anti-CLIC5 (CLIC5) Antikörper

Human Chloride Intracellular Channel 5 (CLIC5) Interaktionspartner

1. loss of ETV6 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 DNA damage accumulation, and thereby contribute to leukemogenesis.

2. EZR, CLIC5 and PODXL 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 and podocalyxin in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.

6. association with Golgi apparatus AKAP350

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.

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

1. These results suggest that KLPH is required for lens-specific expression of Clic5 and that Clic5 has an important role in the machinery that controls lens fiber cell extension and organization.

2. Results indicate CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.

3. The findings indicate that CLIC4/CLIC5A-mediated ERM activation is required for maintenance of the glomerular capillary architecture.

4. 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.

5. 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.

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

7. miR-96 and miR-182 regulate the in vivo expression of CLIC5 in mouse inner ear hair cells

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

9. CLIC5 disrupts proliferation of C2C12 cells and is involved in the differentiation of myoblasts by enhancing the protein expression level of MyHC, myogenin and desmin.

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

11. CLIC5A colocalizes with ezrin and podocalyxin in podocytes and is required for the development/maintenance of the proper glomerular endothelial cell and podocyte architecture.

12. CLIC5 associates with radixin in hair cell stereocilia and may help form or stabilize connections between the plasma membrane and the filamentous actin core.

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

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

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