Curated Information

Javascript is not enabled on this browser. This site will not work properly without Javascript.

Home

Curated Information Page

PubMed Id: 17998334

This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus^®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). 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.

Johnstone CN, et al. (2008) Parvin-beta inhibits breast cancer tumorigenicity and promotes CDK9-mediated peroxisome proliferator-activated receptor gamma 1 phosphorylation. Mol Cell Biol 28, 687-704 17998334

S112-p - PPAR-gamma (human)

▲

Orthologous residues

PPAR‑gamma (human): S112‑p, PPAR‑gamma (mouse): S112‑p, PPAR‑gamma iso2 (mouse): S82‑p, PPAR‑gamma (rat): S112‑p

Characterization

Methods used to characterize site in vivo: phospho-antibody, western blotting

Disease tissue studied: breast cancer

Relevant cell lines - cell types - tissues: MDA-MB231 (breast cell)

Cellular systems studied: cell lines

Species studied: human

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	CDK9 (human)	siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody

Treatments, proteins and their effect on site modification:

Treatments	Manipulated Protein	Referenced Protein	Effect
	PARVB (human)		increase
rosiglitazone		PARVB (human)	no effect upon treatment-induced increase
DRB		PARVB (human)	inhibit treatment-induced increase
rosiglitazone			no change compared to control
DRB			decrease

Home \| Curator Login	With enhanced literature mining using Linguamatics I2E		Produced by 3rd Millennium \| Design by Digizyme
			©2003-2013 Cell Signaling Technology, Inc.