Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
PhosphoSitePlus
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 22137581 
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.
Banko MR, et al. (2011) Chemical genetic screen for AMPKα2 substrates uncovers a network of proteins involved in mitosis. Mol Cell 44, 878-92 22137581
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.
Download Sites

S80-p - ACC1 (human) ▲
Orthologous residues
ACC1 (human): S80‑p, ACC1 iso4 (human): S117‑p, ACC1 (mouse): S79‑p, ACC1 (rat): S79‑p, ACC1 iso2 (rat): S79‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 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
2-deoxyglucose PPP1R12C (human) increase
compound C PPP1R12C (human) decrease
A-769662 increase
glucose starvation increase
starvation medium increase
starvation medium PPP1R12C (human) increase PPP1R12C shRNA inhibits

T172-p - AMPKA2 (human) ▲
Orthologous residues
AMPKA2 (human): T172‑p, AMPKA2 (mouse): T172‑p, AMPKA2 (rat): T172‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 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
glucose starvation increase

S379-p - Cdc27 (human) ▲
Orthologous residues
Cdc27 (human): S379‑p, Cdc27 iso1 (human): S385‑p, Cdc27 (mouse): S380‑p, Cdc27 iso2 (mouse): S361‑p, Cdc27 (rat): S380‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE AMPKA2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

T179-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): T179‑p, FOXO3A (mouse): T178‑p, FOXO3A (rat): T178‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S399-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S399‑p, FOXO3A (mouse): S398‑p, FOXO3A (rat): S398‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S413-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S413‑p, FOXO3A (mouse): S412‑p, FOXO3A (rat): S412‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S555-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S555‑p, FOXO3A (mouse): S554‑p, FOXO3A (rat): S554‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S588-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S588‑p, FOXO3A (mouse): S587‑p, FOXO3A (rat): S587‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S626-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): S626‑p, FOXO3A (mouse): S625‑p, FOXO3A (rat): S625‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S366-p - IRSp53 (human) ▲
Orthologous residues
IRSp53 (human): S366‑p, IRSp53 (mouse): S367‑p, IRSp53 iso2 (mouse): S367‑p, IRSp53 (rat): S367‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE AMPKA2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) mutation in upstream enzyme recognition motif

S20-p - MRLC1 (human) ▲
Orthologous residues
MRLC1 (human): S20‑p, MRLC1 (mouse): S20‑p, MRLC1 (rat): S20‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 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
glucose starvation increase
AMPKA2 (human) increase

S20-p - PAK2 (human) ▲
Orthologous residues
PAK2 (human): S20‑p, PAK2 (mouse): S20‑p, PAK2 (rat): S20‑p, PAK2 (rabbit): S20‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE AMPKA2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) pharmacological inhibitor of upstream enzyme, mutation in upstream enzyme recognition motif, siRNA inhibition of enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
glucose starvation increase

S452-p - PPP1R12C (human) ▲
Orthologous residues
PPP1R12C (human): S452‑p, PPP1R12C (mouse): S454‑p, PPP1R12C (rat): S454‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE AMPKA2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA2 (human) pharmacological inhibitor of upstream enzyme, mutation in upstream enzyme recognition motif, siRNA inhibition of enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
2-deoxyglucose PPP1R12C (human) increase
compound C PPP1R12C (human) decrease
A-769662 increase
glucose starvation increase
starvation medium increase
starvation medium PPP1R12C (human) increase PPP1R12C shRNA inhibits
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 zeta (human) Induces co-immunoprecipitation
 Comments:  mitotic progression


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