Curated Information
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Curated Information Page
PubMed Id: 16488889 
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, Ogura T, Esumi H (2006) NDR2 acts as the upstream kinase of ARK5 during insulin-like growth factor-1 signaling. J Biol Chem 281, 13915-21 16488889
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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T75-p - NDR2 (human) ▲
Orthologous residues
NDR2 (human): T75‑p, NDR2 (mouse): T75‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Relevant cell lines - cell types - tissues:  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
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
S100B (human) Induces

S282-p - NDR2 (human) ▲
Orthologous residues
NDR2 (human): S282‑p, NDR2 (mouse): S282‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Relevant cell lines - cell types - tissues:  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
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced
 Effect of modification (process):  cell growth, altered

T442-p - NDR2 (human) ▲
Orthologous residues
NDR2 (human): T442‑p, NDR2 (mouse): T442‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Relevant cell lines - cell types - tissues:  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
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced
 Effect of modification (process):  cell growth, altered

T211-p - NuaK1 (human) ▲
Orthologous residues
NuaK1 (human): T211‑p, NuaK1 (mouse): T212‑p, NuaK1 (rat): T212‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  DLD1 (intestinal), HCT116 (intestinal), SW480 (intestinal)
 Cellular systems studied:  cell lines
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE NDR2 (human) antisense inhibition of upstream 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):  enzymatic activity, induced
 Effect of modification (process):  cell growth, altered

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
 Relevant cell lines - cell types - tissues:  DLD1 (intestinal), HCT116 (intestinal), SW480 (intestinal)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 increase


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