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Human FRS2 Protein expressed in Wheat germ - ABIN1354441
Krejci, Masri, Salazar, Farrington-Rock, Prats, Thompson, Wilcox: Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteins. in The Journal of biological chemistry 2007
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the FRS2 gene is consistently amplified in classic and dedifferentiated low-grade osteosarcomas
Authors find recurrent ADGRG6 enhancer mutations and FRS2 duplications which are associated with higher protein expression in the tumor and poor prognosis. Functional assays demonstrate that depletion of ADGRG6 or FRS2 expression in UBC cells compromise their abilities to recruit endothelial cells and induce tube formation.
loss of myristoylation of fibroblast growth factor receptor substrate 2 (FRS2alpha), a scaffold protein essential for FGFR signaling, inhibits FGF/FGFR-mediated oncogenic signaling and FGF10-induced tumorigenesis. Moreover, a previously synthesized myristoyl-CoA analog, B13, which targets the activity of N-myristoyltransferases.
These findings suggest that FRS2 is amplified consistently in liposarcoma.
MiR-4653-3p and its target gene FRS2 are may have roles in response of hormone receptor positive breast cancer patients to tamoxifen
we report for the first time that PKD1 was tightly regulated by androgen at the transcriptional level in prostate cancer cells and was a novel androgen-repressed gene. Further analysis identified FRS2 as a novel mediator of androgen-induced PKD1 repression.
They also demonstrate the potential of overexpressed FRS2alpha as a biomarker for prostate cancer diagnosis, prognosis and response to therapies.
Results identify FRS2 as an oncogene in a subset of high-grade serous ovarian cancers that harbor FRS2 amplifications.
Increased expression of FRS2alpha (and FGFR1) was associated with decreased progression-free survival among patients with metastatic renal cell carcinoma treated with sorafenib.
The signaling complex appears to integrate the input from FGFR and EphA4, and release the output signal through FRS2alpha.
These results establish the Frs2alpha-Shp2 complex as the key mediator of FGF signaling in lens development.
The docking protein FRS2alpha is a critical regulator of VEGF receptors signaling.
Patient with pigmentation disorders and vitiligo show decreased expression of mRNA.
Data indicate that the FGFR/FRS2 signaling axis was generally activated in about 75% of FRS2-positive high-grade liposarcomas.
a novel signaling network containing FRS2, CAP and flotillin-1
Validated FRS2 amplification in both Well-differentiated liposarcoma and dedifferentiated liposarcoma.
Microdeformations produced by the combination of polyurethane foam and suction are associated with increased fibroblast proliferation and up-regulation of gene expressions in fibroblasts
Phosphorylation of Fibroblast growth factor receptor substrate 2alpha may function as a molecular switch in the FGF pathway, sensing and participating in crosstalk with other signaling pathways.
FRS2 PTB domain conformation regulates interactions with divergent neurotrophic receptors
FRS2 has a role in fibroblast growth factor-2-induced signaling
FRS2 and FRS3, are together required for postnatal brain development. In the hippocampus, FRS2&3 promote dentate gyrus morphogenesis and dentate granule cell (DGC) maturation during developmental neurogenesis. Frs2,3-double mutants have reduced numbers of dendritic branches and spines in DGCs. Double-mutant mice exhibit fewer excitatory synaptic inputs onto DGCs.
FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis.
controlsConclusionFrs2alpha(ST-/-) embryos have aberrant ureteric induction sites, improper ureteral insertion, shortened intravesicular lengths, and VUR
Embryonic day 18.5 Six2Frs2alphaKO kidneys were hypoplastic and not cystic, postnatal day (P) 7 mutants had proximal tubular-derived cysts that nearly replaced the renal parenchyma by P21. Mutants had high proximal tubular proliferation rates and interstitial fibrosis, similar to known polycystic kidney disease models.
Fgfr signaling in nephron progenitors appears to be mediated predominantly by Frs2alpha.
Analysis of a mutant Fgfr1 allele, unable to bind to the adaptor protein, Frs2/3, indicates that Sox2 maintenance can be regulated by MAP kinase.
data from two models showed that FRS2 played different roles in the regulation of two activity levels of the ERK pathway components in the epididymis.
Genetic evidence further supports that the formation of an Frs2alpha-Shp2 complex and its recruitment to FGF receptors are crucial for downstream ERK signaling in this process.
Frs2alpha enhances fibroblast growth factor-mediated survival and differentiation in lens development.
FRS2alpha-mediated FGF signals suppress premature differentiation of cardiac stem cells through regulating autophagy activity.
The FGF signaling axis activates mTOR via the FGF receptor substrate 2alpha (FRS2alpha)-mediated PI3K/Akt pathway, and suppresses autophagy activity in MEFs.
although Fgfr2 and Frs2alpha have crucial roles in the ureteric lineage, they appear to act separately and additively.
Msx2 and Runx2 likely function together to induce PC-1 gene expression in osteoblastic cells and FGF signaling stimulates Msx2 transcriptional activity through the Frs2 mediated MAPK signaling pathway
FRS2alpha fine-tunes the FGF2-signaling to control self-renewal and proliferation of neural stem cells through Hes1.
Data show that PEA-15 prevents ERK1/2 localization to the plasma membrane, thereby inhibiting ERK1/2-dependent threonine phosphorylation of FRS2alpha to promote activation of the ERK1/2 MAP kinase pathway.
Trophoblast stem cell FRS2alpha mediates activation of the ERK pathway to enhance Cdx2 expression in response to FGF4. Cdx2 in turn binds to an FGF4-responsive enhancer element of the promoter region of Bmp4, leading to production and secretion of Bmp4.
Frs2alpha and Frs2beta have distinct spatio-temporal expression patterns in mouse embryos
FGFR kinase regulates the cell cycle through phosphorylation-dependent release of Cks1 from FGFR substrate 2
FRS2-dependent SRC activation is required for FGFR-induced phosphorylation of Sprouty and suppression of ERK activity
Adapter protein that links activated FGR and NGF receptors to downstream signaling pathways. Plays an important role in the activation of MAP kinases and in the phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3- kinase, in response to ligand-mediated activation of FGFR1. Modulates signaling via SHC1 by competing for a common binding site on NTRK1.
fibroblast growth factor receptor substrate 2
, FGFR signalling adaptor
, FGFR substrate 2
, FGFR-signaling adaptor SNT
, suc1-associated neurotrophic factor target 1