Curated Information
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Curated Information Page
PubMed Id: 18775330 
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.
Casar B, Pinto A, Crespo P (2008) Essential role of ERK dimers in the activation of cytoplasmic but not nuclear substrates by ERK-scaffold complexes. Mol Cell 31, 708-21 18775330
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

S505-p - cPLA2 (human) ▲
Orthologous residues
cPLA2 (human): S505‑p, cPLA2 (mouse): S505‑p, cPLA2 (rat): S505‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
siRNA EGF no effect upon treatment-induced increase control scrambled
siRNA DAGLBETA (human) decrease
siRNA IQGAP1 (human) decrease
siRNA EGF KSR (human) inhibit treatment-induced increase
siRNA EGF ARRB1 (human) inhibit treatment-induced increase
siRNA ARRB2 (human) decrease
siRNA EGF PXN iso2 (human) inhibit treatment-induced increase
siRNA EGF IL17RD (human) inhibit treatment-induced increase
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation, enzymatic activity, induced
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
 Comments:  PLA2 binding to KSR1 is mediated by ERK .

S383-p - ELK1 (human) ▲
Orthologous residues
ELK1 (human): S383‑p, ELK1 (mouse): S384‑p, ELK1 (rat): S382‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
no change compared to control parental
increase HL slight increase
no change compared to control HL-NLS

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:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HRas (human) increase
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation, enzymatic activity, induced, protein conformation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
 Comments:  ERK dimers and and scafolds activate cytoplasmic substrates; PLA2 binding to KSR1 is mediated by ERK .

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:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HRas (human) increase
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation, enzymatic activity, induced, protein conformation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
 Comments:  ERK dimers and and scafolds activate cytoplasmic substrates; PLA2 binding to KSR1 is mediated by ERK .

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:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HRas (human) increase
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
increase parental
increase HL
increase HL-NLS
Downstream Regulation
 Effect of modification (function):  activation, enzymatic activity, induced, protein conformation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
 Comments:  ERK dimers and and scafolds activate cytoplasmic substrates; PLA2 binding to KSR1 is mediated by ERK .

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:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HRas (human) increase
EGF increase Total lysates
siRNA EGF no effect upon treatment-induced increase scramble control
siRNA DAGLBETA (human) no effect upon treatment-induced increase
siRNA IQGAP1 (human) no change compared to control
siRNA KSR (human) no effect upon treatment-induced increase
siRNA ARRB1 (human) no effect upon treatment-induced increase
siRNA ARRB2 (human) no effect upon treatment-induced increase
siRNA PXN iso2 (human) no effect upon treatment-induced increase
siRNA IL17RD (human) augment treatment-induced decrease
increase parental
increase HL
increase HL-NLS
Downstream Regulation
 Effect of modification (function):  activation, enzymatic activity, induced, protein conformation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
KSR (human) Induces molecular association, regulation cell growth, altered co-immunoprecipitation, electrophoretic visualization
 Comments:  ERK dimers and and scafolds activate cytoplasmic substrates; PLA2 binding to KSR1 is mediated by ERK .

T359-p - p90RSK (human) ▲
Orthologous residues
p90RSK (human): T359‑p, p90RSK iso3 (human): T368‑p, p90RSK (mouse): T348‑p, p90RSK iso3 (mouse): ‑, p90RSK (rat): T359‑p, p90RSK (chicken): T377‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
increase parental
increase HL
increase HL-NLS
increase parental
decrease HL
increase HL-NLS

S363-p - p90RSK (human) ▲
Orthologous residues
p90RSK (human): S363‑p, p90RSK iso3 (human): S372‑p, p90RSK (mouse): S352‑p, p90RSK iso3 (mouse): ‑, p90RSK (rat): S363‑p, p90RSK (chicken): S381‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  293 (epithelial), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
increase parental
increase HL
increase HL-NLS
increase parental
decrease HL
increase HL-NLS


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