Curated Information

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PubMed Id: 10949026

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.

Datta SR, et al. (2000) 14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation. Mol Cell 6, 41-51 10949026

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.

S112-p - BAD (mouse)

▲

Orthologous residues

BAD (human): S75‑p, BAD (mouse): S112‑p, BAD (rat): S113‑p

Characterization

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

Relevant cell lines - cell types - tissues: CCL39 (fibroblast)

Cellular systems studied: cell lines

Species studied: hamster

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	PKACa (mouse)

S136-p - BAD (mouse)

▲

Orthologous residues

BAD (human): S99‑p, BAD (mouse): S136‑p, BAD (rat): S137‑p

Characterization

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

Relevant cell lines - cell types - tissues: CCL39 (fibroblast)

Cellular systems studied: cell lines

Species studied: hamster

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	PKACa (mouse)
KINASE	Akt1 (mouse)

Comments: Major phosphoacceptor site for Akt1.

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	Akt1 (mouse)	transfection of constitutively active enzyme
KINASE	PKACa (mouse)	transfection of constitutively active 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): molecular association, regulation

Effect of modification (process): apoptosis, altered

Modification regulates interactions with:

Interacting molecule	Interacting domains	Effect	Consequences (function)	Consequences (process)	Detection assays
14-3-3 beta (mouse)		Induces	activation		co-immunoprecipitation

S155-p - BAD (mouse)

▲

Orthologous residues

BAD (human): S118‑p, BAD (mouse): S155‑p, BAD (rat): S156‑p

Characterization

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

Relevant cell lines - cell types - tissues: CCL39 (fibroblast)

Cellular systems studied: cell lines

Species studied: hamster

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	PKACa (mouse)
KINASE	Akt1 (mouse)

Comments: Major phosphoacceptor site for PKA. Minor phosphoacceptor site for Akt1.

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	PKACa (mouse)	transfection of constitutively active enzyme
KINASE	Akt1 (mouse)	transfection of constitutively active 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): molecular association, regulation

Effect of modification (process): apoptosis, altered

Modification regulates interactions with:

Interacting molecule	Interacting domains	Effect	Consequences (function)	Consequences (process)	Detection assays
Bcl-xL (mouse)		Disrupts

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