Back to search

Article

C-terminal truncation of Pik3r1 in mice models human lipodystrophic insulin resistance uncoupled from dyslipidemia

2017-11-24

Abstract excerpt

<h4>Summary</h4> Heterodimeric class IA phosphatidylinositol-3-kinases (PI3K) transduce signals from many receptor tyrosine kinases including the insulin receptor. PI3K recruitment to phosphotyrosines is mediated by Pik3r1 gene products including the most intensely studied PI3K regulatory subunit, p85α, which also binds and regulates the PIP3 phosphatase Pten, and the lipogenic transcription factor Xbp1. Mutat...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
06a9f211-951b-54dd-a2a1-9f184a6bec83
DOI
10.1101/224485
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
C-terminal truncation of Pik3r1 in mice models human lipodystrophic insulin resistance uncoupled from dyslipidemiaDOI 10.1101/224485
Select a neighboring publication to make it the new centre.