Curated Information
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Curated Information Page
PubMed Id: 15060171 
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.
Suzuki A, et al. (2004) ARK5 is a tumor invasion-associated factor downstream of Akt signaling. Mol Cell Biol 24, 3526-35 15060171
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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T32-p - FOXO3A (human) ▲
Orthologous residues
FOXO3A (human): T32‑p, FOXO3A (mouse): T32‑p, FOXO3A (rat): T32‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, pancreatic cancer, pancreatic carcinoma
 Relevant cell lines - cell types - tissues:  DLD1 (intestinal), PANC-1 (pancreatic), SW480 (intestinal)
 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
IGF-1 increase
IGF-1 NuaK1 (human) no effect upon treatment-induced increase dominant negative
IGF-1 Akt1 (human) inhibit treatment-induced increase dominant negative
LY294002 IGF-1 inhibit treatment-induced increase
siRNA IGF-1 no effect upon treatment-induced increase NuaK1 siRNA

S2448-p - mTOR (human) ▲
Orthologous residues
mTOR (human): S2448‑p, mTOR (mouse): S2448‑p, mTOR (rat): S2448‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, pancreatic cancer, pancreatic carcinoma
 Relevant cell lines - cell types - tissues:  DLD1 (intestinal), PANC-1 (pancreatic), SW480 (intestinal)
 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
IGF-1 increase
IGF-1 NuaK1 (human) inhibit treatment-induced increase dominant negative
IGF-1 Akt1 (human) inhibit treatment-induced increase dominant negative
LY294002 IGF-1 inhibit treatment-induced increase
siRNA IGF-1 inhibit treatment-induced increase NuaK1 siRNA

S600-p - NuaK1 (human) ▲
Orthologous residues
NuaK1 (human): S600‑p, NuaK1 (mouse): S601‑p, NuaK1 (rat): S600‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  colorectal cancer, colorectal carcinoma, pancreatic cancer, pancreatic carcinoma
 Relevant cell lines - cell types - tissues:  DLD1 (intestinal), PANC-1 (pancreatic), SW480 (intestinal)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) pharmacological activator of upstream enzyme, phospho-antibody, transfection of dominant-negative enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase
LY294002 IGF-1 inhibit treatment-induced increase
U0126 IGF-1 no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  activation
 Effect of modification (process):  cell motility, altered


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