CST Guide:

Section I: Research Areas
chapter 02: Signaling
181
2012–2014 citations
CST antibodies for EGFR have been
cited over 181 times in high-impact,
peer-reviewed publications from the
global research community.
Target M P E S C
Phospho-HER2/ErbB2 (pan Tyr) •
Phospho-HER2/ErbB2 (Tyr877) •
Phospho-HER2/ErbB2 (Tyr1196) •
• • •
Phospho-HER2/ErbB2
(Tyr1221/1222)
Phospho-HER2/ErbB2 (Tyr1248)
Phospho-HER2/ErbB2
(Tyr1248)/EGFR (Tyr1173)
•
•
HER3/ErbB3 • • • •
Phospho-HER3/ErbB3 (pan Tyr) •
Phospho-HER3/ErbB3 (Tyr1197) •
Phospho-HER3/ErbB3 (Tyr1222) •
Phospho-HER3/ErbB3 (Tyr1289) •
Phospho-HER3/ErbB3 (Tyr1328) •
HER4/ErbB4 • •
Phospho-HER4/ErbB4 (Pan Tyr) •
Phospho-HER4/ErbB4 (Tyr984) •
Phospho-HER4/ErbB4 (Tyr1284) •
c-Kit • • • •
Phospho-c-Kit (pan Tyr)
•
Phospho-c-Kit (Tyr703) •
Phospho-c-Kit (Tyr719) • •
LRIG1
•
M-CSF Receptor
• •
Phospho-M-CSF Receptor (Tyr546) •
Phospho-M-CSF Receptor (Tyr699) • •
Phospho-M-CSF Receptor (Tyr708) •
Phospho-M-CSF Receptor (Tyr723) • •
Phospho-M-CSF Receptor (Tyr809) •
Phospho-M-CSF Receptor (Tyr923) •
Mer • •
Met
• • • • •
Phospho-Met (pan Tyr)
•
Phospho-Met (Tyr1003) • •
Phospho-Met (Tyr1234/1235) • • • •
Phospho-Met (Tyr1349) • • •
PDGFR-α • • • •
Select Citations:
Wu, J. et al. (2014) EGFR-STAT3 signaling promotes formation
of malignant peripheral nerve sheath tumors. Oncogene
33, 173–180.
Sheu, J.J. et al. (2014) LRIG1 modulates aggressiveness of
head and neck cancers by regulating EGFR-MAPK-SPHK1
signaling and extracellular matrix remodeling. Oncogene 33,
1375–1384.
Bronisz, A. et al. (2014) xtracellular vesicles modulate the
glioblastoma microenvironment via a tumor suppression
signaling network directed by miR-1. Cancer Res. 74,
738–750.
De Cesare, M. et al. (2014) Synergistic antitumor activity
of cetuximab and namitecan in human squamous cell
carcinoma models relies on cooperative inhibition of EGFR
expression and depends on high EGFR gene copy number.
Clin. Cancer Res. 20, 995–1006.
Muller, P.A. et al. (2014) Mutant p53 regulates Dicer through
p63-dependent and -independent mechanisms to promote
an invasive phenotype. J. Biol. Chem. 289, 122–132.
Target M P E S C
Phospho-PDGFR-α (Tyr754) •
Phospho-PDGFR-α (Tyr762) •
Phospho-PDGFR-α (Tyr849) •
Phospho-PDGFR-α (Tyr1018) •
Phospho-PDGF Receptor α/β (pan Tyr) •
Phospho-PDGF Receptor α •
(Tyr849)/PDGF Receptor β (Tyr857)
PDGFR-β • • •
Phospho-PDGFR-β (Tyr740) •
Phospho-PDGFR-β (Tyr751) • • •
Phospho-PDGFR-β (Tyr771) •
Phospho-PDGFR-β (Tyr1009) •
Phospho-PDGFR-β (Tyr1021) •
PTK7
•
Ret
• • •
Phospho-Ret (pan Tyr)
•
Phospho-Ret (Tyr905)
•
Ron • •
ROR1
•
ROR2
•
ROS1 • • •
Phospho-ROS1 (pan Tyr)
•
Phospho-ROS1 (Tyr2274) •
Spry1
•
Tie2
•
Phospho-Tie2 (Tyr992) •
Phospho-Tie2 (Ser1119) •
Tyro3
•
VEGFR1
•
VEGFR2 • • • •
Phospho-VEGFR2 (Tyr951) • •
Phospho-VEGFR2 (Tyr996) •
Phospho-VEGFR2 (Tyr1059) •
Phospho-VEGFR2 (Tyr1175) • •
Phospho-VEGFR2 (Tyr1212) •
VEGFR3
• •
Stahlschmidt, W. et al. (2014) Clathrin terminal domainligand
interactions regulate sorting of mannose 6-phosphate
receptors mediated by AP-1 and GGA adaptors. J Biol Chem.
21, 4906–4918.
Tao, J.J. et al. (2014) Antagonism of EGFR and HER3
enhances the response to inhibitors of the PI3K-Akt pathway
in triple-negative breast cancer. Sci. Signal. 7, ra29.
Zhang, F. et al. (2014) Temporal production of the signaling
lipid phosphatidic acid by phospholipase D2 determines the
output of extracellular signal-regulated kinase signaling in
cancer cells. Mol. Cell Biol. 34, 84–95.
Lee, C.Y. et al. (2014) Neuregulin autocrine signaling
promotes self-renewal of breast tumor-initiating cells by triggering
HER2/HER3 activation. Cancer Res. 74, 341–352.
Bronisz, A. et al. (2014) Extracellular vesicles modulate the
glioblastoma microenvironment via a tumor suppression
signaling network directed by miR-1. Cancer Res. 74,
738–750.
Tyrosine Kinases Kinase-Disease Associations
Name Group Disease Type Molecular Notes
ALK TK Cancer Trans About one third of large-cell lymphomas are caused by a t(2;5)(p23;q35) translocation
that fuses ALK to nucleophosmin (NPM1A). Other cases caused by fusions of ALK to
moesin, non-muscle myosin heavy chain 9, clathrin heavy chain and other genes.
Several fusions also seen in inflammatory myofibroblastic tumors and expression
has been briefly noted in a range of tumors (Medline:15095281). Proposed as tumor
antigen (Medline:11877285). OMIM:105590.
ALK1
(ACVRL1)
ALK2
(ACVR1)
ALK4
(ACVR1B)
TKL Cardiovascular Mut Fourteen distinct mutations linked to hereditary hemorrhagic telangiectasia type 2
(Osler-Rendu-Weber syndrome 2) [OMIM:600376], associated with intestinal bleeding,
arterial hypertension and arteriovenous malformations. OMIM:601284.
TKL Development Mut Single heterozygous mutation seen in many independent cases of fibrodysplasia ossificans
progressiva [OMIM:135100], causing skeletal malformations and extra-skeletal
bone formation. OMIM:102576.
TKL Cancer Mut, Splice Two somatic truncation mutations seen in pancreatic carcinoma. Unique splice forms
with predicted dominant negative activity. OMIM:601300.
Axl TK Cancer OE Overexpression in tissue culture causes oncogenic transformation. Overexpressed in
several cancers including thyroid (Medline:10411118), ovarian (Medline:15452374),
gastric (Medline:12168903), ER+ breast cancer (Medline:11484958) and acute
myeloid leukemia, where it is associated with poor prognosis (Medline:10482985).
OMIM:109135.
BTK TK Cancer,
Immunity
LOF Mut
EGFR TK Cancer Amp, OE,
GOF Mut
Eph
family
TK
Cancer,
Sensory
LOF mutations cause X-linked agammaglobulinemia [OMIM:300300], arresting
development of B cells and causing recurrent bacterial infections. Truncated splice
forms found in childhood leukemias may underlie radiation resistance of tumors
through inhibition of apoptosis (Medline: 12854903). Inhibitors developed to target B
cell maturation and function. Inhibitor: dasatinib. OMIM:300300.
Overexpressed in breast, head and neck cancers (Medline:15254682) and correlated
with poor survival. Activating somatic mutations seen in lung cancer, corresponding
to minority of patients with strong response to EGFR inhibitor gefinitib. Mutations and
amplification also seen in glioblastoma, and upregulation seen in colon cancer and
neoplasms. In xenografts, inhibitors synergized with cytotoxic drugs in inhibition of many
tumor types (Medline:10815932). Inhibitors: gefinitib/ZD1839 (Astra Zeneca), cetuximab
(mAb, Imclone), erlotinib (OSI/Genentech) lapatinib (Glaxo Smith Kline). OMIM:131550.
A 14-member family of receptor tyrosine kinases with similar functions in intercellular
communication, migration, patterning and angiogenesis. Ephrins are implicated in
development of tumor vasculature and intercellular contacts required for metastasis.
Several members are overexpressed in cancers. Soluble forms (competitive receptors)
have shown some anti-tumor activity and extracellular domains have been used as
tumor-specific antigens.
EphA1 TK Cancer Expr Misexpressed in several cancers and upregulated in head and neck cancer
(Medline:15023838). Downregulated in invasive breast cancer cell lines (Medline:15147954)
and glioblastoma (Medline:14726470). OMIM:179610.
EphA2 TK Cancer OE Overexpressed in many cancers including aggressive ovarian (Medline:15297418),
cervical (Medline:15297167), breast carcinomas (Medline: 15147954) and lung
cancer (Medline:12576426). Expression correlates with degree of angiogenesis
(Medline:14965363), metastasis (Medline: 14767510) and xenograft tumor growth
(Medline:14973554). Soluble receptor inhibits tumor growth and angiogenesis in mice
(Medline:12370823, 14670182). OMIM:176946.
EphA3
(HEK)
TK Cancer Mut Two point mutations seen in a survey of colorectal tumors (Medline:12738854).
Soluble receptors reduce tumor growth and angiogenesis in mouse models (Medline:12370823,
14670182). Nine point mutations found in 294 colon and lung tumors
(Medline:16941478) OMIM:179611.
EphB2 TK Cancer OE, Mut Point mutations seen in prostate cancer (Medline:15300251). Overexpressed and
required for migration of glioblastoma (Medline:15126357). Overexpressed and correlated
with poor survival in breast cancer (Medline:15029258). Overexpression and loss
of heterozygosity seen in colorectal cancers (Medline:11920461, 11166921). Target
for immunoconjugate drug therapy (Medline:14871799). OMIM:600997.
EphB4
(HTK)
TK Cancer OE Required for normal development and angiogenesis of the mammary gland. Angiogenic
functions may be kinase-independent by means of retrograde signaling through its
ephrin-B2 ligand (Medline:15067119). High expression correlates with malignancy in
breast, ovarian and other cancers, but appears to be a survival factor (Medline:16816380,
17353927). Also upregulated in head and neck (Medline:14661437),
endometrial (Medline:12562648) and colon carcinomas (Medline:11801186).
OMIM:600011.
FGFR1 TK Cancer,
Development
Mut, Trans
Point mutations cause Pfeffer syndrome [OMIM:101600] (finger and toe malformations
and other skeletal errors) and dominant Kallmann syndrome 2 [OMIM:147950]. Stem
cell leukemia lymphoma syndrome (SCLL) may be caused by a t(8;13)(p12;q12)
translocation that fuses a zinc finger gene (ZNF198) to FGFR1. Various myeloproliferative
disorders have been linked to translocations that fuse FGFR1 to FOP, FIM, CEP1 or
the atypical kinase, BCR. Inhibitor: SU5402. OMIM:136350.
70 For Research Use Only. Not For Use in Diagnostic Procedures. See pages 302 & 303 for Pathway Diagrams, Application, and Reactivity keys.
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