Liang Y, et al. (2021) PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production. Cell Death Differ 33934104

This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.

Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.

Click on the protein name to open the protein page, and on the RSD number to open the site page.

Download

T645-p - STAT6 (mouse) ▲

Modsite: GRGyVSTtIKMTVER SwissProt Entrez-Gene Orthologous residues STAT6 (human): T645‑p, STAT6 iso2 (human): T471‑p, STAT6 (mouse): T645‑p, STAT6 (rat): T645‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  kidney, lymphocyte, macrophage-bone marrow Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes LPS increase LPS PPP2CA (human) inhibit treatment-induced increase PPP2CA-/- genetic knock out augments Downstream Regulation Effect of modification (process):  apoptosis, inhibited, cell motility, inhibited, transcription, inhibited Comments:  reduce TNF alpha production and tubular cell death