- decreased bone mineral density / MGI
- abnormal kidney cortex morphology / MGI
- kidney cortex cysts / MGI
- abnormal kidney development / MGI
- premature death / MGI
- abnormal kidney morphology / MGI
- abnormal kidney physiology / MGI
- abnormal renal tubule morphology / MGI
- dilated renal tubules / MGI
- abnormal Leydig cell morphology / MGI
- abnormal juxtaglomerular apparatus morphology / MGI
- abnormal nephron morphology / MGI
- abnormal proximal convoluted tubule morphology / MGI
- abnormal renal glomerulus morphology / MGI
- renal/urinary system phenotype / MGI
- homeostasis/metabolism phenotype / MGI
- cardiovascular system phenotype / MGI
- behavior/neurological phenotype / MGI
- increased circulating creatinine level / MGI
- increased blood urea nitrogen level / MGI
- decreased blood urea nitrogen level / MGI
- abnormal renal tubule epithelium morphology / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- postnatal lethality, incomplete penetrance / MGI
- abnormal juxtaglomerular cell morphology / MGI
- abnormal glomerular capillary morphology / MGI
- abnormal kidney medullary ray morphology / MGI
- increased glomerular capsule space / MGI
- abnormal mitochondrial chromosome morphology / MGI
- decreased urine nitrite level / MGI
B6;129S7-Bdkrb2tm1Jfh/Cnrm
Status | Available to order |
EMMA ID | EM:02483 |
International strain name | B6;129S7-Bdkrb2tm1Jfh/Cnrm |
Alternative name | B2 knockout |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Bdkrb2tm1Jfh |
Gene/Transgene symbol | Bdkrb2 |
Information from provider
Provider | J. Fred Hess |
Provider affiliation | Department of Neuroscience Drug Discovery, Merck Research Laboratories |
Genetic information | Targeting construct is derived from 129/SvEvJ DNA. The coding sequence of the B2 (Bdkrb2) receptor, which lies on a single exon (exon 4), was replaced by a PGKneo cassette. |
Phenotypic information | Adult and juvenile B2 (Bdkrb2) knockout animals are indistinguishable from wild type littermates by visual inspection. No abnormalities were seen in either the gross pathology or the histopathology. |
Breeding history | The animals were backcrossed on a C57BL/6J background. |
References |
|
Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- decreased bone mineral density / MGI
- abnormal kidney cortex morphology / MGI
- kidney cortex cysts / MGI
- abnormal kidney development / MGI
- premature death / MGI
- abnormal kidney morphology / MGI
- abnormal kidney physiology / MGI
- no abnormal phenotype detected / MGI
- abnormal renal tubule morphology / MGI
- dilated renal tubules / MGI
- abnormal Leydig cell morphology / MGI
- abnormal juxtaglomerular apparatus morphology / MGI
- abnormal nephron morphology / MGI
- abnormal proximal convoluted tubule morphology / MGI
- abnormal renal glomerulus morphology / MGI
- renal/urinary system phenotype / MGI
- homeostasis/metabolism phenotype / MGI
- cardiovascular system phenotype / MGI
- behavior/neurological phenotype / MGI
- increased circulating creatinine level / MGI
- increased blood urea nitrogen level / MGI
- decreased blood urea nitrogen level / MGI
- abnormal renal tubule epithelium morphology / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- postnatal lethality, incomplete penetrance / MGI
- abnormal juxtaglomerular cell morphology / MGI
- abnormal glomerular capillary morphology / MGI
- abnormal kidney medullary ray morphology / MGI
- increased glomerular capsule space / MGI
- abnormal mitochondrial chromosome morphology / MGI
- decreased urine nitrite level / MGI
Literature references
- Targeted disruption of a B2 bradykinin receptor gene in mice eliminates bradykinin action in smooth muscle and neurons.;Borkowski J A, Ransom R W, Seabrook G R, Trumbauer M, Chen H, Hill R G, Strader C D, Hess J F, ;1995;The Journal of biological chemistry;270;13706-10; 7775424
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