Curated Information
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Curated Information Page
PubMed Id: 17785202 
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.
Kang S, et al. (2007) FGFR3 activates RSK2 to mediate hematopoietic transformation through tyrosine phosphorylation of RSK2 and activation of the MEK/ERK pathway. Cancer Cell 12, 201-14 17785202
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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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:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [FGFR3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 FGFR3 (human) inhibit treatment-induced decrease
wortmannin FGFR3 (human) inhibit treatment-induced decrease

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:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [FGFR3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 FGFR3 (human) inhibit treatment-induced decrease
wortmannin FGFR3 (human) inhibit treatment-induced decrease

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:  mass spectrometry
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [RSK3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse

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:  mass spectrometry
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [RSK3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse

S380-p - p90RSK (human) ▲
Orthologous residues
p90RSK (human): S380‑p, p90RSK iso3 (human): S389‑p, p90RSK (mouse): S369‑p, p90RSK iso3 (mouse): ‑, p90RSK (rat): S380‑p, p90RSK (chicken): S398‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [RSK3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse

T573-p - p90RSK (human) ▲
Orthologous residues
p90RSK (human): T573‑p, p90RSK iso3 (human): T582‑p, p90RSK (mouse): T562‑p, p90RSK iso3 (mouse): ‑, p90RSK (rat): T573‑p, p90RSK (chicken): T590‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [RSK3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse

S386-p - RSK2 (human) ▲
Orthologous residues
RSK2 (human): S386‑p, RSK2 (mouse): S386‑p, RSK2 (rat): S386‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  myeloproliferative disorder
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [FGFR3 (human)], CCLP1 (hepatic), KMS-11 (B lymphocyte), KMS-11 (B lymphocyte) [FGFR3 (mouse)], NCI-H929 (B lymphocyte), OPM-1 (B lymphocyte), RPMI-8266 (B lymphocyte), U266 (B lymphocyte)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  Phosphorylation of RSK2 Y29 and S386was induced in T(14:4) posative lines (KMS-11, OPM-1, LP1, H929), but not in t(14:4) lines(RPMI8226, ANBL6, U266) myeloma cell lines.
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IL-3 withdrawal, IL-3 FGFR3 (human) increase
U0126 FGFR3 (human) inhibit treatment-induced decrease
wortmannin FGFR3 (human) inhibit treatment-induced decrease
Boc-D-FMK RSK2 (human) inhibit treatment-induced decrease RSK inhibitor fmk-BODIPY, inhibits cytokine -independent proliferation of Ba/F3 cells.
Boc-D-FMK RSK2 (human) inhibit treatment-induced decrease Inhibition of RSK2 by fmk in FRFR3-expressing t(14:4)-positive Human myeloma cell lines and primary human myeloma cells induces apoptosis.

Y488-p - RSK2 (human) ▲
Orthologous residues
RSK2 (human): Y488‑p, RSK2 (mouse): Y488‑p, RSK2 (rat): Y488‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [FGFR3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE FGFR3 (human)
 Comments:  FGFR3 (constitutively activated) directly phosphorylates RSK2 Y529 in an in vitro kinase assay. This facitates binding of ERK to RSK2 (co-immunoprecipitation).

Y529-p - RSK2 (human) ▲
Orthologous residues
RSK2 (human): Y529‑p, RSK2 (mouse): Y529‑p, RSK2 (rat): Y529‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  myeloproliferative disorder
 Relevant cell lines - cell types - tissues:  BaF3 ('B lymphocyte, precursor') [FGFR3 (human)], CCLP1 (hepatic), KMS-11 (B lymphocyte), KMS-11 (B lymphocyte) [FGFR3 (mouse)], NCI-H929 (B lymphocyte), OPM-1 (B lymphocyte), RPMI-8266 (B lymphocyte), U266 (B lymphocyte)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  Phosphorylation of RSK2 Y29 and S386was induced in T(14:4) posative lines (KMS-11, OPM-1, LP1, H929), but not in t(14:4) lines(RPMI8226, ANBL6, U266) myeloma cell lines.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE FGFR3 (human)
 Comments:  FGFR3 (constitutively activated) directly phosphorylates RSK2 Y529 in an in vitro kinase assay. This facitates binding of ERK to RSK2 (co-immunoprecipitation).
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK1 (human) modification site within consensus motif
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  apoptosis, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
FGFR3 (human) Induces phosphorylation cell growth, altered co-immunoprecipitation
 Comments:  FGFR3 phosphorylates RSK2 at Y529 which facilitates inactive ERK binding to RSK2.


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