the post-prandial state

increased incidence of tumors by chemical induction
- 100% of mice develop tumors at 12 weeks of age compared to 10% of wild-type mice
- mutants are more susceptible to DMBA (7,12-dimethylbenzanthracene)-induced skin carcinogenesis
- tumor multiplicity is greatly increased

immune system phenotype

abnormal chemokine level
- increased production of the chemokines CCL3, CXCL10 and CXCL10 at 3 days post Salmonella infection

abnormal cytokine level

abnormal macrophage physiology
- macrophages exhibit increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS
- Normal - macrophages show no differences in the uptake of opsonized bacteria from wild-type

abnormal neutrophil physiology
- polymorphonuclear neutrophil (PMN) sequestration in lungs is reduced in mutants compared to wild-type after LPS challenge

abnormal osteoclast morphology
- marrow cultures from mutants generate about 20% more osteoclasts than wild-type cultures

decreased susceptibility to endotoxin shock
- adhesion of wild-type PMN to mutant endothelial cells is reduced after LPS challenge
- lungs are protected from LPS-induced lung injury, showing no increase in lung microvascular permeability or edema formation as in wild-type mice
- mutants show reduced mortality compared to wild-type mice following LPS challenge due to elevated nitric oxide as mutants treated with an NOS3 inhibitor show 100% mortality

impaired neutrophil recruitment
- mutants lack infiltration of white pulp by neutrophils when infected with Salmonella

increased circulating interferon-gamma level
- increased production of interferon-gamma at 3 days post Salmonella infection

increased circulating interleukin-6 level
- increased production of IL-6 at 3 days post Salmonella infection

increased circulating tumor necrosis factor level
- increased production of TNF-alpha at 3 days post Salmonella infection

increased susceptibility to bacterial infection
- mutants exhibit increased production of inflammatory cytokines, chemokines, and nitric oxide in response to Salmonella infection but are unable to control the systemic infection and have higher bacterial burden in spleen and liver

increased susceptibility to bacterial infection induced morbidity/mortality
- mutants exhibit a decrease in survival (7 days vs. 13 days in wild-type) when challenged with Salmonella enterica serovar Typhimurium

lung inflammation
- increase in inflammatory infiltrates in the lung

integument phenotype

abnormal mammary gland duct morphology
- the mammary ductal epithelia exhibits hyperproliferation
- the number of mammary ducts per field is increased

abnormal mammary gland epithelium morphology
- mammary epithelial cell hyperplasia, even in 6 week old virgin mice

abnormal mammary gland morphology
- size of mammary glands is reduced, however overall architecture is intact

absent subcutaneous adipose tissue
- the hypodermal fat layer is absent in both males and females at 12 weeks of age

decreased subcutaneous adipose tissue amount
- at 36 weeks of age on a high fat diet, subcutaneous fat is severely perturbed in females, with reduced numbers of adipoctyes that are heterogeneous in size and marked interstitial fibrosis and hypercellularity
- underdeveloped subcutaneous fat pads

epidermal hyperplasia
- mutants develop extensive epidermal hyperplasia in response to DMBA treatment before tumor formation

mammary gland duct hyperplasia
- intraductal hyperplasia, with the epithelial cell layer 3-4 cells thick

mammary gland hyperplasia
- mammary epithelial cell hyperplasia, even in 6 week old virgin mice

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
STOCK Cav1/J

cardiovascular system phenotype

decreased vasoconstriction
- erence
- phenylephrine causes vascular contraction that is significantly reduced compared to wild-type on a high salt diet, however when the phenylephrine contraction is presented as a percentage of maximum and the ED50 is calculated, there is no significant difference
- vascular contraction in response to membrane depolarization by high KCl is reduced in mutants compared to wild-type mice on a high salt diet

increased systemic arterial blood pressure
- mice on a high salt diet treated with N-G-nitro-L-arginine methyl ester (L-NAME) exhibit a more elevated blood pressure than similarly treated wild-type mice, however no differences are seen on a low salt diet

increased vasodilation
- acetylcholine causes enhanced aortic relaxation compared to wild-type on a high salt and low salt diet

endocrine/exocrine gland phenotype

abnormal thyroid follicular cell morphology
- more than a 4-fold increase in thyrocyte proliferation, however mice do not develop a goiter because there is an increase in thyrocyte apoptosis

growth/size/body region phenotype

decreased body weight
- total body weight is reduced in mutants compared to wild-type on both high salt and low salt diets

muscle phenotype

decreased vasoconstriction
- erence
- phenylephrine causes vascular contraction that is significantly reduced compared to wild-type on a high salt diet, however when the phenylephrine contraction is presented as a percentage of maximum and the ED50 is calculated, there is no significant difference
- vascular contraction in response to membrane depolarization by high KCl is reduced in mutants compared to wild-type mice on a high salt diet

increased vasodilation
- acetylcholine causes enhanced aortic relaxation compared to wild-type on a high salt and low salt diet

References

Razani B; Engelman JA; Wang XB; Schubert W; Zhang XL; Marks CB; Macaluso F; Russell RG; Li M; Pestell RG; Di Vizio D; Hou H Jr; Kneitz B; Lagaud G; Christ GJ; Edelmann W; Lisanti MP. 2001. Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities. J Biol Chem 276(41):38121-38PubMed: 11457855 MGI: J:75193

Additional References

Capozza F; Williams TM; Schubert W; McClain S; Bouzahzah B; Sotgia F; Lisanti MP. 2003. Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation. Am J Pathol 162(6):2029-39PubMed: 12759258 MGI: J:83485
Cohen AW; Razani B; Schubert W; Williams TM; Wang XB; Iyengar P; Brasaemle DL; Scherer PE; Lisanti MP. 2004. Role of caveolin-1 in the modulation of lipolysis and lipid droplet formation. Diabetes 53(5):1261-70PubMed: 15111495 MGI: J:89326
Cohen AW; Razani B; Wang XB; Combs TP; Williams TM; Scherer PE; Lisanti MP. 2003. Caveolin-1-deficient mice show insulin resistance and defective insulin receptor protein expression in adipose tissue. Am J Physiol Cell Physiol 285(1):C222-35PubMed: 12660144 MGI: J:84260
Park DS; Woodman SE; Schubert W; Cohen AW; Frank PG; Chandra M; Shirani J; Razani B; Tang B; Jelicks LA; Factor SM; Weiss LM; Tanowitz HB; Lisanti MP. 2002. Caveolin-1/3 double-knockout mice are viable, but lack both muscle and non-muscle caveolae, and develop a severe cardiomyopathic phenotype. Am J Pathol 160(6):2207-17PubMed: 12057923 MGI: J:77372
Razani B; Combs TP; Wang XB; Frank PG; Park DS; Russell RG; Li M; Tang B; Jelicks LA; Scherer PE; Lisanti MP. 2002. Caveolin-1-deficient Mice Are Lean, Resistant to Diet-induced Obesity, and Show Hypertriglyceridemia with Adipocyte Abnormalities. J Biol Chem 277(10):8635-47PubMed: 11739396 MGI: J:75192
Schubert W; Frank PG; Woodman SE; Hyogo H; Cohen DE; Chow CW; Lisanti MP. 2002. Microvascular hyperpermeability in caveolin-1 (-/-) knock-out mice. Treatment with a specific nitric-oxide synthase inhibitor, L-name, restores normal microvascular permeability in Cav-1 null mice. J Biol Chem 277(42):40091-8PubMed: 12167625 MGI: J:79595
Sheen MR; Fields JL; Northan B; Lacoste J; Ang LH; Fiering S; Iorns E; Tsui R; Denis A; Perfito N; Errington TM. 2019. Replication Study: Biomechanical remodeling of the microenvironment by stromal caveolin-1 favors tumor invasion and metastasis. Elife 8PubMed: 31845647 MGI: J:283644

Additional - Cav1^tm1Mls related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Cav1alternate1
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes. The donating investigator noted diminished reproductive performance as the backcross to C57BL/6J background progressed and backcrossed to a 129S6/SvEv background for 1 generation. The mice are now maintained as homozygotes and are primarily a mix of 129 and C57BL/6, but a minor contribution from the SJL background (contributed from the originating ES cell line) should not be discounted. Coat color expected from breeding: Black and Agouti.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the Cav-1 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #004585 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

FGB29 (Standard)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Homozygous for Cav1<tm1Mls>, 1 pair minimum

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Frozen Mouse Embryo	STOCK Cav1<tm1Mls>/J Frozen Embryos	$2595.00
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Frozen Mouse Embryo	STOCK Cav1<tm1Mls>/J Frozen Embryos	$3373.50
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:Cav-1 KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Cav1tm1Mls

Allele Symbol: Cav1tm1Mls

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Cav1tm1Mls related

Mammalian Phenotype Terms by Genotype

Genotype: Cav1tm1Mls/Cav1tm1Mlsinvolves: 129/Sv * C57BL/6J * SJL

adipose tissue phenotype

cardiovascular system phenotype

cellular phenotype

behavior/neurological phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

muscle phenotype

nervous system phenotype

skeleton phenotype

Genotype: Cav1tm1Mls/Cav1tm1Mlsinvolves: 129/Sv * C57BL/6 * FVB/N * SJL

endocrine/exocrine gland phenotype

neoplasm

integument phenotype

Genotype: Cav1tm1Mls/Cav1tm1MlsB6.Cg-Cav1

adipose tissue phenotype

homeostasis/metabolism phenotype

integument phenotype

reproductive system phenotype

respiratory system phenotype

cardiovascular system phenotype

cellular phenotype

endocrine/exocrine gland phenotype

Genotype: Cav1tm1Mls/Cav1tm1MlsB6.Cg-Cav1/J

cardiovascular system phenotype

cellular phenotype

homeostasis/metabolism phenotype

reproductive system phenotype

respiratory system phenotype

Genotype: Cav1tm1Mls/Cav1tm1MlsNot Specified

cardiovascular system phenotype

cellular phenotype

homeostasis/metabolism phenotype

nervous system phenotype

Genotype: Cav1tm1Mls/Cav1tm1MlsFVB.Cg-Cav1

adipose tissue phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

liver/biliary system phenotype

cellular phenotype

muscle phenotype

growth/size/body region phenotype

Genotype: Cav1tm1Mls/Cav1tm1Mlsinvolves: 129/Sv * C57BL/6 * SJL

adipose tissue phenotype

mammalian phenotype

mortality/aging

muscle phenotype

neoplasm

nervous system phenotype

respiratory system phenotype

skeleton phenotype

behavior/neurological phenotype

cardiovascular system phenotype

cellular phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Cav1^tm1Mls

Allele Symbol: Cav1^tm1Mls

Genotype: Cav1^tm1Mls related

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6J * SJL

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6 * FVB/N * SJL

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
B6.Cg-Cav1

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
B6.Cg-Cav1/J

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
Not Specified

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
FVB.Cg-Cav1

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
involves: 129/Sv * C57BL/6 * SJL

Genotype: Cav1^tm1Mls/Cav1^tm1Mls
STOCK Cav1/J

Additional - Cav1^tm1Mls related