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PubMed Id: 19940129

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.

Yuan Z, et al. (2010) Phosphoinositide 3-kinase/Akt inhibits MST1-mediated pro-apoptotic signaling through phosphorylation of threonine 120. J Biol Chem 285, 3815-24 19940129

Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.

T120-p - MST1 (human)

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Orthologous residues

MST1 (human): T120‑p, MST1 (mouse): T120‑p, MST1 (rat): T120‑p

Characterization

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

Disease tissue studied: ovarian cancer

Relevant cell lines - cell types - tissues: 293 (epithelial), 293T (epithelial), COS (fibroblast), MEF (fibroblast), ovary

Cellular systems studied: cell lines, tissue

Species studied: human, monkey, mouse

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	Akt1 (human)

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	Akt1 (human)	genetic knockout/knockin of upstream enzyme, co-immunoprecipitation, transfection of inactive enzyme, phospho-motif antibody, transfection of wild-type enzyme

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
IGF-1				increase

Downstream Regulation

Effect of modification (function): enzymatic activity, inhibited, intracellular localization, phosphorylation

Effect of modification (process): apoptosis, altered

Comments: regulates autophosphorylation of MST1 T183

Associated Diseases

Diseases:	Alterations:	Comments:
ovarian cancer	increased

T183-p - MST1 (human)

▲

Orthologous residues

MST1 (human): T183‑p, MST1 (mouse): T183‑p, MST1 (rat): T183‑p

Characterization

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

Relevant cell lines - cell types - tissues: MEF (fibroblast)

Cellular systems studied: cell lines

Species studied: mouse

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	MST1 (human)	activation of upstream enzyme

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
		Akt2 (human)		increase	siRNA Akt2
		Akt1 (human)		increase	Akt1 -/- cells

Associated Diseases

Diseases:	Alterations:	Comments:
ovarian cancer	decreased

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