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Article

Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney.

American journal of physiology. Renal physiology - 15 Dec 2012

Vashistha Himanshu, Singhal Pravin C, Malhotra Ashwani, Husain Mohammad, Mathieson Peter, Saleem Moin A, Kuriakose Cyril, Seshan Surya, Wilk Anna, Delvalle Luis, Peruzzi Francesca, Giorgio Marco, Pelicci Pier Giuseppe, Smithies Oliver, Kim Hyung-Suk, Kakoki Masao, Reiss Krzysztof, Meggs Leonard G

Abstract excerpt

Candidate genes have been identified that confer increased risk for diabetic glomerulosclerosis (DG). Mice heterozygous for the Akita (Ins2(+/C96Y)) diabetogenic mutation with a second mutation introduced at the bradykinin 2 receptor (B2R(-/-)) locus express a disease phenotype that approximates human DG. Src homology 2 domain transforming protein 1 (p66) controls mitochondrial metabolism and cellular responses...

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Identifiers

PMID: 23019230
DOI: 10.1152/ajprenal.00246.2012
PMCID: PMC3532473

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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