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loss of ETV6 (show ETV6 ELISA Kits) leads to significant overexpression of CLIC5, which in turn leads to decreased lysosome-mediated apoptosis. Our data suggest that heightened CLIC5 activity could promote a permissive environment for oxidative stress-induced (show SQSTM1 ELISA Kits) DNA damage accumulation, and thereby contribute to leukemogenesis.
EZR (show EZR ELISA Kits), CLIC5 and PODXL (show PODXL ELISA Kits) are overexpressed in hepatocellular carcinoma and may have a role in cell migration and invasiveness
The mechanism of CLIC5A action involves clustered plasma membrane phosphatidylinositol 4,5-bisphosphate accumulation, in turn facilitating ezrin activation and actin-dependent cell surface remodeling.
CLIC5 is a novel gene involved in progressive hearing impairment, vestibular and possibly mild renal dysfunction.
CLIC5A colocalizes with ezrin (show EZR ELISA Kits) and podocalyxin (show PODXL ELISA Kits) in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.
association with Golgi apparatus AKAP350 (show AKAP9 ELISA Kits)
CLIC-5A has a role as a chloride channel in vitro and binds to cortical actin cytoskeleton
CLIC5 was demonstrated in cultured lymphoblasts.
Data showed that CLIC1 and CLIC5, but not CLIC4, were strongly and reversibly inhibited (or inactivated) by F-actin.
results suggest that CLIC5 might be a crucial regulator of adipose accumulation in skeletal muscle of pigs
Results indicate CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (show NLRP3 ELISA Kits) activation.
The findings indicate that CLIC4/CLIC5A-mediated ERM activation is required for maintenance of the glomerular capillary architecture.
Augmented hypertension-induced glomerular capillary injury in mice lacking CLIC5 results from abrogation of Rac1-dependent Pak and ezrin activation, perhaps reducing the tensile strength of the podocyte actin cytoskeleton.
Biochemical assays showed interaction of CLIC5 with ERM proteins, TPRN (show TPRN ELISA Kits), and possibly myosin VI (MYO6 (show MYO6 ELISA Kits)). In addition, CLIC5 and RDX (show RDX ELISA Kits) failed to localize normally in fused stereocilia of MYO6 (show MYO6 ELISA Kits) mutant mice
miR (show MLXIP ELISA Kits)-96 and miR (show MLXIP ELISA Kits)-182 regulate the in vivo expression of CLIC5 in mouse inner ear hair cells
Study identifies CLIC5 as a new component that is enriched in and necessary for foot process integrity and podocyte function in vivo.
CLIC5 disrupts proliferation of C2C12 cells and is involved in the differentiation of myoblasts by enhancing the protein expression level of MyHC, myogenin (show MYOG ELISA Kits) and desmin (show DES ELISA Kits).
Clic5 mutant mice are resistant to diet-induced obesity.
This gene encodes a member of the chloride intracellular channel (CLIC) family of chloride ion channels. The encoded protein associates with actin-based cytoskeletal structures and may play a role in multiple processes including hair cell stereocilia formation, myoblast proliferation and glomerular podocyte and endothelial cell maintenance. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
chloride intracellular channel 5
, chloride intracellular channel protein 6
, chloride intracellular channel protein 5-like
, chloride intracellular channel protein 5
, chloride channel protein p64
, chlorine channel protein p64