Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Fibroblast growth factor 3, a protein with a dual subcellular fate, is interacting with human ribosomal protein S2.
BMP-mediated inhibition of FGF signaling promotes cardiomyocyte differentiation of anterior heart field progenitors.
Sequence organization of the human int-2 gene and its expression in teratocarcinoma cells.
Receptor specificity of the fibroblast growth factor family.
PI3K-containing complexes phosphorylate PIP2 to PIP3
Autocatalytic phosphorylation of FGFR2b
Autocatalytic phosphorylation of FGFR1b
FGFR2b mutants bind an expanded range of ligands
Autocatalytic phosphorylation of FGFR2b mutants with enhanced ligand binding
FP-1039 acts as a ligand-trap for FGFR2b-binding ligands in endometrial cancer
Point mutants of FGFR2 bind and are inactivated by tyrosine kinase inhibitors
PI3K phosphorylates PIP2 to PIP3
PI3K inhibitors block PI3K catalytic activity
Activated FGFR2 phosphorylates PLCG1
Activated FGFR1 phosphorylates PLCG1
p-4Y-PLCG1 dissociates from activated FGFR2
Activated FGFR2 binds PLCG1
p-4Y-PLCG1 dissociates from activated FGFR1
Activated FGFR1 binds PLCG1
Activated FGFR1:p-FRS:GRB2:SOS1 activates RAS nucleotide exchange
Activated FGFR2 phosphorylates FRS2
Activated FGFR2 binds FRS2
Activated FGFR2:p-SHC1:GRB2:SOS1 activates RAS nucleotide exchange
Activated FGFR2 binds SHC1
Activated FGFR2:p-SHC1 binds GRB2:SOS1
Activated FGFR2 phosphorylates SHC1
Activated ERK1/2 threonine-phosphorylates FGFR1-associated FRS2
Activated ERK1/2 threonine-phosphorylates FGFR2-associated FRS2
Activated FGFR1 binds FRS2
Activated FGFR1 binds FRS3
Activated FGFR1 binds SHC1
Activated FGFR1 phosphorylates FRS2
Activated FGFR1 phosphorylates FRS3
Activated FGFR1 phosphorylates SHC1
Activated FGFR1:p-FRS bind to PPTN11
Activated FGFR1:p-FRS binds GRB2:SOS1
Activated FGFR1:p-FRS phosphorylates PPTN11
Activated FGFR1:p-FRS2:GRB2:GAB1:PI3KR1 binds PIK3CA
Activated FGFR1:p-FRS2 binds GRB2:GAB1:PIK3R1
Activated FGFR1:p-FRS2:p-PPTN11 binds GRB2:GAB1:PI3KR1
Activated FGFR1:p-FRS2:p-PPTN11:GRB2:GAB1:PIK3R1 binds PIK3CA
Activated FGFR1:p-SHC1 binds GRB2:SOS1
Activated FGFR1:p-SHC1:GRB2:SOS1 activates RAS nucleotide exchange
Activated FGFR2 binds FRS3
Activated FGFR2 phosphorylates FRS3
Activated FGFR2 phosphorylates PPTN11
Activated FGFR2:p-FRS bind to PPTN11
Activated FGFR2:p-FRS2 binds GRB2:GAB1:PIK3R1
Activated FGFR2:p-FRS2:GRB2:GAB1:PI3KR1 binds PIK3CA
Activated FGFR2:pFRS binds GRB2:SOS1
Activated FGFR2:p-FRS2:GRB2:SOS1 activates RAS nucleotide exchange
Activated FGFR2:p-FRS2:p-PPTN11 binds GRB2:GAB1:PI3KR1
Activated FGFR2:p-FRS2:p-PPTN11:GRB2:GAB1:PIK3R1 binds PIK3CA
CBL ubiquitinates FRS2 and FGFR1
p-CBL:GRB2 binds p-FRS2:activated FGFR1
CBL ubiquitinates FRS2 and FGFR2
FGFR1-associated PI3K phosphorylates PIP2 to PIP3
FGFR1- and PTPN11- associated PI3K phosphorylates PIP2 to PIP3
FGFR2- and PTPN11- associated PI3K phosphorylates PIP2 to PIP3
FGFR2-associated PI3K phosphorylates PIP2 to PIP3
p-CBL:GRB2 binds p-FRS2:activated FGFR2
p-4Y-PLCG1 dissociates from activated FGFR2 mutants
Activated FGFR2 mutants:p-FRS2 binds GRB2-SOS1
Activated FGFR2 mutants:p-FRS2:GRB2:SOS1 activates RAS nucleotide exchange
Activated FGFR2 mutants:p-FRS2:GRB2:GAB1:PIK3R1 binds PIK3CA
Activated FGFR2 mutants phosphorylate FRS2
Activated FGFR2 mutants phosphorylate PLCG1
Activated FGFR2 mutants:p-FRS2 binds GRB2:GAB1:PIK3R1
Activated FGFR2 mutant-associated PI3K phosphorylates PIP2 to PIP3
Activated FGFR2 mutants bind FRS2
Activated FGFR2 mutants bind PLCG1
Activated FGFR1 binds FLRT1,2,3
RAS GEFs promote RAS nucleotide exchange
Homozygous mutations in fibroblast growth factor 3 are associated with a new form of syndromic deafness characterized by inner ear agenesis, microtia, and microdontia.
Homozygous FGF3 mutations result in congenital deafness with inner ear agenesis, microtia, and microdontia.
Competition between nuclear localization and secretory signals determines the subcellular fate of a single CUG-initiated form of FGF3.
NoBP, a nuclear fibroblast growth factor 3 binding protein, is cell cycle regulated and promotes cell growth.
UniProtKB P11487 (FGF3_HUMAN) reviewed record
FGF3 source mechanism and phylogeny evidence