FGFR2IIIa TM binds ligand and full length receptors to inhibit signaling

Stable Identifier
R-HSA-8853320
Type
Reaction [binding]
Species
Homo sapiens
Compartment
plasma membrane
ReviewStatus
5/5
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FGFR2IIIa TM binds ligand and full length receptors to inhibit signaling
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By BIAcore assay, FGFR2 IIIa TM has been shown to bind FGF1, and in the presence of chip-bound FGFR2b or 2c, to form an FGF1-dependent heterodimer. In COS cells stimulated with FGF2, expression of FGFR IIIa TM abrogates FGF signaling and stabilizes the full length receptors at the cell surface. Consistent with this, in vivo expression of FGFR2 IIIa TM abrogates expression of the FGFR target gene MKP3. These data support the idea that FGFR2 IIIa TM inhibits FGFR signaling by binding and sequestering ligand and/or forming non-functional heterodimers with full-length receptors (Wheldon et al, 2011).
Literature References
PubMed ID Title Journal Year
21355848 Identification and characterization of an inhibitory fibroblast growth factor receptor 2 (FGFR2) molecule, up-regulated in an Apert Syndrome mouse model

Hajihosseini, MK, Khodabukus, N, Heath, JK, Smith, TG, Patey, SJ, Wheldon, LM

Biochem. J. 2011
Participants
Input
Output
Participates
as an event of
Functional status

Gain of function of FGFR2 IIIa TM [extracellular region]

Disease Entity
Status
Inferred From
Mouse FGFR2 IIIa TM binds FGF1,2 and full-length receptors (Homo sapiens)
Disease
Name Identifier Synonyms
acrocephalosyndactylia DOID:12960 Apert syndrome
Authored
Rothfels, K  (2016-01-09)
Reviewed
Grose, RP  (2016-01-25)
Created
Rothfels, K  (2016-01-22)
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