anti-CLIC5 (CLIC5) Antikörper

Human Chloride Intracellular Channel 5 (CLIC5) Interaktionspartner

1. loss of ETV6 (zeige ETV6 Antikörper) 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 (zeige SQSTM1 Antikörper) DNA damage accumulation, and thereby contribute to leukemogenesis.

2. EZR (zeige EZR Antikörper), CLIC5 and PODXL (zeige PODXL Antikörper) are overexpressed in hepatocellular carcinoma and may have a role in cell migration and invasiveness

3. 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.

4. CLIC5 is a novel gene involved in progressive hearing impairment, vestibular and possibly mild renal dysfunction.

5. CLIC5A colocalizes with ezrin (zeige EZR Antikörper) and podocalyxin (zeige PODXL Antikörper) in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.

6. association with Golgi apparatus AKAP350 (zeige AKAP9 Antikörper)

7. CLIC-5A has a role as a chloride channel in vitro and binds to cortical actin cytoskeleton

8. CLIC5 was demonstrated in cultured lymphoblasts.

9. Data showed that CLIC1 and CLIC5, but not CLIC4, were strongly and reversibly inhibited (or inactivated) by F-actin.

Pig (Porcine) Chloride Intracellular Channel 5 (CLIC5) Interaktionspartner

1. results suggest that CLIC5 might be a crucial regulator of adipose accumulation in skeletal muscle of pigs

Cow (Bovine) Chloride Intracellular Channel 5 (CLIC5) Interaktionspartner

1. CLIC5A colocalizes with ezrin (zeige EZR Antikörper) and podocalyxin (zeige PODXL Antikörper) in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.

Mouse (Murine) Chloride Intracellular Channel 5 (CLIC5) Interaktionspartner

1. Results indicate CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (zeige NLRP3 Antikörper) activation.

2. The findings indicate that CLIC4 (zeige CLIC4 Antikörper)/CLIC5A-mediated ERM (zeige ETV5 Antikörper) activation is required for maintenance of the glomerular capillary architecture.

3. 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.

4. 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.

5. Biochemical assays showed interaction of CLIC5 with ERM (zeige ETV5 Antikörper) proteins, TPRN (zeige TPRN Antikörper), and possibly myosin VI (MYO6 (zeige MYO6 Antikörper)). In addition, CLIC5 and RDX (zeige RDX Antikörper) failed to localize normally in fused stereocilia of MYO6 (zeige MYO6 Antikörper) mutant mice

6. miR (zeige MLXIP Antikörper)-96 and miR (zeige MLXIP Antikörper)-182 regulate the in vivo expression of CLIC5 in mouse inner ear hair cells

7. Study identifies CLIC5 as a new component that is enriched in and necessary for foot process integrity and podocyte function in vivo.

8. CLIC5 disrupts proliferation of C2C12 cells and is involved in the differentiation of myoblasts by enhancing the protein expression level of MyHC (zeige MYH13 Antikörper), myogenin (zeige MYOG Antikörper) and desmin (zeige DES Antikörper).

9. Clic5 mutant mice are resistant to diet-induced obesity.

10. CLIC5A colocalizes with ezrin (zeige EZR Antikörper) and podocalyxin (zeige PODXL Antikörper) in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.