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: 20870721 
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.
Frijns E, et al. (2010) EGF-induced MAPK signaling inhibits hemidesmosome formation through phosphorylation of the integrin {beta}4. J Biol Chem 285, 37650-62 20870721
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

S1356-p - ITGB4 (human)
Orthologous residues
ITGB4 (human): S1356‑p, ITGB4 iso2 (human): S1356‑p, ITGB4 iso3 (human): S1356‑p, ITGB4 (mouse): S1358‑p, ITGB4 iso2 (mouse): S1358‑p, ITGB4 iso3 (mouse): S1358‑p, ITGB4 (rat): S1358‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  PA-JEB
 Relevant cell lines - cell types - tissues:  COS (fibroblast), PA-JEB (keratinocyte)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK1 (human) transfection of inactive enzyme, transfection of wild-type enzyme, pharmacological inhibitor of upstream enzyme, modification site within consensus motif, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
phorbol ester increase
Go 6983 phorbol ester inhibit treatment-induced increase
U0126 phorbol ester inhibit treatment-induced increase
PD98059 phorbol ester inhibit treatment-induced increase
SB203580 phorbol ester no effect upon treatment-induced increase
EGF increase
Go 6983 EGF no effect upon treatment-induced increase
U0126 EGF inhibit treatment-induced increase
PD98059 EGF inhibit treatment-induced increase
SB203580 EGF no effect upon treatment-induced increase
sorbitol no change compared to control
IBMX, forskolin no change compared to control
phorbol ester increase
BI-D1870 phorbol ester no effect upon treatment-induced increase
EGF increase
BI-D1870 EGF no effect upon treatment-induced increase
nocodazole increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell motility, altered, cytoskeletal reorganization
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Plectin-1 (human) Disrupts co-immunoprecipitation

S1360-p - ITGB4 (human)
Orthologous residues
ITGB4 (human): S1360‑p, ITGB4 iso2 (human): S1360‑p, ITGB4 iso3 (human): S1360‑p, ITGB4 (mouse): S1362‑p, ITGB4 iso2 (mouse): S1362‑p, ITGB4 iso3 (mouse): S1362‑p, ITGB4 (rat): S1362‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  PA-JEB
 Relevant cell lines - cell types - tissues:  COS (fibroblast), PA-JEB (keratinocyte)
 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
phorbol ester no change compared to control
EGF no change compared to control

S1364-p - ITGB4 (human)
Orthologous residues
ITGB4 (human): S1364‑p, ITGB4 iso2 (human): S1364‑p, ITGB4 iso3 (human): S1364‑p, ITGB4 (mouse): S1366‑p, ITGB4 iso2 (mouse): S1366‑p, ITGB4 iso3 (mouse): S1366‑p, ITGB4 (rat): S1366‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  PA-JEB
 Relevant cell lines - cell types - tissues:  COS (fibroblast), PA-JEB (keratinocyte)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE p90RSK (human) transfection of wild-type enzyme, pharmacological inhibitor of upstream enzyme, modification site within consensus motif, pharmacological activator of upstream enzyme, transfection of dominant-negative enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
phorbol ester increase
Go 6983 phorbol ester inhibit treatment-induced increase
U0126 phorbol ester inhibit treatment-induced increase
PD98059 phorbol ester inhibit treatment-induced increase
SB203580 phorbol ester no effect upon treatment-induced increase
EGF increase
Go 6983 EGF no effect upon treatment-induced increase
U0126 EGF inhibit treatment-induced increase
PD98059 EGF inhibit treatment-induced increase
SB203580 EGF no effect upon treatment-induced increase
sorbitol no change compared to control
IBMX, forskolin increase
phorbol ester increase
BI-D1870 phorbol ester inhibit treatment-induced increase
EGF increase
BI-D1870 EGF inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell motility, altered, cytoskeletal reorganization
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Plectin-1 (human) Disrupts co-immunoprecipitation


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.