Curated Information
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Curated Information Page
PubMed Id: 21383122 
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.
Shang L, et al. (2011) Nutrient starvation elicits an acute autophagic response mediated by Ulk1 dephosphorylation and its subsequent dissociation from AMPK. Proc Natl Acad Sci U S A 108, 4788-93 21383122
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.
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S638-p - ULK1 (human) ▲
Orthologous residues
ULK1 (human): S638‑p, ULK1 (mouse): S637‑p, ULK1 (rat): S637‑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:  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 mTOR (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme
KINASE AMPKA1 (human) siRNA inhibition of enzyme, co-immunoprecipitation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum starvation no change compared to control
starvation medium decrease
Ca(2+) starvation medium inhibit treatment-induced decrease
rapamycin decrease
siRNA decrease siRNA mTOR
siRNA decrease shRNA AMPKalpha and AMPKbeta
Downstream Regulation
 Effect of modification (function):  phosphorylation
 Effect of modification (process):  autophagy, altered
 Comments:  facilitates rephosphorylation at S758

S758-p - ULK1 (human) ▲
Orthologous residues
ULK1 (human): S758‑p, ULK1 (mouse): S757‑p, ULK1 (rat): S757‑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:  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 mTOR (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
starvation medium decrease
serum starvation decrease
Ca(2+) starvation medium no effect upon treatment-induced decrease
rapamycin decrease
siRNA decrease siRNA mTOR
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  autophagy, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
AMPKA1 (human) Induces co-immunoprecipitation


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