Curated Information
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PubMed Id: 20656472 
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.
Habib SL, et al. (2010) Novel mechanism of reducing tumourigenesis: upregulation of the DNA repair enzyme OGG1 by rapamycin-mediated AMPK activation and mTOR inhibition. Eur J Cancer 46, 2806-20 20656472
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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T183-p - AMPKA1 (human) ▲
Orthologous residues
AMPKA1 (human): T183‑p, AMPKA1 (mouse): T183‑p, AMPKA1 (rat): T183‑p, AMPKA1 (fruit fly): T184‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  kidney cancer
 Relevant cell lines - cell types - tissues:  'kidney, tubule' [TSC2 (mouse), homozygous knockout], 786-O (renal), HK2 (epithelial), MEF (fibroblast) [TSC2 (mouse), heterozygous knockout]
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
rapamycin increase HK2 and 786-O cells
AICAR increase 786-O cells

T412-p - p70S6K (human) ▲
Orthologous residues
p70S6K (human): T412‑p, p70S6K iso2 (human): T389‑p, p70S6K (mouse): T412‑p, p70S6K (rat): T412‑p, p70S6K iso2 (rat): T389‑p, p70S6K (fruit fly): T398‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  kidney cancer
 Relevant cell lines - cell types - tissues:  'kidney, tubule' [TSC2 (mouse), homozygous knockout], 786-O (renal), HK2 (epithelial), MEF (fibroblast) [TSC2 (mouse), heterozygous knockout]
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
rapamycin decrease HK2 and 786-O cells
AICAR decrease 786-O cells

S79-p - ACC1 (mouse) ▲
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:  phospho-antibody, western blotting
 Disease tissue studied:  kidney cancer
 Relevant cell lines - cell types - tissues:  'kidney, tubule' [TSC2 (mouse), homozygous knockout], 786-O (renal), HK2 (epithelial), MEF (fibroblast) [TSC2 (mouse), heterozygous knockout]
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
rapamycin increase TSC2 +/- cells, in vivo kidney cortex TSC2 +/-
AMPKA1 (human) decrease dominant negative AMPK, TCSC2 +/- cells
AICAR AMPKA1 (human) increase

T183-p - AMPKA1 (mouse) ▲
Orthologous residues
AMPKA1 (human): T183‑p, AMPKA1 (mouse): T183‑p, AMPKA1 (rat): T183‑p, AMPKA1 (fruit fly): T184‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  kidney cancer
 Relevant cell lines - cell types - tissues:  'kidney, tubule' [TSC2 (mouse), homozygous knockout], 786-O (renal), HK2 (epithelial), MEF (fibroblast) [TSC2 (mouse), heterozygous knockout]
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
rapamycin increase TSC2 +/+, +/-, -/- cells, in vivo kidney cortex TSC2 +/-
AICAR increase TSC2+/-, -/- cells
glucose decrease TSC2 +/- cells
rapamycin glucose inhibit treatment-induced decrease TSC2 +/- cells
AMPKA1 (human) decrease dominant negative AMPK, TSC2 +/- cells
AICAR AMPKA1 (human) increase

T412-p - p70S6K (mouse) ▲
Orthologous residues
p70S6K (human): T412‑p, p70S6K iso2 (human): T389‑p, p70S6K (mouse): T412‑p, p70S6K (rat): T412‑p, p70S6K iso2 (rat): T389‑p, p70S6K (fruit fly): T398‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  kidney cancer
 Relevant cell lines - cell types - tissues:  'kidney, tubule' [TSC2 (mouse), homozygous knockout], 786-O (renal), HK2 (epithelial), MEF (fibroblast) [TSC2 (mouse), heterozygous knockout]
 Cellular systems studied:  cell lines, primary cells, tissue
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
rapamycin decrease TSC2 +/+, +/-, -/- cells, in vivo kidney cortex TSC2 +/-
AICAR decrease TSC2+/-, -/- cells
glucose increase TSC2 +/- cells
rapamycin glucose inhibit treatment-induced increase TSC2 +/- cells
p70S6K (human) decrease dominant negative p70S6K, TSC2 +/- cells


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