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Adapter protein involved in invadopodia and podosome formation, extracellular matrix degradation and invasiveness of some cancer cells. Additionally we are shipping and many more products for this protein.
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Rheumatoid arthritis T cells abundantly express the podosome scaffolding protein TKS5, which enables them to form tissue-invasive membrane structures. TKS5 overexpression was regulated by the intracellular metabolic environment of RA T cells-specifically, by reduced glycolytic flux that led to deficiencies in ATP and pyruvate.
Results show that the interaction between Girdin (show CCDC88A Antibodies) and Tks5 might be important for Tks5 phosphorylation in HCC (show FAM126A Antibodies) cells.
This is the first study that identifies a new Rab40b (show RAB40B Antibodies)-Tks5- and miR (show MLXIP Antibodies)-204-dependent invadopodia transport pathway that regulates MMP2 (show MMP2 Antibodies) and MMP9 (show MMP9 Antibodies) secretion, and extracellular matrix remodeling during cancer progression.
Results suggest that Tks5, similar to XB130 (show AFAP1L2 Antibodies), plays a role in cell proliferation and cell survival and that the interaction between XB130 (show AFAP1L2 Antibodies) and Tks5 appears to be critical for regulation of Src (show SRC Antibodies)-mediated cellular homeostasis.
TKS5 and MYLK (show MYLK Antibodies) represent two mediators of invasive behavior of cancer cells that are regulated by the ZEB1 (show ZEB1 Antibodies)/miR (show MLXIP Antibodies)-200 feedback loop
establishes an important role for Tks5 in tumor growth in vivo, and suggests that invadopodia may play broad roles in tumor progression
Results show that TKS5 is highly expressed in many cancer types with strong correlation with increased metastatic events and a poorer prognosis suggesting a clinical importance.
Inhibiting the function of Tks5 both reduced extracellular matrix degradation in vitro and disrupted motoneuron axons from exiting the spinal cord and extending into the periphery.
Tks5 is needed for breast carcinoma cell invadopodium precursor stabilization, where the phox homology (PX) domain of Tks5 interacts with PI(3,4)P2. SHIP2 (show INPPL1 Antibodies) arrival at the invadopodium precursor coincides with the onset of PI(3,4)P2 accumulation.
Src (show SRC Antibodies)-dependent Tks5 phosphorylation regulates invadopodia-associated invasion in prostate cancer cells.
Signaling leading to Tks5 activation in peritoneal mesothelial cells may be a suitable therapeutic target for prevention of peritoneal carcinomatosis.
Tks5 undergoes an isoform switch during metastatic progression in a genetically engineered mouse model of lung adenocarcinoma
Tks5, a master regulator of invadopodia in cancer cells, is crucial for osteoclast fusion downstream of phosphoinositide 3-kinase and Src (show SRC Antibodies).
Src (show SRC Antibodies)-Tks5 pathway is required for neural crest cell migration during embryonic development
Examination of the initial stages of podosome formation has revealed an important role for the phosphoinositide PI(3,4)P(2) in anchoring the scaffold protein (show HOMER1 Antibodies) Tks5 to the plasma membrane.
Data suggest that Src (show SRC Antibodies)-dependent phosphorylation of beta-dystroglycan results in the formation of a Src (show SRC Antibodies)/dystroglycan complex that drives the SH3-mediated association between dystroglycan and Tks5 which together regulate podosome formation in myoblasts.
The tandem SH3A and SH3B domains of Tks5 constitute a versatile module for the implementation of isoform-specific protein-protein interactions.
Tks5 facilitates the production of ROS (show ROS1 Antibodies) necessary for invadopodia formation, and in turn ROS (show ROS1 Antibodies) modulate Tks5 tyrosine phosphorylation in a positive feedback loop.
Src (show SRC Antibodies)-Tks5 pathway is required for neural crest cell migration during embryonic development [TKS5]
Adapter protein involved in invadopodia and podosome formation, extracellular matrix degradation and invasiveness of some cancer cells. Binds matrix metalloproteinases (ADAMs), NADPH oxidases (NOXs) and phosphoinositides. Acts as an organizer protein that allows NOX1- or NOX3-dependent reactive oxygen species (ROS) generation and ROS localization. In association with ADAM12, mediates the neurotoxic effect of beta-amyloid peptide (By similarity).
SH3 and PX domain-containing protein 2A
, SH3 multiple domains 1
, adapter protein TKS5
, adaptor protein TKS5
, five SH3 domain-containing protein
, tyrosine kinase substrate with five SH3 domains
, SH3 multiple domains protein 1
, five SH3 domains
, SH3 and PX domains 2A