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anti-Human FES Antibodies:
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Human Monoclonal FES Primary Antibody for ELISA, WB - ABIN969135
Delfino, Stevenson, Smithgall: A growth-suppressive function for the c-fes protein-tyrosine kinase in colorectal cancer. in The Journal of biological chemistry 2006
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Human Monoclonal FES Primary Antibody for IHC, ELISA - ABIN969134
Durfee, Rivard: Design and simulation of a pneumatic, stored-energy, hybrid orthosis for gait restoration. in Journal of biomechanical engineering 2006
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Human Monoclonal FES Primary Antibody for ELISA, WB - ABIN966135
Vitenzon, Mironov, Petrushanskaya: Functional electrostimulation of muscles as a method for restoring motor functions. in Neuroscience and behavioral physiology 2006
Show all 3 Pubmed References
analysis of the JAK-Fes-phospholipase D signaling pathway that is enhanced in highly proliferative breast cancer cells
c-fes gene expression was found in myeloid leukemias, whereas low or no expression in lymphocytic leukemias.
FES kinase is a mediator of wild-type KIT signalling implicated in cell migration.
Closing in on the biological functions of Fps/Fes and Fer. A review.
Fes naturally adopts an inactive conformation in vivo, and maintenance of the inactive structure requires the coiled-coil and SH2 domains.
Fps/Fes and Fer are expressed in human and mouse platelets, and are activated following stimulation with collagen and collagen-related peptide (CRP), suggesting a role in GPVI receptor signaling
Fes transduces inductive signals for terminal macrophage and granulocyte differentiation, and this biological activity is mediated through the activation of lineage-specific transcription factors.
FPS mediates enhanced sensitization to VEGF and PDGF signaling in ECs; this hypersensitization contributes to excessive angiogenic signaling and underlies the observed hypervascular phenotype of human myristoylated FPS expressed in transgenic mice.
c-Fes is a regulator of the tubulin cytoskeleton and may contribute to Fes-induced morphological changes in myeloid hematopoietic and neuronal cells
NMR assignment of the SH2 domain
PEDF downregulates Fyn through Fes, resulting in inhibition of FGF-2-induced capillary morphogenesis of endothelial cells
NMR analysis of Src homology 2 domain from the human feline sarcoma oncogene Fes
FES has a growth suppressive function in colorectal neoplasms.
A novel Fes-KAP-1 interaction is reported, suggesting a dual role for KAP-1 as both a Fes activator and downstream effector.
These novel results indicate the involvement of Fes in VEGF-A-induced cellular responses by cultured endothelial cells.
shows a major function of FES downstream of activated KIT receptor and thereby points to FES as a novel target in KIT-related pathologi
Ezrin/Fes interaction at cell-cell contacts plays an essential role in hepatocyte growth factor-induced cell scattering and implicates Fes in the cross-talk between cell-cell and cell-matrix adhesion.
The SH2 and catalytic domains of active Fes and Abl pro-oncogenic kinases form integrated structures essential for effective tyrosine kinase signaling.
study shows Fes phosphorylates C-terminal tyrosine residues in HS1 implicated in actin stabilization; coordinated action of F-BAR & SH2 domains of Fes allow for coupling to FcepsilonRI signaling & potential regulation of actin reorganization in mast cells
Study of promoter methylation as important mechanism responsible for downregulation of FES gene expression in colorectal cancer cells. Treatment with DNA methyltransferase inhibitor resulted in expression of functional FES transcripts in CRC cell lines.
FES is a driver of melanoma progression in a mouse model.
Fes inhibition might provide therapeutic benefits in breast cancer, in part by attenuating tumor-associated angiogenesis and the metastasis-promoting functions of tumor-associated macrophages.
Fes protein is activated downstream of activated Kit receptor, and this is facilitated by the Fes SH2 domain binding to Kit, and by trans-phosphorylation by Fyn kinase.
Truncation of c-fes via gene targeting results in embryonic lethality and hyperproliferation of hematopoietic cells.
Fes was expressed in mouse brain. Experiments with transfected mouse cDNA show that Fes links Sema3A signals to CRMP-CRAM.
Fes may be a key component of the granulocyte differentiation machinery, may regulate granulocyte-specific gene expression
Hematopoiesis is deregulated in the absence of Fps and Fer kinases. Qualitative differences in myeloid colonies from compound mutant mice suggested a role for Fps and Fer kinases in regulating cell-cell adhesion or a skewing in cellularity of colonies.
Fps/Fes may act synergistically with Flk1 to modulate hemangioblast differentiation into the endothelium.
plays a critical role in microtubule dynamics including microtubule nucleation and bundling through its FCH domain
The increased numbers and survival of erythroid progenitors from fps(MF) mice, and their differential responsiveness to SCF and EPO, implicates Fps/Fes in the commitment of multilineage progenitors to the erythroid lineage.
studies suggest that Fps/Fes influences both angiogenic and hemostatic function through regulatory effects on the endothelium
Tumor onset in a mouse model of breast epithelial cancer occurred earlier in mice targeted with either null or kinase-inactivating fps/fes mutations.
Lyn and Fer/Fps kinases cooperate to phosphorylate Pecam-1 and activate Shp1/Shp2 phosphatases that function in part to limit mast cell activation
These findings suggest that activation of Fes by fibroblast growth factor-2 (FGF-2) enhances FAK-dependent activation of Src within focal adhesions, promoting FGF-2-induced disassembly of focal adhesions.
Fps/Fes is not essential for the maintenance of mammary epithelial cell adherens junctions in lactating mammae.
This gene encodes the human cellular counterpart of a feline sarcoma retrovirus protein with transforming capabilities. The gene product has tyrosine-specific protein kinase activity and that activity is required for maintenance of cellular transformation. Its chromosomal location has linked it to a specific translocation event identified in patients with acute promyelocytic leukemia but it is also involved in normal hematopoiesis as well as growth factor and cytokine receptor signaling. Alternative splicing results in multiple variants encoding different isoforms.
Oncogene FES, feline sarcoma virus
, feline sarcoma (Snyder-Theilen) viral (v-fes)/Fujinami avian sarcoma (PRCII) viral (v-fps) oncogene homolog
, feline sarcoma/Fujinami avian sarcoma oncogene homolog
, proto-oncogene c-Fes
, proto-oncogene c-Fps
, proto-oncogene tyrosine-protein kinase Fes/Fps
, tyrosine-protein kinase Fes/Fps
, V-FES feline sarcoma viral/V-FPS fujinami avian sarcoma viral oncogene homolog
, c-fes proto-oncogene protein
, feline sarcoma viral (v-fes) oncogene
, v-fps oncogene homolog
, tyrosine kinase Fps/Fes
, feline sarcoma oncogene
, c-fps proto oncogene
, tyrosine-protein kinase Fes/Fps-like