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Human FAK Protein expressed in HEK-293 Cells - ABIN2720714
Banerjee, de Freitas, Friggeri, Zmijewski, Liu, Abraham: Intracellular HMGB1 negatively regulates efferocytosis. in Journal of immunology (Baltimore, Md. : 1950) 2011
The ectopic overexpression of miR-379 inhibited cell migration, invasion and EMT progress, while downregulated miR-379 reversed the effect. In addition, miR-379 regulated the focal adhesion kinase (FAK) by directly binding to its 3'-UTR, resulting in suppression of AKT signaling. In clinical samples of gastric cancer (GC), miR-379 inversely correlated with FAK, which was upregulated in GC.
Building upon previous work suggesting that FAK-Akt1 (show AKT1 Proteins) binding is mediated by the FAK F1 lobe, we demonstrated that independently expressing the F1 domain in human Caco-2 or murine CT-26 (show DDX53 Proteins) colon cancer cells by transient or stable inducible plasmid expression respectively prevents the stimulation of cancer cell adhesion by increased extracellular pressure.
functional activation of FAK1 in metastases and provide preclinical rationale for targeting this kinase in the setting of advanced ccRCC
this study shows that simultaneous deactivation of FAK and Src (show SRC Proteins) improves the pathology of hypertrophic scar
Silencing of p130Cas (show BCAR1 Proteins) and inhibition of FAK activity both strongly reduced imatinib and nilotinib stimulated invasion.
IP6K1 (show IP6K1 Proteins) physiologically regulates neuronal migration by binding to alpha-actinin (show ACTN1 Proteins) and influencing phosphorylation of both FAK and alpha-actinin (show ACTN1 Proteins) through its product 5-diphosphoinositol pentakisphosphate.
These data indicate that Ang II (show AGT Proteins)-AT2R (show AGTR2 Proteins) regulates human bone marrow MSC (show MSC Proteins) migration by signaling through the FAK and RhoA (show RHOA Proteins)/Cdc42 (show CDC42 Proteins) pathways.
upregulated FAK expression correlates with poor prognosis and tumor dissemination in surgically treated patients with hypopharyngeal cancer
These findings suggest that the integrin beta4-FAK/Src (show SRC Proteins) signaling axis may play a crucial role in clonorchiasis-associated cholangiocarcinoma metastasis during tumor progression.
whereas Src (show SRC Proteins) activation under shear stress is dominantly ligand-dependent, FAK signaling seems to be mostly shear induced.
evidence that despite the fact that FAK is in the active, open conformation at CAs (show CSE1L Proteins), its kinase activity is dispensable for ciliogenesis and ciliary function revealing that FAK plays a scaffolding role in multiciliated cells.
FAK is required for external force-induced spindle reorientation, suggesting that FAK's involvement in this process stems from a role in the transduction of external forces to the cell cortex.
FAK is required for tension-dependent organization of collective cell movements in Xenopus mesendoderm.
work identifies new roles for the FERM domain in the regulation of the dynamics of FAK on its signaling complexes in vivo and in vitro and identifies epiboly as the earliest developmental process in which FAK plays a crucial role during development
These data suggest an important role for the FERM domain in the activation of FAK.
FAK phosphorylation at Y861 is essential for lamellipodial protrusion induced by BDNF (show BDNF Proteins), while phosphorylation at Y925 controls the rate of point contact turnover.
Data imply that FAK plays an essential role in chamber outgrowth and looping morphogenesis.
FAK is required for proper topographic positioning of retinal axons along the anterior-posterior axis of the optic tectum in Xenopus and zebrafish, a guidance decision mediated in part by A-type ephrins.
RhoA (show RHOA Proteins) and membrane fluidity mediates the spatially polarized Src (show SRC Proteins)/FAK activation in response to shear stress.
XIAP (show XIAP Proteins) plays an essential role in shear stress-stimulated FAK phosphorylation.
mitochondrial oxidants generated in response to endothelial strain trigger FAK phosphorylation through a signaling pathway that involves protein kinase C
These results suggest that TGF-beta1 (show TGFB1 Proteins)-induced monolayer permeability involves focal adhesion and cytoskeletal rearrangement through both FAK/Src (show SRC Proteins)-dependent and -independent pathways.
Results suggest focal adhesion kinase is involved in thrombospondin-1 (show THBS1 Proteins)-induced vascular smooth muscle cell migration.
In conclusion, our observations reveal that PRRSV triggers the activation of FAK-PI3K-AKT-Rac1 signaling pathway to facilitate its entry into cells.
Data suggest that focal adhesion kinase (FAK)-SMAD 2/3 mediate signal crosstalk between type II collagen and TGF-beta1 and regulate glycosaminoglycan secretion in chondrocytic cells.
FAK is essentially required in chondrocyte communication with type II collagen (show COL2A1 Proteins) by regulating type II collagen (show COL2A1 Proteins) expression and cell proliferation.
The results suggest that FAK is not required for monocyte migration to the perivascular space and that vascular remodeling following arterial occlusion occurs independently of myeloid specific FAK.
These results provide a molecular explanation of how initiation of B cell activation (show BLNK Proteins) discriminates substrate stiffness through a PKCbeta-mediated FAK activation dependent manner.
An FAK-YAP (show YAP1 Proteins)-mTOR (show FRAP1 Proteins) Signaling Axis Regulates Stem Cell-Based Tissue Renewal in Mice.
loss of FAK signaling during endoplasmic reticulum stress causes mitochondrial dysfunction by reducing the protective effects of mitochondrial STAT3 (show STAT3 Proteins), leading to endothelial cell death.
Hypoxia activated the focal adhesion kinase (FAK) pathway through upregulation of BNIP3, while FAK inhibition attenuated hypoxic keratinocyte migration.
Among a group of tumor cells, there is correlation between activation of the MRTF-dependent transcription and activated FAK-dependent regulation of cell migration.
It has been demonstrated that FAK depletion reduces hepatocellular carcinoma cell growth by affecting cancer-promoting genes including the pro-oncogene (show RAB1A Proteins) EZH2 (show EZH2 Proteins).
miR (show MLXIP Proteins)-7a was a necessary mediator in FADD (show FADD Proteins)-regulated FAK expression. In contrast to its classical apoptotic role, FADD (show FADD Proteins) interference could reduce the rate of cell migration, which could be rescued by inhibiting miR (show MLXIP Proteins)-7a expression.
These data support a crucial role for miR (show MYLIP Proteins)-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
findings highlight an essential role of Paxillin (show PXN Proteins) and FAK in controlling cardiac contractility via the recruitment of Vinculin (show VCL Proteins) to mechano-sensitive sites in cardiomyocytes.
Data indicate that focal adhesion kinase (FAK) activity may be a mediator of the integrin alpha5/Fn1 interaction during zebrafish lens fiber morphogenesis.
Focal adhesion kinase (FAK) mediates regulation of growth cone adhesion in the optic tectum of zebrafish.
This gene encodes a cytoplasmic protein tyrosine kinase which is found concentrated in the focal adhesions that form between cells growing in the presence of extracellular matrix constituents. The encoded protein is a member of the FAK subfamily of protein tyrosine kinases but lacks significant sequence similarity to kinases from other subfamilies. Activation of this gene may be an important early step in cell growth and intracellular signal transduction pathways triggered in response to certain neural peptides or to cell interactions with the extracellular matrix. Several transcript variants encoding different isoforms have been found for this gene, but the full-length natures of only three of them have been determined.
, FAK-related non-kinase polypeptide
, PTK2 protein tyrosine kinase 2
, focal adhesion kinase 1
, focal adhesion kinase-related nonkinase
, protein phosphatase 1 regulatory subunit 71
, protein phosphatase 1, regulatory subunit 71
, focal adhesion kinase pp125FAK
, protein-tyrosine kinase 2
, focal adhesion kinase
, focal ashension kinase 1
, protein tyrosine kinase 2.1