JAX
Mouse Strain Datasheet - 006233
B6N.129S1-Casp3tm1Flv/J
Also Known As: CPP32-
Brain development in Casp3-deficient mice shows a variety of hyperplasias and disorganized cell deployment, and ovaries from female homozygotes show aberrant development. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development
Donating Investigator
Dr. Richard A. Flavell, Yale University School of Medicine
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N10+N2F4
|
Casp3tm1Flv
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Null/Knockout) | Casp3 | caspase 3 |
Research Applications
- Apoptosis Research
- Cardiovascular Research
- Developmental Biology Research
- Immunology, Inflammation and Autoimmunity Research
- Reproductive Biology Research
- Research Tools
- Sensorineural Research
Base Price
Starting at:
| $255.00 Domestic price for female |
| $329.00 Domestic price for breeder pair |
Detailed Description
On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development.
Development
A targeting vector was designed to replace the caspase protease-conserved catalytic site of the endogenous gene with a PGK-neo cassette. The construct was electroporated into 129S1/Sv-derived W9.5 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts, and the resulting chimeric males were bred to C57BL/6 females. Heterozygous mice were backcrossed to C57BL/6 mice for ten generations (see SNP results below) prior to sending females and males to The Jackson Laboratory Repository in 2006. Upon arrival, these females and males were used to establish our living mouse colony.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be C57BL/6N allele-type. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background, the living colony is on a C57BL/6N genetic background, and the sperm frozen in 2008 is on a C57BL/6N genetic background.
Control Suggestions
Selected References
- Kuida K; Zheng TS; Na S; Kuan C; Yang D; Karasuyama H; Rakic P; Flavell RA. 1996. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 384(6607):368-72. PubMed: 8934524MGI: J:36821
Casp3tm1Flv
Allele Symbol: Casp3tm1Flv
| Allele Name | targeted mutation 1, Richard Flavell |
|---|---|
| Allele Type | Targeted (Null/Knockout) |
| Allele Synonym(s) | CPP32-; Casp3-; caspase-3- |
| Gene Symbol and Name | Casp3, caspase 3 |
| Gene Synonym(s) | A830040C14Rik; A830040C14Rik; AC-3; Apopain; CC3; CPP32; CPP32-beta; CPP32B; Caspase-3; Lice; RIKEN cDNA A830040C14 gene; SCA-1; Yama; melody; mldy; mldy |
| Strain of Origin | 129S1/Sv-Oca2<+> Tyr<+> Kitl<+> |
| Chromosome | 8 |
| Molecular Note | A genomic fragment containing sequences encoding a conserved motif was replaced with a neomycin selection cassette. RT-PCR analysis on samples derived from brain and liver of homozygous mice demonstrated that no detectable transcript is produced from this allele. Western blot analysis on samples derived from thymocytes of homozygous mice confirmed that no detectable protein was produced. |
| Mutations Made By | Dr. Richard Flavell, Yale University School of Medicine |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Apoptosis Research
- Endogenous Regulators
- Cardiovascular Research
- Ischemia studies
- Developmental Biology Research
- Eye Defects
- Internal/Organ Defects
- ovary; uterus
- Immunology, Inflammation and Autoimmunity Research
- Intracellular Signaling Molecules
- Reproductive Biology Research
- Developmental Defects Affecting Gonads
- Research Tools
- Apoptosis Research
- Reproductive Biology Research
- Sensorineural Research
- Cataracts
- Eye Defects
- Hearing Defects
Mammalian Phenotype Terms by Genotype
Genotype: Casp3tm1Flv/Casp3+
B6.129S1-Casp3tm1Flv
hearing/vestibular/ear phenotype
- hearing/vestibular/ear phenotype
- hearing and cochlear morphology normal (MGI Ref ID J:68122)
Genotype: Casp3tm1Flv/Casp3tm1Flv
B6.129S1-Casp3tm1Flv
reproductive system phenotype
- abnormal granulosa cell morphology
- granulosa cells of atretic follicles are not eliminated by apoptosis and when cultured in the absence of serum fail to complete nuclear fragmentation after initial DNA condensation (MGI Ref ID J:70205)
- abnormal ovarian follicle morphology
- shrunken and disorganized atretic follicles lacking blood cell infiltration (MGI Ref ID J:70205)
- reproductive system phenotype
vision/eye phenotype
- abnormal lens development
- slight reduction in lysis of fluorogenic substrate DEVD-AMC in both the core and cortex of the lens (MGI Ref ID J:101037)
- abnormal lens epithelium morphology
- the epithelium at the anterior lens pole is multilayered and disorganized and the lens capsule above the opaque region has irregular folds (MGI Ref ID J:101037)
- cataract
- marked cataracts on the optic acis due to accumulation of epithelial cells at the anterior pole of the lens evident by the end of the first postnatal week, mature by 3 weeks of age, but most 6 month to 2 year old homozygotes no longer have cataracts (MGI Ref ID J:101037)
- vision/eye phenotype
- the size of the lens organelle free zone is normal (MGI Ref ID J:101037)
hearing/vestibular/ear phenotype
- abnormal auditory brainstem response waveform shape
- ABR analysis at 2 weeks of age shows atypical waves at all frequencies with sound pressures above 70 dB (MGI Ref ID J:68122)
- abnormal ear morphology
- (MGI Ref ID J:68122)
- abnormal organ of Corti morphology
- hyperplasia and stratified arrangement of border cells throughout all turns of the cochlea at 2 and 5 weeks of age (MGI Ref ID J:68122)
- the greater epithelial ridge persists at 2 weeks of age throughout all turns of the cochlea (MGI Ref ID J:68122)
- the tunnel of Corti and other pericellular spaces are collapsed at 5 weeks of age (MGI Ref ID J:68122)
- abnormal outer hair cell stereociliary bundle morphology
- (MGI Ref ID J:68122)
- cochlear degeneration
- (MGI Ref ID J:68122)
- cochlear inner hair cell degeneration
- at 5 weeks of age degeneration of inner hair cells is apparent with only 1 row of inner hair cells present in the apical to middle turn (MGI Ref ID J:68122)
- cochlear outer hair cell degeneration
- at 5 weeks of age degeneration of outer hair cells is apparent with only 3 rows of outer hair cells present in the apical to middle turn (MGI Ref ID J:68122)
- deafness
- (MGI Ref ID J:68122)
- fused outer hair cell stereocilia
- at 2 weeks of age there is fusion of stereocilia and at 5 weeks of age all outer hair cell stereocilia are fused at the tips to an unidentified V shaped object (MGI Ref ID J:68122)
- increased or absent threshold for auditory brainstem response
- at 5 weeks of age no significant waves are detected even at 100 dB (MGI Ref ID J:68122)
nervous system phenotype
- abnormal outer hair cell stereociliary bundle morphology
- (MGI Ref ID J:68122)
- cochlear ganglion degeneration
- at 5 weeks of age neurons are lost from the basal spiral ganglion (MGI Ref ID J:68122)
- cochlear inner hair cell degeneration
- at 5 weeks of age degeneration of inner hair cells is apparent with only 1 row of inner hair cells present in the apical to middle turn (MGI Ref ID J:68122)
- cochlear outer hair cell degeneration
- at 5 weeks of age degeneration of outer hair cells is apparent with only 3 rows of outer hair cells present in the apical to middle turn (MGI Ref ID J:68122)
- fused outer hair cell stereocilia
- at 2 weeks of age there is fusion of stereocilia and at 5 weeks of age all outer hair cell stereocilia are fused at the tips to an unidentified V shaped object (MGI Ref ID J:68122)
endocrine/exocrine gland phenotype
- abnormal granulosa cell morphology
- granulosa cells of atretic follicles are not eliminated by apoptosis and when cultured in the absence of serum fail to complete nuclear fragmentation after initial DNA condensation (MGI Ref ID J:70205)
- abnormal ovarian follicle morphology
- shrunken and disorganized atretic follicles lacking blood cell infiltration (MGI Ref ID J:70205)
cellular phenotype
- abnormal apoptosis
- hemorrhagic response and destruction of the hepatic enothelium and subsequent death in response to injection with anti-Fas antibody Jo2 are delayed at least 12 hours relative to that in wildtype mice and the apoptotic pathway aberrently involves activation, but not altered expression, of caspases 2, 6, and 7n, but not altered expression, of caspases 2, 6, and 7 (MGI Ref ID J:65496)
- decreased fibroblast apoptosis
- following UV irradiation and staurosporine treatment, mouse embryonic fibroblasts (MEFs) exhibit increased survival compared to wild type MEFs but not as much as Casp7tm1Flv MEFs (MGI Ref ID J:105496)
- decreased sensitivity to induced cell death
- mouse embryonic fibroblasts treated to initiate apoptosis fail to exhibit DNA fragmentation (MGI Ref ID J:105496)
Genotype: Casp3tm1Flv/Casp3tm1Flv
B6N.129S1-Casp3tm1Flv/J
cellular phenotype
- decreased keratinocyte apoptosis
- mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice (MGI Ref ID J:189241)
- increased cardiomyocyte apoptosis
- in mice treated with doxorubicin (MGI Ref ID J:189241)
- increased cellular sensitivity to ultraviolet irradiation
- mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice (MGI Ref ID J:189241)
- mice exposed to UV-B radiation exhibit increased cell death (apoptotic and necrosis-like combined) compared with wild-type mice (MGI Ref ID J:189241)
- mice exposed to UV-B radiation exhibit increased keratinocytes undergoing necrosis-like death compared with wild-type mice (MGI Ref ID J:189241)
- increased sensitivity to induced cell death
- in the cardiomyocytes of mice treated with doxorubicin (MGI Ref ID J:189241)
cardiovascular system phenotype
- increased cardiomyocyte apoptosis
- in mice treated with doxorubicin (MGI Ref ID J:189241)
integument phenotype
- abnormal keratinocyte physiology
- mice exposed to UV-B radiation exhibit increased keratinocytes undergoing necrosis-like death compared with wild-type mice (MGI Ref ID J:189241)
- decreased keratinocyte apoptosis
- mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice (MGI Ref ID J:189241)
muscle phenotype
- increased cardiomyocyte apoptosis
- in mice treated with doxorubicin (MGI Ref ID J:189241)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Casp3tm1Flv/Casp3+
involves: 129S1/Sv * C57BL/6J
craniofacial phenotype
- abnormal sagittal suture morphology
- incomplete closure of sagittal suture of anterior frontal bone at 7 weeks of age (MGI Ref ID J:94703)
- cranioschisis
- (MGI Ref ID J:94703)
skeleton phenotype
- abnormal bone ossification
- abnormal bone remodeling
- (MGI Ref ID J:94703)
- abnormal sagittal suture morphology
- incomplete closure of sagittal suture of anterior frontal bone at 7 weeks of age (MGI Ref ID J:94703)
- cranioschisis
- (MGI Ref ID J:94703)
- decreased bone mineral density
- decreased bone mineral density with age with onset beginning at 3 weeks of age (MGI Ref ID J:94703)
Genotype: Casp3tm1Flv/Casp3tm1Flv
involves: 129S1/Sv * C57BL/6
mortality/aging
- postnatal lethality, complete penetrance
- Background Sensitivity - animals surviving to birth die between 1-3 weeks of age (MGI Ref ID J:36821)
- prenatal lethality, incomplete penetrance
- incomplete penetrance with only 7% homozygous offspring from heterozygote x heterozygote breeders (MGI Ref ID J:36821)
hematopoietic system phenotype
- abnormal osteoclast physiology
- osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells (MGI Ref ID J:94703)
- decreased thymocyte number
- fewer total thymocytes at 2 weeks of age, however the spleen is histologically normal (MGI Ref ID J:36821)
immune system phenotype
- abnormal bone marrow development
- increased replicative senescence in bone marrow stromal stem cells from attenuated cell cycle (MGI Ref ID J:94703)
- abnormal osteoclast physiology
- osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells (MGI Ref ID J:94703)
- decreased thymocyte number
- fewer total thymocytes at 2 weeks of age, however the spleen is histologically normal (MGI Ref ID J:36821)
- immune system phenotype
- normal thymocyte expression patterns of CD4, CD8, CD25, CD69, and heat stable antigen (MGI Ref ID J:36821)
renal/urinary system phenotype
- renal/urinary system phenotype
- kidney is histologically normal (MGI Ref ID J:36821)
respiratory system phenotype
- respiratory system phenotype
- lung is histologically normal (MGI Ref ID J:36821)
reproductive system phenotype
- reproductive system phenotype
- testis is histologically normal (MGI Ref ID J:36821)
endocrine/exocrine gland phenotype
- decreased thymocyte number
- fewer total thymocytes at 2 weeks of age, however the spleen is histologically normal (MGI Ref ID J:36821)
growth/size/body region phenotype
- decreased body size
- smaller than littermates (MGI Ref ID J:36821)
vision/eye phenotype
- abnormal eye development
- delayed regression of vitreal vasculature (MGI Ref ID J:88367)
- abnormal eye morphology
- protrusions of the neuroepithelium in the retina, causing compression on the lens (MGI Ref ID J:36821)
- abnormal optic stalk morphology
- optic stalk contains fewer pyknotic cells and is much larger than in wild-type (MGI Ref ID J:36821)
- abnormal retina morphology
- abnormal retinal inner nuclear layer morphology
- delayed apoptotic kinetics result in thickened inner nuclear layer at 5 days of age which resolves after 13 days of age (MGI Ref ID J:88367)
- abnormal retinal pigment epithelium morphology
- absence of the retinal pigment epithelium in a region encircling the optic nerve (MGI Ref ID J:88367)
- microphthalmia
- eyes are 85% to 90% smaller than those of heterozygotes or wild-type (MGI Ref ID J:88367)
- vision/eye phenotype
- normal cell number and apoptotic kinetics within the retinal ganglion cell layer and normal width of the nerve fiber and plexiform layers (MGI Ref ID J:88367)
nervous system phenotype
- abnormal brain morphology
- abnormal brainstem morphology
- increase in cell number and density of the brainstem at E12 (MGI Ref ID J:36821)
- abnormal cerebellar granule layer morphology
- thickness of the internal granular layer is increased (MGI Ref ID J:36821)
- abnormal cerebellar molecular layer
- numerous spindle-shaped granule cells are seen traversing the molecular layer (MGI Ref ID J:36821)
- abnormal cerebellum development
- the germinal layer is thick and mitotically active at P16, at a time when it is normally absent, and spindle-shaped granule cells traverse the molecular layer (MGI Ref ID J:36821)
- abnormal cerebellum external granule cell layer morphology
- the germinal layer is thick and mitotically active at P16, at a time when it is normally absent (MGI Ref ID J:36821)
- abnormal diencephalon morphology
- thicker diencephalic wall with supernumerary cell masses is seen at E12 (MGI Ref ID J:36821)
- abnormal forebrain morphology
- ectopic cell masses are found between the cerebral cortex, the hippocampus and the striatum (MGI Ref ID J:36821)
- hydroencephaly
- diencephalic lumen is frequently obstructed at E17 (MGI Ref ID J:36821)
- nervous system phenotype
- normal cell number and apoptotic kinetics within the retinal ganglion cell layer and normal width of the nerve fiber and plexiform layers (MGI Ref ID J:88367)
skeleton phenotype
- abnormal bone ossification
- abnormal osteoclast physiology
- osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells (MGI Ref ID J:94703)
- abnormal sagittal suture morphology
- open sagittal suture of anterior frontal bone at 7 weeks of age (MGI Ref ID J:94703)
- abnormal skeleton development
- skeleton is smaller than normal at 1 week of age (MGI Ref ID J:94703)
- cranioschisis
- either completely open sagittal suture or incomplete closure at 7 weeks of age (MGI Ref ID J:94703)
- decreased trabecular bone thickness
- (MGI Ref ID J:94703)
- delayed bone ossification
- evident at E14.5 in skull, metacarpi, phalanges, and sternum and at E17.5 in interparietal bones and metatarsi (MGI Ref ID J:94703)
craniofacial phenotype
- abnormal sagittal suture morphology
- open sagittal suture of anterior frontal bone at 7 weeks of age (MGI Ref ID J:94703)
- cranioschisis
- either completely open sagittal suture or incomplete closure at 7 weeks of age (MGI Ref ID J:94703)
cardiovascular system phenotype
- abnormal blood vessel morphology
- delayed regression of vitreal vasculature, however the heart is histologically normal (MGI Ref ID J:88367)
pigmentation phenotype
- abnormal retinal pigment epithelium morphology
- absence of the retinal pigment epithelium in a region encircling the optic nerve (MGI Ref ID J:88367)
cellular phenotype
- cellular phenotype
References
- Kuida K; Zheng TS; Na S; Kuan C; Yang D; Karasuyama H; Rakic P; Flavell RA. 1996. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 384(6607):368-72. PubMed: 8934524MGI: J:36821
Additional - Casp3tm1Flv related
- Akhter A; Gavrilin MA; Frantz L; Washington S; Ditty C; Limoli D; Day C; Sarkar A; Newland C; Butchar J; Marsh CB; Wewers MD; Tridandapani S; Kanneganti TD; Amer AO. 2009. Caspase-7 activation by the Nlrc4/Ipaf inflammasome restricts Legionella pneumophila infection. PLoS Pathog 5(4):e1000361. PubMed: 19343209MGI: J:162695
- Amin S; Matalova E; Simpson C; Yoshida H; Tucker AS. 2007. Incudomalleal joint formation: the roles of apoptosis, migration and downregulation. BMC Dev Biol 7:134. PubMed: 18053235MGI: J:132300
- Carambula SF; Matikainen T; Lynch MP; Flavell RA; Goncalves PB; Tilly JL; Rueda BR. 2002. Caspase-3 is a pivotal mediator of apoptosis during regression of the ovarian corpus luteum. Endocrinology 143(4):1495-501. PubMed: 11897708MGI: J:109249
- Carambula SF; Pru JK; Lynch MP; Matikainen T; Goncalves PB; Flavell RA; Tilly JL; Rueda BR. 2003. Prostaglandin F2alpha- and FAS-activating antibody-induced regression of the corpus luteum involves caspase-8 and is defective in caspase-3 deficient mice. Reprod Biol Endocrinol 1:15. PubMed: 12657159MGI: J:102441
- D'Sa-Eipper C; Leonard JR; Putcha G; Zheng TS; Flavell RA; Rakic P; Kuida K; Roth KA. 2001. DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3. Development 128(1):137-46. PubMed: 11092819MGI: J:115386
- Delhase M; Kim SY; Lee H; Naiki-Ito A; Chen Y; Ahn ER; Murata K; Kim SJ; Lautsch N; Kobayashi KS; Shirai T; Karin M; Nakanishi M. 2011. TANK-binding kinase 1 (TBK1) controls cell survival through PAI-2/serpinB2 and transglutaminase 2. Proc Natl Acad Sci U S A :. PubMed: 22203995MGI: J:179973
- Fujita E; Egashira J; Urase K; Kuida K; Momoi T. 2001. Caspase-9 processing by caspase-3 via a feedback amplification loop in vivo. Cell Death Differ 8(4):335-44. PubMed: 11550085MGI: J:115634
- Gibon J; Unsain N; Gamache K; Thomas RA; De Leon A; Johnstone A; Nader K; Seguela P; Barker PA. 2016. The X-linked inhibitor of apoptosis regulates long-term depression and learning rate. FASEB J 30(9):3083-90. PubMed: 27189977MGI: J:239645
- Guo YH; Hernandez I; Isermann B; Kang TB; Medved L; Sood R; Kerschen EJ; Holyst T; Mosesson MW; Weiler H. 2009. Caveolin-1-dependent apoptosis induced by fibrin degradation products. Blood 113(18):4431-9. PubMed: 19074731MGI: J:148438
- Jiao S; Li Z. 2011. Nonapoptotic function of BAD and BAX in long-term depression of synaptic transmission. Neuron 70(4):758-72. PubMed: 21609830MGI: J:174982
- Jo J; Whitcomb DJ; Olsen KM; Kerrigan TL; Lo SC; Bru-Mercier G; Dickinson B; Scullion S; Sheng M; Collingridge G; Cho K. 2011. Abeta(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3beta. Nat Neurosci 14(5):545-7. PubMed: 21441921MGI: J:172292
- Josefsson EC; Burnett DL; Lebois M; Debrincat MA; White MJ; Henley KJ; Lane RM; Moujalled D; Preston SP; O'Reilly LA; Pellegrini M; Metcalf D; Strasser A; Kile BT. 2014. Platelet production proceeds independently of the intrinsic and extrinsic apoptosis pathways. Nat Commun 5:3455. PubMed: 24632563MGI: J:210320
- Kang SJ; Wang S; Kuida K; Yuan J. 2002. Distinct downstream pathways of caspase-11 in regulating apoptosis and cytokine maturation during septic shock response. Cell Death Differ 9(10):1115-25. PubMed: 12232800MGI: J:115554
- Khalil H; Peltzer N; Walicki J; Yang JY; Dubuis G; Gardiol N; Held W; Bigliardi P; Marsland B; Liaudet L; Widmann C. 2012. Caspase-3 Protects Stressed Organs against Cell Death. Mol Cell Biol 32(22):4523-33. PubMed: 22949508MGI: J:189241
- Kirkland RA; Saavedra GM; Cummings BS; Franklin JL. 2010. Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases. J Neurosci 30(48):16114-27. PubMed: 21123558MGI: J:166748
- Koenig A; Fortner KA; King BR; Madden J; Buskiewicz IA; Budd RC. 2012. Proliferating gammadelta T cells manifest high and spatially confined caspase-3 activity. Immunology 135(4):276-86. PubMed: 22117649MGI: J:184101
- Koike M; Shibata M; Tadakoshi M; Gotoh K; Komatsu M; Waguri S; Kawahara N; Kuida K; Nagata S; Kominami E; Tanaka K; Uchiyama Y. 2008. Inhibition of autophagy prevents hippocampal pyramidal neuron death after hypoxic-ischemic injury. Am J Pathol 172(2):454-69. PubMed: 18187572MGI: J:131320
- Lakhani SA; Masud A; Kuida K; Porter GA Jr; Booth CJ; Mehal WZ; Inayat I; Flavell RA. 2006. Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311(5762):847-51. PubMed: 16469926MGI: J:105496
- Lamkanfi M; Moreira LO; Makena P; Spierings DC; Boyd K; Murray PJ; Green DR; Kanneganti TD. 2009. Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. Blood 113(12):2742-5. PubMed: 19168786MGI: J:146876
- Le DA; Wu Y; Huang Z; Matsushita K; Plesnila N; Augustinack JC; Hyman BT; Yuan J; Kuida K; Flavell RA; Moskowitz MA. 2002. Caspase activation and neuroprotection in caspase-3- deficient mice after in vivo cerebral ischemia and in vitro oxygen glucose deprivation. Proc Natl Acad Sci U S A 99(23):15188-93. PubMed: 12415117MGI: J:126184
- Leonard JR; Klocke BJ; D'Sa C; Flavell RA; Roth KA. 2002. Strain-dependent neurodevelopmental abnormalities in caspase-3-deficient mice. J Neuropathol Exp Neurol 61(8):673-7. PubMed: 12152782MGI: J:104966
- Li F; He Z; Shen J; Huang Q; Li W; Liu X; He Y; Wolf F; Li CY. 2010. Apoptotic caspases regulate induction of iPSCs from human fibroblasts. Cell Stem Cell 7(4):508-20. PubMed: 20887956MGI: J:165654
- Li Z; Jo J; Jia JM; Lo SC; Whitcomb DJ; Jiao S; Cho K; Sheng M. 2010. Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization. Cell 141(5):859-71. PubMed: 20510932MGI: J:167946
- Lin L; Ye Y; Zakeri Z. 2006. p53, Apaf-1, caspase-3, and -9 are dispensable for Cdk5 activation during cell death. Cell Death Differ 13(1):141-50. PubMed: 16021178MGI: J:121028
- Liu F; Cheng G; Hamard PJ; Greenblatt S; Wang L; Man N; Perna F; Xu H; Tadi M; Luciani L; Nimer SD. 2015. Arginine methyltransferase PRMT5 is essential for sustaining normal adult hematopoiesis. J Clin Invest 125(9):3532-44. PubMed: 26258414MGI: J:226257
- Lo SC; Wang Y; Weber M; Larson JL; Scearce-Levie K; Sheng M. 2015. Caspase-3 deficiency results in disrupted synaptic homeostasis and impaired attention control. J Neurosci 35(5):2118-32. PubMed: 25653368MGI: J:219897
- Man SM; Zhu Q; Zhu L; Liu Z; Karki R; Malik A; Sharma D; Li L; Malireddi RK; Gurung P; Neale G; Olsen SR; Carter RA; McGoldrick DJ; Wu G; Finkelstein D; Vogel P; Gilbertson RJ; Kanneganti TD. 2015. Critical Role for the DNA Sensor AIM2 in Stem Cell Proliferation and Cancer. Cell 162(1):45-58. PubMed: 26095253MGI: J:224547
- Massa V; Savery D; Ybot-Gonzalez P; Ferraro E; Rongvaux A; Cecconi F; Flavell R; Greene ND; Copp AJ. 2009. Apoptosis is not required for mammalian neural tube closure. Proc Natl Acad Sci U S A 106(20):8233-8. PubMed: 19420217MGI: J:148528
- Matalova E; Sharpe PT; Lakhani SA; Roth KA; Flavell RA; Setkova J; Misek I; Tucker AS. 2006. Molar tooth development in caspase-3 deficient mice. Int J Dev Biol 50(5):491-7. PubMed: 16586350MGI: J:109513
- Matikainen T; Perez GI; Zheng TS; Kluzak TR; Rueda BR; Flavell RA; Tilly JL. 2001. Caspase-3 gene knockout defines cell lineage specificity for programmed cell death signaling in the ovary. Endocrinology 142(6):2468-80. PubMed: 11356696MGI: J:70205
- Miura M; Chen XD; Allen MR; Bi Y; Gronthos S; Seo BM; Lakhani S; Flavell RA; Feng XH; Robey PG; Young M; Shi S. 2004. A crucial role of caspase-3 in osteogenic differentiation of bone marrow stromal stem cells. J Clin Invest 114(12):1704-13. PubMed: 15599395MGI: J:94703
- Nogueira CV; Lindsten T; Jamieson AM; Case CL; Shin S; Thompson CB; Roy CR. 2009. Rapid pathogen-induced apoptosis: a mechanism used by dendritic cells to limit intracellular replication of Legionella pneumophila. PLoS Pathog 5(6):e1000478. PubMed: 19521510MGI: J:211458
- Oppenheim RW; Flavell RA; Vinsant S; Prevette D; Kuan CY; Rakic P. 2001. Programmed cell death of developing mammalian neurons after genetic deletion of caspases. J Neurosci 21(13):4752-60. PubMed: 11425902MGI: J:70079
- Park E; Kim Y; Noh H; Lee H; Yoo S; Park S. 2013. EphA/ephrin-A signaling is critically involved in region-specific apoptosis during early brain development. Cell Death Differ 20(1):169-80. PubMed: 22976838MGI: J:205629
- Parker A; Hardisty-Hughes RE; Wisby L; Joyce S; Brown SD. 2010. Melody, an ENU mutation in Caspase 3, alters the catalytic cysteine residue and causes sensorineural hearing loss in mice. Mamm Genome 21(11-12):565-76. PubMed: 21116635MGI: J:166750
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