JAX Mouse Strain Datasheet - 004374

129-Npr1^tm1Gar/J

Stock No:: 004374 |; GC-A KO

Targeted Mutation

Cryo Recovery

Overview

Also Known As: GC-A KO

These Npr1 knock-out mice exhibit elevated systolic, diastolic and mean blood pressure.

Donating Investigator

David L. Garbers, U.T. Southwestern Medical Center

Genetic overview

Genetic Background	Generation

Npr1^tm1Gar

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Npr1	natriuretic peptide receptor 1

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Research Applications

Cardiovascular Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) was detected. Homozygous mutant mice have elevated systolic, diastolic and mean blood pressure when compared to wildtype. Heterozygous mutant mice display systolic, diastolic and mean blood pressure that are slightly elevated above wildtype levels. Blood pressure in mutant mice remains elevated independent of salt content in diet. Infusion treatment of atrial natriuretic peptide in mutant mice does not result in the increased urine output or sodium excretion response seen in wildtype mice. Plasma volume expansion to release natriuretic/diuretic factors from the heart fails to induce increased urine output, sodium excretion and cyclic GMP excretion in the mutant. The same plasma volume expansion in wildtype mice results in a 12-fold increase in urine output, a 6-fold increase in sodium excretion and a 4-fold increase in cyclic GMP excretion in the urine. Mutant mice excrete only 30% of the normal level of urinary cyclic GMP. The Donating Investigator reports this mutant strain also exhibits cardiac hypertrophy and cardiac fibrosis. The phenotype of this mutant strain, salt insensitive hypertension, resembles that of half of all human patients with essential hypertension. This mutant mouse strain represents a model that may be useful in studies related to essential hypertension.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 4 of the targeted gene. The construct was electroporated into 129S7/SvEvBrd-Hprt⁺ derived AB-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts.

Control Suggestions

002448 129S1/SvImJ

Additional Information

Considerations for Choosing Controls

Selected References

Lopez MJ; Wong SK; Kishimoto I; Dubois S; Mach V; Friesen J; Garbers DL; Beuve A. 1995. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide. Nature 378(6552):65-8. PubMed: 7477288 MGI: J:30007

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Genetics

Npr1^tm1Gar

Allele Symbol: Npr1^tm1Gar

Allele Name	targeted mutation 1, David L Garbers
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	GC-A KO; GC-A^-
Gene Symbol and Name	Npr1, natriuretic peptide receptor 1
Gene Synonym(s)	AI893888; ANPRA; ANPa; Anpra; GC-A; GUC2A; GUCY2A; Gca; NPR-A; NPRA; Npra; Pndr; expressed sequence AI893888; guanylyl cyclase-A
Strain of Origin	129S7/SvEvBrd-Hprt<+>
Chromosome	3
Molecular Note	Insertion of a neomycin resistance cassette into exon 4, which encodes part of the extra-cellular putative ligand-binding domain, disrupted the gene. Stable, wild-type size transcript was not detected in liver or kidney from homozygous mutant mice.
Mutations Made By	David Garbers, U.T. Southwestern Medical Center

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Npr1^tm1Gar related

Cardiovascular Research
- Heart Abnormalities
- Hypertension

Mammalian Phenotype Terms by Genotype

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

Genotype: Npr1^tm1Gar/Npr1⁺
involves: 129S7/SvEvBrd * C57BL/6J

cardiovascular system phenotype

increased systemic arterial blood pressure
- on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 7.7 mm Hg increase in mean blood pressure relative to wild-type mice; no significant changes in heart rates are observed

increased systemic arterial diastolic blood pressure
- on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 5.9 mm Hg increase in diastolic blood pressure relative to wild-type mice

increased systemic arterial systolic blood pressure
- on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 10.5 mm Hg increase in systolic blood pressure relative to wild-type mice

salt-resistant hypertension
- a high (8% NaCl) salt diet fails to change hematocrit or body weight, suggesting the possibility of increased natriuresis; no differences in aldosterone and atrial natriuretic peptide concentrations are observed
- heterozygotes display salt-resistant hypertension: on a low (0.008% NaCl), normal (0.7% NaCl) and high (8% NaCl) salt diet, their blood pressures and heart rates remain unchanged

Genotype: Npr1^tm1Gar/Npr1^tm1Gar
B6.129S7-Npr1^tm1Gar

cardiovascular system phenotype

decreased myocardial infarction size
- at 2 days after myocardial ischemia/reperfusion, homozygotes exhibit a 20% reduction in myocardial infarct size relative to wild-type mice
- reduced infarct size is associated with concomitant reductions in PMN infiltration, coronary endothelial cell expression of P-selectin, and activation of NF-kappaB

immune system phenotype

impaired neutrophil chemotaxis
- in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice
- reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice

homeostasis/metabolism phenotype

decreased myocardial infarction size
- at 2 days after myocardial ischemia/reperfusion, homozygotes exhibit a 20% reduction in myocardial infarct size relative to wild-type mice
- reduced infarct size is associated with concomitant reductions in PMN infiltration, coronary endothelial cell expression of P-selectin, and activation of NF-kappaB

cellular phenotype

impaired neutrophil chemotaxis
- in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice
- reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice

hematopoietic system phenotype

impaired neutrophil chemotaxis
- in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice
- reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice

Genotype: Npr1^tm1Gar/Npr1^tm1Gar
involves: 129S7/SvEvBrd * C57BL/6J

mortality/aging

mortality/aging
- at 3 weeks, homozygotes are slightly (but significantly) underrepresented, at least partly due to the presence of hydrops fetalis in 10% of mutant embryos; however, stage of lethality is not speficied
- no histological abnormalities are detected in heart, vasculature or kidneys at less than 5 months of age

cardiovascular system phenotype

abnormal systemic arterial blood pressure
- CNP evoked a significant reduction in BP at much higher infusion rates (50 g/kg/min), resulting in a plasma concentration of 18.3 nM, with no significant differences between wild-type and mutant mice
- in wild-type mice, ANP evoked a significant reduction in BP at 500 ng/kg/min, a rate which resulted in a plasma concentration of 0.8 nM; in contrast, ANP failed to lower BP in mutant mice even at infusion rates of 50 g/kg/min

abnormal vasodilation
- atrial natriuretic peptide (ANP) or B-type natriuretic peptide (BNP) half-maximally relaxed KCl-precontracted aortic rings in wild-type mice at ~24 nM, but failed to relax aortas in mutant mice, even at micromolar concentrations
- in contrast, C-type natriuretic peptide (CNP) caused half-maximal relaxation at 335 and 146 nM in aortas from either wild-type or null mice, respectively (no significant difference)

increased systemic arterial blood pressure
- on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 19.7 mm Hg increase in mean blood pressure relative to wild-type mice; no significant changes in heart rates are observed

increased systemic arterial diastolic blood pressure
- on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 15.3 mm Hg increase in diastolic blood pressure relative to wild-type mice

increased systemic arterial systolic blood pressure
- on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 27.4 mm Hg increase in systolic blood pressure relative to wild-type mice

salt-resistant hypertension
- a high (8% NaCl) salt diet fails to change hematocrit or body weight, suggesting the possibility of increased natriuresis; no differences in aldosterone and atrial natriuretic peptide concentrations are observed
- homozygotes display salt-resistant hypertension: on a low (0.008% NaCl), normal (0.7% NaCl) and high (8% NaCl) salt diet, their blood pressures and heart rates remain unchanged

homeostasis/metabolism phenotype

hydrops fetalis
- ~10% of homozygotes exhibit hydrops fetalis

increased circulating atrial natriuretic factor
- homozygous mutant mice exhibit increased basal concentrations of ANP relative to wild-type mice (~279 109 pM vs ~159 111 pM, respectively)
- in contrast, basal concentrations of circulating CNP are below the detectable limit in both wild-type and mutant mice

muscle phenotype

abnormal vasodilation
- atrial natriuretic peptide (ANP) or B-type natriuretic peptide (BNP) half-maximally relaxed KCl-precontracted aortic rings in wild-type mice at ~24 nM, but failed to relax aortas in mutant mice, even at micromolar concentrations
- in contrast, C-type natriuretic peptide (CNP) caused half-maximal relaxation at 335 and 146 nM in aortas from either wild-type or null mice, respectively (no significant difference)

References

Lopez MJ; Wong SK; Kishimoto I; Dubois S; Mach V; Friesen J; Garbers DL; Beuve A. 1995. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide. Nature 378(6552):65-8. PubMed: 7477288 MGI: J:30007

Additional - Npr1^tm1Gar related

Chen S; Grigsby CL; Law CS; Ni X; Nekrep N; Olsen K; Humphreys MH; Gardner DG. 2009. Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents. J Clin Invest 119(6):1647-58. PubMed: 19436108 MGI: J:150581
Chusho H; Ogawa Y; Tamura N; Suda M; Yasoda A; Miyazawa T; Kishimoto I; Komatsu Y; Itoh H; Tanaka K; Saito Y; Garbers DL; Nakao K. 2000. Genetic models reveal that brain natriuretic peptide can signal through different tissue-specific receptor-mediated pathways. Endocrinology 141(10):3807-13. PubMed: 11014237 MGI: J:108806
Demerath T; Staffel J; Schreiber A; Valletta D; Schweda F. 2014. Natriuretic peptides buffer renin-dependent hypertension. Am J Physiol Renal Physiol 306(12):F1489-98. PubMed: 24717731 MGI: J:210961
Dubois SK; Kishimoto I; Lillis TO; Garbers DL. 2000. A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function. Proc Natl Acad Sci U S A 97(8):4369-73. PubMed: 10760303 MGI: J:126140
Hunt LM; Hogeland EW; Henry MK; Swoap SJ. 2004. Hypotension and bradycardia during caloric restriction in mice are independent of salt balance and do not require ANP receptor. Am J Physiol Heart Circ Physiol 287(4):H1446-51. PubMed: 15191892 MGI: J:95588
Izumi T; Saito Y; Kishimoto I; Harada M; Kuwahara K; Hamanaka I; Takahashi N; Kawakami R; Li Y; Takemura G; Fujiwara H; Garbers DL; Mochizuki S; Nakao K. 2001. Blockade of the natriuretic peptide receptor guanylyl cyclase-A inhibits NF-kappaB activation and alleviates myocardial ischemia/reperfusion injury. J Clin Invest 108(2):203-13. PubMed: 11457873 MGI: J:70496
Kilic A; Velic A; De Windt LJ; Fabritz L; Voss M; Mitko D; Zwiener M; Baba HA; van Eickels M; Schlatter E; Kuhn M. 2005. Enhanced activity of the myocardial Na+/H+ exchanger NHE-1 contributes to cardiac remodeling in atrial natriuretic peptide receptor-deficient mice. Circulation 112(15):2307-17. PubMed: 16216978 MGI: J:116814
Kinoshita H; Kuwahara K; Nishida M; Jian Z; Rong X; Kiyonaka S; Kuwabara Y; Kurose H; Inoue R; Mori Y; Li Y; Nakagawa Y; Usami S; Fujiwara M; Yamada Y; Minami T; Ueshima K; Nakao K. 2010. Inhibition of TRPC6 channel activity contributes to the antihypertrophic effects of natriuretic peptides-guanylyl cyclase-A signaling in the heart. Circ Res 106(12):1849-60. PubMed: 20448219 MGI: J:175052
Kirchhof P; Fabritz L; Kilic A; Begrow F; Breithardt G; Kuhn M. 2004. Ventricular arrhythmias, increased cardiac calmodulin kinase II expression, and altered repolarization kinetics in ANP receptor deficient mice. J Mol Cell Cardiol 36(5):691-700. PubMed: 15135664 MGI: J:102133
Kong X; Wang X; Xu W; Behera S; Hellermann G; Kumar A; Lockey RF; Mohapatra S; Mohapatra SS. 2008. Natriuretic peptide receptor a as a novel anticancer target. Cancer Res 68(1):249-56. PubMed: 18172317 MGI: J:131033
Kuhn M; Volker K; Schwarz K; Carbajo-Lozoya J; Flogel U; Jacoby C; Stypmann J; van Eickels M; Gambaryan S; Hartmann M; Werner M; Wieland T; Schrader J; Baba HA. 2009. The natriuretic peptide/guanylyl cyclase--a system functions as a stress-responsive regulator of angiogenesis in mice. J Clin Invest 119(7):2019-30. PubMed: 19487812 MGI: J:152580
Li Y; Kishimoto I; Saito Y; Harada M; Kuwahara K; Izumi T; Hamanaka I; Takahashi N; Kawakami R; Tanimoto K; Nakagawa Y; Nakanishi M; Adachi Y; Garbers DL; Fukamizu A; Nakao K. 2004. Androgen contributes to gender-related cardiac hypertrophy and fibrosis in mice lacking the gene encoding guanylyl cyclase-A. Endocrinology 145(2):951-8. PubMed: 14592959 MGI: J:88703
Li Y; Kishimoto I; Saito Y; Harada M; Kuwahara K; Izumi T; Takahashi N; Kawakami R; Tanimoto K; Nakagawa Y; Nakanishi M; Adachi Y; Garbers DL; Fukamizu A; Nakao K. 2002. Guanylyl cyclase-A inhibits angiotensin II type 1A receptor-mediated cardiac remodeling, an endogenous protective mechanism in the heart. Circulation 106(13):1722-8. PubMed: 12270869 MGI: J:103221
Li Y; Saito Y; Kuwahara K; Rong X; Kishimoto I; Harada M; Adachi Y; Nakanishi M; Kinoshita H; Horiuchi M; Murray M; Nakao K. 2009. Guanylyl cyclase-A inhibits angiotensin II type 2 receptor-mediated pro-hypertrophic signaling in the heart. Endocrinology 150(8):3759-65. PubMed: 19372206 MGI: J:158158
Lopez MJ; Garbers DL; Kuhn M. 1997. The guanylyl cyclase-deficient mouse defines differential pathways of natriuretic peptide signaling. J Biol Chem 272(37):23064-8. PubMed: 9287305 MGI: J:42893
Madhani M; Hall AR; Cuello F; Charles RL; Burgoyne JR; Fuller W; Hobbs AJ; Shattock MJ; Eaton P. 2010. Phospholemman Ser69 phosphorylation contributes to sildenafil-induced cardioprotection against reperfusion injury. Am J Physiol Heart Circ Physiol 299(3):H827-36. PubMed: 20543084 MGI: J:164509
Miyashita K; Itoh H; Tsujimoto H; Tamura N; Fukunaga Y; Sone M; Yamahara K; Taura D; Inuzuka M; Sonoyama T; Nakao K. 2009. Natriuretic peptides/cGMP/cGMP-dependent protein kinase cascades promote muscle mitochondrial biogenesis and prevent obesity. Diabetes 58(12):2880-92. PubMed: 19690065 MGI: J:158488
Nakanishi M; Saito Y; Kishimoto I; Harada M; Kuwahara K; Takahashi N; Kawakami R; Nakagawa Y; Tanimoto K; Yasuno S; Usami S; Li Y; Adachi Y; Fukamizu A; Garbers DL; Nakao K. 2005. Role of natriuretic peptide receptor guanylyl cyclase-A in myocardial infarction evaluated using genetically engineered mice. Hypertension 46(2):441-7. PubMed: 15998711 MGI: J:114365
Ropero AB; Soriano S; Tuduri E; Marroqui L; Tellez N; Gassner B; Juan-Pico P; Montanya E; Quesada I; Kuhn M; Nadal A. 2010. The atrial natriuretic peptide and guanylyl cyclase-A system modulates pancreatic beta-cell function. Endocrinology 151(8):3665-74. PubMed: 20555029 MGI: J:168515
Sasaki H; Nagayama T; Blanton RM; Seo K; Zhang M; Zhu G; Lee DI; Bedja D; Hsu S; Tsukamoto O; Takashima S; Kitakaze M; Mendelsohn ME; Karas RH; Kass DA; Takimoto E. 2014. PDE5 inhibitor efficacy is estrogen dependent in female heart disease. J Clin Invest 124(6):2464-71. PubMed: 24837433 MGI: J:213223
Schreier B; Borner S; Volker K; Gambaryan S; Schafer SC; Kuhlencordt P; Gassner B; Kuhn M. 2008. The heart communicates with the endothelium through the guanylyl cyclase-A receptor: acute handling of intravascular volume in response to volume expansion. Endocrinology 149(8):4193-9. PubMed: 18450968 MGI: J:145509
Soriano S; Ropero AB; Alonso-Magdalena P; Ripoll C; Quesada I; Gassner B; Kuhn M; Gustafsson JA; Nadal A. 2009. Rapid regulation of K(ATP) channel activity by 17{beta}-estradiol in pancreatic {beta}-cells involves the estrogen receptor {beta} and the atrial natriuretic peptide receptor. Mol Endocrinol 23(12):1973-82. PubMed: 19855088 MGI: J:154658
Steinmetz M; Potthast R; Sabrane K; Kuhn M. 2004. Diverging vasorelaxing effects of C-type natriuretic peptide in renal resistance arteries and aortas of GC-A-deficient mice. Regul Pept 119(1-2):31-7. PubMed: 15093694 MGI: J:102436
Tokudome T; Horio T; Kishimoto I; Soeki T; Mori K; Kawano Y; Kohno M; Garbers DL; Nakao K; Kangawa K. 2005. Calcineurin-nuclear factor of activated T cells pathway-dependent cardiac remodeling in mice deficient in guanylyl cyclase A, a receptor for atrial and brain natriuretic peptides. Circulation 111(23):3095-104. PubMed: 15939815 MGI: J:112245
Tokudome T; Kishimoto I; Horio T; Arai Y; Schwenke DO; Hino J; Okano I; Kawano Y; Kohno M; Miyazato M; Nakao K; Kangawa K. 2008. Regulator of G-protein signaling subtype 4 mediates antihypertrophic effect of locally secreted natriuretic peptides in the heart. Circulation 117(18):2329-39. PubMed: 18443239 MGI: J:155088
Tokudome T; Kishimoto I; Shindo T; Kawakami H; Koyama T; Otani K; Nishimura H; Miyazato M; Kohno M; Nakao K; Kangawa K. 2016. Importance of Endogenous Atrial and Brain Natriuretic Peptides in Murine Embryonic Vascular and Organ Development. Endocrinology 157(1):358-67. PubMed: 26517044 MGI: J:233635
Tokudome T; Kishimoto I; Yamahara K; Osaki T; Minamino N; Horio T; Sawai K; Kawano Y; Miyazato M; Sata M; Kohno M; Nakao K; Kangawa K. 2009. Impaired recovery of blood flow after hind-limb ischemia in mice lacking guanylyl cyclase-A, a receptor for atrial and brain natriuretic peptides. Arterioscler Thromb Vasc Biol 29(10):1516-21. PubMed: 19628785 MGI: J:167805
Yasuno S; Usami S; Kuwahara K; Nakanishi M; Arai Y; Kinoshita H; Nakagawa Y; Fujiwara M; Murakami M; Ueshima K; Harada M; Nakao K. 2009. Endogenous cardiac natriuretic peptides protect the heart in a mouse model of dilated cardiomyopathy and sudden death. Am J Physiol Heart Circ Physiol 296(6):H1804-10. PubMed: 19346456 MGI: J:150878
Zhao L; Long L; Morrell NW; Wilkins MR. 1999. NPR-A-Deficient mice show increased susceptibility to hypoxia-induced pulmonary hypertension. Circulation 99(5):605-7. PubMed: 9950655 MGI: J:53666

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Also Known As: GC-A KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Npr1tm1Gar

Allele Symbol: Npr1tm1Gar

Disease Terms

Research Areas By Genotype

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

Genotype: Npr1tm1Gar related

Mammalian Phenotype Terms by Genotype

Genotype: Npr1tm1Gar/Npr1+involves: 129S7/SvEvBrd * C57BL/6J

cardiovascular system phenotype

Genotype: Npr1tm1Gar/Npr1tm1GarB6.129S7-Npr1tm1Gar

cardiovascular system phenotype

immune system phenotype

homeostasis/metabolism phenotype

cellular phenotype

hematopoietic system phenotype

Genotype: Npr1tm1Gar/Npr1tm1Garinvolves: 129S7/SvEvBrd * C57BL/6J

mortality/aging

cardiovascular system phenotype

homeostasis/metabolism phenotype

muscle phenotype

References

Additional - Npr1tm1Gar related

Genotyping Protocols

Breeding Considerations

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

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The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Npr1^tm1Gar

Allele Symbol: Npr1^tm1Gar

Genotype: Npr1^tm1Gar related

Genotype: Npr1^tm1Gar/Npr1⁺
involves: 129S7/SvEvBrd * C57BL/6J

Genotype: Npr1^tm1Gar/Npr1^tm1Gar
B6.129S7-Npr1^tm1Gar

Genotype: Npr1^tm1Gar/Npr1^tm1Gar
involves: 129S7/SvEvBrd * C57BL/6J

Additional - Npr1^tm1Gar related