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: 19118012 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Cho YY, et al. (2009) Cyclin-dependent kinase-3-mediated c-Jun phosphorylation at Ser63 and Ser73 enhances cell transformation. Cancer Res 69, 272-81 19118012
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.
Download Sites

T202-p - ERK1 (human) ▲
Orthologous residues
ERK1 (human): T202‑p, ERK1 (mouse): T203‑p, ERK1 (rat): T203‑p, ERK1 (hamster): T192‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF increase
PD98059 EGF inhibit treatment-induced increase
SP600125 EGF inhibit treatment-induced increase

Y204-p - ERK1 (human) ▲
Orthologous residues
ERK1 (human): Y204‑p, ERK1 (mouse): Y205‑p, ERK1 (rat): Y205‑p, ERK1 (hamster): Y194‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF increase
PD98059 EGF inhibit treatment-induced increase
SP600125 EGF inhibit treatment-induced increase

T185-p - ERK2 (human) ▲
Orthologous residues
ERK2 (human): T185‑p, ERK2 (mouse): T183‑p, ERK2 (rat): T183‑p, ERK2 (chicken): T193‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF increase
PD98059 EGF inhibit treatment-induced increase
SP600125 EGF inhibit treatment-induced increase

Y187-p - ERK2 (human) ▲
Orthologous residues
ERK2 (human): Y187‑p, ERK2 (mouse): Y185‑p, ERK2 (rat): Y185‑p, ERK2 (chicken): Y195‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF increase
PD98059 EGF inhibit treatment-induced increase
SP600125 EGF inhibit treatment-induced increase

T183-p - JNK1 (human) ▲
Orthologous residues
JNK1 (human): T183‑p, JNK1 iso2 (human): T183‑p, JNK1 iso3 (human): T183‑p, JNK1 (mouse): T183‑p, JNK1 (rat): T183‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF no change compared to control
SP600125 EGF no change compared to control

Y185-p - JNK1 (human) ▲
Orthologous residues
JNK1 (human): Y185‑p, JNK1 iso2 (human): Y185‑p, JNK1 iso3 (human): Y185‑p, JNK1 (mouse): Y185‑p, JNK1 (rat): Y185‑p
Characterization
 Methods used to characterize site in vivo:  phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), Saos-2 (bone cell)
 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
EGF no change compared to control
SP600125 EGF no change compared to control

S63-p - Jun (human) ▲
Orthologous residues
Jun (human): S63‑p, Jun (mouse): S63‑p, Jun (rat): S63‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), JB6 C141 (epidermal), Saos-2 (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK1 (human)
KINASE CDK3 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK3 (human) co-immunoprecipitation, phospho-antibody, transfection of dominant-negative enzyme, transfection of wild-type enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
EKI-785 EGF inhibit treatment-induced increase
PD98059 EGF no effect upon treatment-induced increase
SP600125 EGF no effect upon treatment-induced increase
siRNA EGF CDK3 (human) inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  activation
 Effect of modification (process):  cell growth, altered, transcription, altered

S73-p - Jun (human) ▲
Orthologous residues
Jun (human): S73‑p, Jun (mouse): S73‑p, Jun (rat): S73‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phosphoamino acid analysis, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), JB6 C141 (epidermal), Saos-2 (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK1 (human)
KINASE CDK3 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK3 (human) co-immunoprecipitation, phospho-antibody, transfection of dominant-negative enzyme, transfection of wild-type enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
EKI-785 EGF inhibit treatment-induced increase
PD98059 EGF no effect upon treatment-induced increase
SP600125 EGF no effect upon treatment-induced increase
siRNA EGF CDK3 (human) inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  activation
 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.