AI Article Synopsis
- Cell growth depends on special signals called insulin and IGF1, which help cells multiply.
- Researchers found 40 proteins that interact with a key player in this process named IRS1, including one called DCAF7.
- When they reduced DCAF7 in cells, it stopped them from growing properly by causing them to get stuck in a certain phase of the cell cycle (G2), and also changed the location of a protein called FOXO1 that affects cell growth.
Article Abstract
Cell proliferation is dependent on growth factors insulin and IGF1. We sought to identify interactors of IRS1, the most proximal mediator of insulin/IGF1 signaling, that regulate cell proliferation. Using proximity-dependent biotin identification (BioID), we detected 40 proteins displaying proximal interactions with IRS1, including DCAF7 and its interacting partners DYRK1A and DYRK1B. In HepG2 cells, DCAF7 knockdown attenuated cell proliferation by inducing cell cycle arrest at G2. DCAF7 expression was required for insulin-stimulated AKT phosphorylation, and its absence promoted nuclear localization of the transcription factor FOXO1. DCAF7 knockdown induced expression of FOXO1-target genes implicated in G2 cell cycle inhibition, correlating with G2 cell cycle arrest. In , wing-specific knockdown of DCAF7/ caused smaller wing size and lower wing cell number; the latter recovered upon double knockdown of and . We propose that DCAF7 regulates cell proliferation and cell cycle via IRS1-FOXO1 signaling, of relevance to whole organism growth.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9556925 | PMC |
| http://dx.doi.org/10.1016/j.isci.2022.105188 | DOI Listing |
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