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: 18451027 
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.
Zhu J, Blenis J, Yuan J (2008) Activation of PI3K/Akt and MAPK pathways regulates Myc-mediated transcription by phosphorylating and promoting the degradation of Mad1. Proc Natl Acad Sci U S A 105, 6584-9 18451027
Download Sites

S145-p - Mad1 (human) ▲
Orthologous residues
Mad1 (human): S145‑p, Mad1 (mouse): S144‑p
Characterization
 Methods used to characterize site in vivo:  electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), HeLa (cervical), MCF-10A (breast cell), MCF-7 (breast cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE p70S6K (human)
KINASE p90RSK (human)
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE p70S6K (human) transfection of constitutively active enzyme, inhibition of upstream enzyme, siRNA inhibition of enzyme, transfection of dominant-negative enzyme, pharmacological activator of upstream enzyme, modification site within consensus motif, pharmacological inhibitor of upstream enzyme, transfection of wild-type enzyme, phospho-antibody
KINASE p90RSK (human) siRNA inhibition of enzyme, transfection of dominant-negative enzyme, pharmacological activator of upstream enzyme, modification site within consensus motif, pharmacological inhibitor of upstream enzyme, transfection of wild-type enzyme, phospho-antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum increase
LY294002 serum no effect upon treatment-induced increase
PD98059 serum no effect upon treatment-induced increase
LY294002, PD98059 serum inhibit treatment-induced increase
PD98059, rapamycin serum inhibit treatment-induced increase
serum Akt1 (human) inhibit treatment-induced increase dominant negative Akt1
serum p70S6K (human) inhibit treatment-induced increase dominant negative p70S6K
serum p90RSK (human) inhibit treatment-induced increase dominant negative p90RSK
siRNA serum p70S6K (human) no effect upon treatment-induced increase
siRNA serum p90RSK (human) no effect upon treatment-induced increase
siRNA serum p70S6K (human), p90RSK (human) inhibit treatment-induced increase
insulin increase
LY294002 insulin no effect upon treatment-induced increase
PD98059 insulin no effect upon treatment-induced increase
LY294002, PD98059 insulin inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  protein degradation
 Effect of modification (process):  cell growth, altered, transcription, altered


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.