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Human FAK ELISA Kit for Sandwich ELISA - ABIN416964
Gupta, Khan, Kumar, Kumar, Sharma: Versican and its associated molecules: potential diagnostic markers for multiple myeloma. in Clinica chimica acta; international journal of clinical chemistry 2015
In contrast to mice, the analysis of human olfactory bulbs revealed a late activation of FAK in advanced AAlzheimer's disease stages, whereas ERK1/2 activation was enhanced across AD staging
focal adhesion kinase (FAK) transduces integrin activation and supports Human embryonic stem cell survival, substrate adhesion, and maintenance of the undifferentiated state.
Data show that miR (show MLXIP ELISA Kits)-193b, by directly targeting focal adhesion kinase (FAK), CRK (show CRK ELISA Kits)-like proto-oncogene (show RAB1A ELISA Kits) (CRKL (show CRKL ELISA Kits)), and methionine sulfoxide reductase A (MSRA (show MSRA ELISA Kits)), regulates focal adhesion signaling and ROS (show ROS1 ELISA Kits) signaling, which play pivotal roles in liposarcomagenesis and adipogenic differentiation.
PTK2 inhibition-induced sustained levels of ATG3 (show ATG3 ELISA Kits) were able to sensitize cancer cells to DNA-damaging agents.
High FAK expression is associated with Ovarian Cancer.
Generally, this study indicates that miR (show MLXIP ELISA Kits)-3173 negatively regulates PTK2 and inhibits proliferation and invasion of B-ALL cell lines. Thus, miR (show MLXIP ELISA Kits)-3173 may represent a potential therapeutic molecule for B-ALL intervention.
elevated levels of bile acid increase the tumorigenic potential of pancreatic cancer cells by inducing FXR (show NR1H4 ELISA Kits)/FAK/c-Jun (show JUN ELISA Kits) axis to upregulate MUC4 (show MUC4 ELISA Kits) expression.
Osteoprotegerin (show TNFRSF11B ELISA Kits) facilitates pulmonary arterial hypertension pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation via integrin alphavbeta3 (show ITGAV ELISA Kits)/FAK/AKT (show AKT1 ELISA Kits) signaling pathway.
the active phosphorylated form of Src (Src (show SRC ELISA Kits)(pY416) ) is co-expressed in Exo with phosphorylated FAK (FAK(pY861) ), a known target site of Src (show SRC ELISA Kits), which enhances proliferation and migration.
our findings identified FAK as a common aberrant protein overexpression in various subtypes of osteosarcoma. pFAK-Y397 overexpression can be used as a prognostic biomarker predicting poor OS for patients with metastatic osteosarcoma, and the expression of pFAK-Y397 differentiated good and poor responders to neoadjuvant chemotherapy.
evidence that despite the fact that FAK is in the active, open conformation at CAs (show CSE1L ELISA Kits), 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 ELISA Kits), 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 ELISA Kits) and membrane fluidity mediates the spatially polarized Src (show SRC ELISA Kits)/FAK activation in response to shear stress.
XIAP (show XIAP ELISA Kits) 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 (show PKC ELISA Kits)
These results suggest that TGF-beta1 (show TGFB1 ELISA Kits)-induced monolayer permeability involves focal adhesion and cytoskeletal rearrangement through both FAK/Src (show SRC ELISA Kits)-dependent and -independent pathways.
Results suggest focal adhesion kinase is involved in thrombospondin-1 (show THBS1 ELISA Kits)-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 ELISA Kits) by regulating type II collagen (show COL2A1 ELISA Kits) expression and cell proliferation.
In mouse olfactory bulbs, beta-amyloid induced an inactivation of focal adhesion kinase (FAK) together with a transient activation of MEK1/2, leading to inactivation of ERK1/2.
High FAK expression is associated with skin squamous cell carcinoma.
In cardiomyocytes exposed to biomechanical stimulation, FAK accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c (show MEF2C ELISA Kits) through an interaction with the FAK focal adhesion targeting (FAT) domain.
FAK-knockout mice were shorter and showed reduced bone volume. Disruptions of FAK function in osteoblasts reduced mRNA and protein expression of Runx2 (show RUNX2 ELISA Kits) Osterix (show SP7 ELISA Kits) and collagen-1.
The remodeling of the stromal matrix by CAFs has been shown to increase tumor rigidity to indirectly regulate FAK Y397 phosphorylation in tumor cells to promote their growth and invasion. Accordingly, the Hic-5(-/-);PyMT tumor cells exhibited a reduction in FAK Y397 phosphorylation. Isolated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exhibited reduced contractility
Focal adhesion kinase (FAK) in platelets regulated their migration into the tumor microenvironment, and FAK-deficient platelets completely prevented the rebound tumor growth.
dynamic changes to the extracellular matrix after injury promote fibroblast activation and inhibition of epithelial cell apoptosis in response to TGF-beta (show TGFB1 ELISA Kits) through FAK activation.
Results suggest that interleukin-6 (IL-6 (show IL6 ELISA Kits)) increases VEGF-C (show VEGFC ELISA Kits) induction and lymphangiogenesis may involve, at least in part, Src (show SRC ELISA Kits)-FAK-STAT3 (show STAT3 ELISA Kits) cascade in lymphatic endothelial cells (LECs).
identify FAK as a novel negative regulator of Beclin1 (show BECN1 ELISA Kits)-mediated autophagy and indicate that this pathway can facilitate the promotion of compensatory hypertrophic growth
These data support a crucial role for miR (show MYLIP ELISA Kits)-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
findings highlight an essential role of Paxillin (show PXN ELISA Kits) and FAK in controlling cardiac contractility via the recruitment of Vinculin (show VCL ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)+-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
, activated Cdc42 kinase-like
, tyrosine kinase
, focal adhesion kinase homolog