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Article

Stim1 Polymorphism Disrupts Immune Signaling and Creates Renal Injury in Hypertension.

Journal of the American Heart Association - 3 Mar 2020

Dhande Isha S, Zhu Yaming, Kneedler Sterling C, Joshi Aniket S, Hicks M John, Wenderfer Scott E, Braun Michael C, Doris Peter A

Abstract excerpt

Background Spontaneously hypertensive rats of the stroke-prone line (SHR-A3) develop hypertensive renal disease as a result of naturally occurring genetic variation. Our prior work identified a single-nucleotide polymorphism unique to SHR-A3 that results in truncation of the carboxy terminus of STIM1. The SHR-B2 line, which is also hypertensive but resists hypertensive renal injury, expresses the wild-type STIM1....

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Open in PubMed Open full text

Identifiers

PMID: 32075490
DOI: 10.1161/JAHA.119.014142
PMCID: PMC7335582

Genes

STIM1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Stim1 Polymorphism Disrupts Immune Signaling and Creates Renal Injury in Hypertension.PMID 32075490Read ↗

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