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抗Human FAK 抗体:
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Human Polyclonal FAK Primary Antibody for IHC - ABIN966125
Sanders, Basson: p130cas but not paxillin is essential for Caco-2 intestinal epithelial cell spreading and migration on collagen IV. in The Journal of biological chemistry 2005
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Human Polyclonal FAK Primary Antibody for WB - ABIN361988
Shi, Boettiger: A novel mode for integrin-mediated signaling: tethering is required for phosphorylation of FAK Y397. in Molecular biology of the cell 2003
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Human Monoclonal FAK Primary Antibody for ICS - ABIN1177061
Ma, Richardson, Schaefer, Parsons: Serine phosphorylation of focal adhesion kinase in interphase and mitosis: a possible role in modulating binding to p130(Cas). in Molecular biology of the cell 2001
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Human Monoclonal FAK Primary Antibody for ICS - ABIN1177060
Schlaepfer, Mitra, Ilic: Control of motile and invasive cell phenotypes by focal adhesion kinase. in Biochimica et biophysica acta 2004
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Human Monoclonal FAK Primary Antibody for ICS - ABIN1177062
Yamakita, Totsukawa, Yamashiro, Fry, Zhang, Hanks, Matsumura: Dissociation of FAK/p130(CAS)/c-Src complex during mitosis: role of mitosis-specific serine phosphorylation of FAK. in The Journal of cell biology 1999
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Human Monoclonal FAK Primary Antibody for WB - ABIN1882052
Whitney, Chan, Blake, Cosand, Neubauer, Aruffo, Kanner: Human T and B lymphocytes express a structurally conserved focal adhesion kinase, pp125FAK. in DNA and cell biology 1993
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Human Polyclonal FAK Primary Antibody for ELISA, ICC - ABIN6256730
Zhang, Zhou, Meng, Zhang, Zhou: Down-regulating Myoferlin inhibits the vasculogenic mimicry of melanoma via decreasing MMP-2 and inducing mesenchymal-to-epithelial transition. in Journal of cellular and molecular medicine 2018
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Human Polyclonal FAK Primary Antibody for ELISA, ICC - ABIN6261663
Wu, Huang, Jiao, Ding, Zhang, Chen, Wang, Li, Huo: Olaquindox disrupts tight junction integrity and cytoskeleton architecture in mouse Sertoli cells. in Oncotarget 2017
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Human Monoclonal FAK Primary Antibody for ELISA, WB - ABIN969128
Tse, Dang-Lawson, Lee, Vong, Bulic, Buckbinder, Gold: B cell receptor-induced phosphorylation of Pyk2 and focal adhesion kinase involves integrins and the Rap GTPases and is required for B cell spreading. in The Journal of biological chemistry 2009
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Human Monoclonal FAK Primary Antibody for ICC, FACS - ABIN969129
Zheng, Kurenova, Ucar, Golubovskaya, Magis, Ostrov, Cance, Hochwald: Targeting of the protein interaction site between FAK and IGF-1R. in Biochemical and biophysical research communications 2009
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tumor cells incubated with LGRFYAASG-pen showed disruption of filamentous actin, focal adhesions and caveolae-mediated membrane trafficking, resulting in impaired cell adhesion and migration in vitro. These effects were paralleled by a decrease in the phosphorylation of both focal adhesion kinase (Fak) and protein kinase B (Akt).
LFA-1 cross-linking recruits and activates FAK1 and PYK2 to phosphorylate LAT selectively on a single Y-171 site that binds to the GRB2-SKAP1 complex and limits dwell times of T-cells with dendritic cells
Results identified FAK mRNA as a direct target of miR-433. Its activation inhibits the effect of microRNA433 on the growth of cervical cancer cells.
This study shows that Leu33Pro polymorphism of integrin beta 3 modulates platelet Src pY418 and focal adhesion kinase pY397 phosphorylation in response to abnormally high shear stress. Whereas physiological shear stress does not affect platelet signaling, abnormally high-shear stress considerably elevates Src and FAK phosphorylation in both Pro33 and Leu33 platelets.
High FAK expression is associated with gastric cancer.
These results indicate that PCTK3 controls actin cytoskeleton dynamics by negatively regulating the FAK/Rho signaling pathway.
FAK is required for adipocyte survival and maintenance of insulin sensitivity, particularly in the context of adipose tissue expansion as a result of caloric excess.
Data suggest that TYRO3-mediated phosphorylation of ACTN4 is involved in invasiveness of melanoma cells; TYRO3-mediated phosphorylation of ACTN4 requires FAK activation at tyrosine 397. (TYRO3 = TYRO3 protein tyrosine kinase; ACTN4 = actinin alpha 4; FAK = focal adhesion kinase isoform FAK1)
FAK controls invasiveness of tumor cells by regulating focal adhesion-mediated motility.
FAK controls the nuclear translocation and activation of YAP in response to mechanical activation and submit that the YAP-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, Rac1 and Cdc42, all of which are critical proteins for the regulation of cell movement.
This study demonstrated that the Cas scaffolding protein family member 4 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), and inhibiting cell motility by reducing the levels of Rho GTPases (Rac1, Cdc42 and RhoA).
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 phosphorylation.
MUC4/X facilitated pancreatic cancer (PC) tumorigenesis via integrin-beta1/FAK/ERK signaling pathway. Overall, these findings revealed the novel role of MUC4/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.
MPAP suppressed cancer cell proliferation and the phosphorylation of FAK1. Combined treatment with MPAP and irradiation (IR) showed enhanced suppression of cancer cell proliferation in wild-type p53 cells and more intense suppression in p53-null cells
evidence that despite the fact that FAK is in the active, open conformation at CAs, 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, 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 and membrane fluidity mediates the spatially polarized Src/FAK activation in response to shear stress.
XIAP 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-induced monolayer permeability involves focal adhesion and cytoskeletal rearrangement through both FAK/Src-dependent and -independent pathways.
Results suggest focal adhesion kinase is involved in thrombospondin-1-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 by regulating type II collagen expression and cell proliferation.
FAK appears to regulate inflammation in chondrocytes under Cyclic Tensile Strain via MAPK pathways.
FAK Y397 is required for the highly dynamic tissue remodeling during development but dispensable for normal homeostasis of avascular epidermis. In contrast to the Y397F mutation, FAK Y397E retains sufficient biological activity to allow for development beyond mid-gestation.
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.
These findings suggest that NG2 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.
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 physiologically regulates neuronal migration by binding to alpha-actinin and influencing phosphorylation of both FAK and alpha-actinin 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 discriminates substrate stiffness through a PKCbeta-mediated FAK activation dependent manner.
An FAK-YAP-mTOR 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, 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 EZH2.
miR-7a was a necessary mediator in FADD-regulated FAK expression. In contrast to its classical apoptotic role, FADD interference could reduce the rate of cell migration, which could be rescued by inhibiting miR-7a expression.
Irradiation coupled with JNK inhibition in beta1 integrin -/- transgenic adenocarcinoma of prostate (TRAMP) leads to increased levels of nuclear focal adhesion kinase (FAK) in tumor cells.
Ablation of Cyclophilin D Results in an Activation of FAK, Akt, and ERK Pathways in the Mouse Heart.
These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
findings highlight an essential role of Paxillin and FAK in controlling cardiac contractility via the recruitment of Vinculin 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 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+-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