Gene interactions and pathways from curated databases and text-mining

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FGFR3 — STAT1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Britto et al., Cleft Palate Craniofac J 2002 (Acrocephalosyndactylia...) : In addition, the immunolocalization of the ligand FGFs 2, 4, and 7 was undertaken together with the intracellular transcription factor STAT1 , which is activated by FGFR signaling
Nakajima et al., Endocrinology 2003 (Femoral Fractures) : Furthermore, FGFR3, STAT1, and p21 exhibited a similar temporal expression profile, suggesting that FGFR3 mediated STAT1-p21 signaling plays a role in fracture repair
Citores et al., J Cell Physiol 2007 (Breast Neoplasms) : Both FGFR1 and FGFR2 induced strong phosphorylation of STAT1 causing redistribution of the Golgi apparatus, while FGFR3 and FGFR4 induced less phosphorylation of STAT1 and little or no redistribution of the Golgi apparatus
Harada et al., Bone 2007 (Dwarfism) : Here we reveal that phospholipase C gamma ( PLCgamma ) mediates FGFR3 induced STAT1 activation ... Both PLCgamma and STAT1 were activated by FGFR3 signaling, but a dominant negative form of PLCgamma ( DN-PLCgamma ) remarkably reduced STAT1 phosphorylation
Krejci et al., PloS one 2008 (Bone Diseases, Developmental) : Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage ... In a cell-free kinase assay, only K650M and K650E-FGFR3 caused activatory STAT1 ( Y701 ) phosphorylation ... Similarly, in RCS chondrocytes, HeLa, and 293T cellular environments, only K650M and K650E-FGFR3 caused strong STAT1 activation
Su et al., Nature 1997 (Thanatophoric Dysplasia) : Activation of Stat1 by mutant fibroblast growth-factor receptor in thanatophoric dysplasia type II dwarfism ... Furthermore, expression of TDII FGFR3 induced nuclear translocation of Stat1 , expression of the cell-cycle inhibitor p21 ( WAF1/CIP1 ), and growth arrest of the cell