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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
FAK controls the nuclear translocation and activation of YAP (show YAP1 Proteins) in response to mechanical activation and submit that the YAP (show YAP1 Proteins)-dependent process of durotaxis requires a cell with an asymmetric distribution of active and inactive FAK molecules.
Results show thatproto-Oncogene Protein ets-1 (ETS1) drives ovarian cancer (OC) metastasis phenotypes through its transcriptional target PTK2 (focal adhesion kinase FAK).
Methylmercury chloride negatively affects the activation of Src (show SRC Proteins), Rac1 and Cdc42 (show CDC42 Proteins), all of which are critical proteins for the regulation of cell movement.
This study demonstrated that the Cas scaffolding protein family member 4 (show CASS4 Proteins) and protein tyrosine kinase 2 proteins and their significant role in the activation of downstream signaling pathways in Alzheimer's disease.
Calpain small subunit 1 (Capn4) overexpression increased the protein level of cleaved talin and and activated the focal adhesion kinase (FAK)/AKT/MAPK signaling in 786-O cells, while Capn4 silencing decreased the protein level of cleaved talin in Caki-1 cells.
mitochondria are present at the leading edge of migrating cells, SIRT3 expression is down-regulated during migration, resulting in elevated ROS levels. This SIRT3-mediated control of ROS represses Src oxidation and attenuates focal adhesion kinase (FAK) activation.
These results demonstrated that the inhibition of FAK promoted cell detachment by decreasing the expression of focal adhesions components (talin and paxillin (show PXN Proteins)), and inhibiting cell motility by reducing the levels of Rho GTPases (Rac1, Cdc42 (show CDC42 Proteins) and RhoA (show RHOA Proteins)).
The results showed that in cervical cancer cells Rac1 activation by hypoxia could stimulate invasion and migration, and this process was mediated by integrin a5b3-facilitated FAK and PI3K (show PIK3CA Proteins) phosphorylation.
MUC4 (show MUC4 Proteins)/X facilitated pancreatic cancer (PC) tumorigenesis via integrin-beta1/FAK/ERK (show EPHB2 Proteins) signaling pathway. Overall, these findings revealed the novel role of MUC4 (show MUC4 Proteins)/X in promoting and sustaining the oncogenic features of PC.
The addition of LCS to capecitabine treatment led to an increase in the proteolysis of the FAK signaling cascade components.
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 C-terminal DSP domain induced phosphorylation of occludin Ser(490) and focal adhesion kinase (FAK) Ser(722) and Tyr(576). Coexpression of DSP, occludin and FAK was detected in dental mesenchymal cells during tooth development. Occludin physically interacts with FAK, and occludin and FAK phosphorylation can be blocked by DSP and occludin antibodies.
Overexpression of FAK impaired neuronal migration through Tyr925 phosphorylation during corticogenesis.
these data provide mechanistic insight into how FAK controls the tumor immune environment, namely, through a transcriptional regulatory network mediated by nuclear IL-33 (show IL33 Proteins).
These findings suggest that NG2 (show Vcan Proteins) expression mediates inflammatory reactions and neurodegeneration in microglial cells in response to central nervous system injury, potentially by regulating FAK phosphorylation.
FAK tyrosine 397 autophosphorylation is required for FAK function and is positively regulated by MYO1E (show MYO1E Proteins).
Building upon previous work suggesting that FAK-Akt1 binding is mediated by the FAK F1 lobe, we demonstrated that independently expressing the F1 domain in human Caco-2 or murine CT-26 colon cancer cells by transient or stable inducible plasmid expression respectively prevents the stimulation of cancer cell adhesion by increased extracellular pressure.
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.
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.
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.
presynaptic FAK signaling may be disrupted, causing abnormal synaptic growth and transmission in the NF1 (show NF1 Proteins) genetic
Fak56 may play a subtle role in the negative regulation of integrin adhesion
Fak56D mutation causes severe disruption of the optic stalk structure. These phenotypes were completely rescued by Fak56D transgene expression in the SG cells but not in photoreceptor cells.
An intron loss of Dfak gene in species of the Drosophila melanogaster subgroup.
Together these findings suggest that modulation of Fak56 function is important for action potential propagation and Ca2 (show CA2 Proteins)+-regulated neuromuscular transmission in vivo.
Data show that Fak56 is required to restrict larval neuromuscular junctions (NMJ)growth during NMJ development and mediates an extracellular signal through the integrin receptor.
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
, focal adhesion kinase homolog