Dimberg A, Nilsson K, Oberg F (2000) Phosphorylation-deficient Stat1 inhibits retinoic acid-induced differentiation and cell cycle arrest in U-937 monoblasts. Blood 96, 2870-8 11023524

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.

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

Download

Y701-p - STAT1 (human) ▲

Modsite: DGPkGtGyIktELIs SwissProt Entrez-Gene Orthologous residues STAT1 (human): Y701‑p, STAT1 iso2 (human): Y701‑p, STAT1 (mouse): Y701‑p, STAT1 (rat): Y701‑p Characterization Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  lymphoma Relevant cell lines - cell types - tissues:  U-937 (myeloid) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes retinoic_acid increase Downstream Regulation Effect of modification (function):  activity, induced, intracellular localization Effect of modification (process):  cell cycle regulation, cell differentiation, altered, transcription, altered Comments:  ATRA induced effects