Autocatalytic phosphorylation of FGFR4 Y367C mutant

Stable Identifier
R-HSA-2012087
Type
Reaction [transition]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
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Expression of the FGFR4 Y367C mutant in MDA-MB453 breast cancer cell line results in constitutive tyrosine phosphorylation of the receptor and serum-independent activation of downstream signaling as monitored by Erk phosphorylation. Ectopic expression of FGFR4 Y367C in HEK cells also leads to Erk activation and enhanced cellular proliferation. Akt and phospho-AKT levels were not affected by overexpression of the FGFR4 Y367C mutant, however (Roidl, 2010)
Literature References
PubMed ID Title Journal Year
19946327 The FGFR4 Y367C mutant is a dominant oncogene in MDA-MB453 breast cancer cells

Hart, S, Streit, S, Bechtold, S, Berger, HJ, Foo, P, Mann, C, Ullrich, A, Ruhe, JE, Roidl, A, Ho, HK, Wong, W

Oncogene 2010
Participants
Participates
Catalyst Activity

protein tyrosine kinase activity of FGFR4 Y367C mutant dimer [plasma membrane]

Normal reaction
Functional status

Gain of function of FGFR4 Y367C mutant dimer [plasma membrane]

Status
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
breast cancer DOID:1612 malignant tumor of the breast, mammary cancer, malignant neoplasm of breast, mammary tumor, primary breast cancer, breast cancer, Ca breast - NOS, breast tumor
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