anti-Chloride Intracellular Channel 4 (CLIC4) Antibodies

Human Chloride Intracellular Channel 4 (CLIC4) interaction partners

1. through profilin-1 binding, CLIC4 functions in a RhoA-mDia2-regulated signaling network to integrate cortical actin assembly and membrane protrusion

2. High CLIC4 expression is associated with Merkel cell polyomavirus positive Merkel cell carcinoma.

3. Results provide evidence that the G4 structure formed in the CLIC4 promoter region may act as a regulatory element in regulating CLIC4 gene transcription.

4. CLIC4 and Ihh could serve as biological markers for the progression, metastasis and/or invasiveness of pancreatic ductal adenocarcinoma.

5. in malignant pleural mesothelioma, the gene expressions of CLIC3 and CLIC4 were significantly increased compared to controls

6. CLIC1 and CLIC4 are overexpressed in specific tumor types or their corresponding stroma and change localization and function from hydrophilic cytosolic to integral transmembrane proteins. (Review)

7. CLIC4 knockdown decreases cell-matrix adhesion, cell spreading and integrin signaling, whereas it increases cell motility.

8. CLIC4, ERp29, and Smac/DIABLO integrated into a novel panel based on cancer stem-like cells in association with metastasis stratify the prognostic risks of colorectal cancer.

9. This study investigated the proteome modulated by oncogenic KRAS in immortalized airway epithelial cells.

10. Increased CLIC4 expression is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension.

11. CLIC4 increases tumor cell migration and invasion in a TGF-beta-dependent manner.

12. In addition to CLIC1 and TPM1, which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2, TPM3, and TPM4 were present in ovarian cancer patient sera at significantly elevated levels compared with controls.

13. Our data indicate that CLIC4 protein may be a key element in the apoptotic response to oxidative stress.

14. These results demonstrate that CLIC4 nuclear translocation is an integral part of the cellular response to starvation.

15. Reduced CLIC4 expression and nuclear residence detected in cancer cells is associated with the altered redox state of tumor cells and the absence of detectable nuclear CLIC4 in cancers contributes to TGF-beta resistance and enhances tumor development.

16. CLIC4 may not be responsible for benign familial infantile seizures (BFIS) in a Chinese family affected with BFIS.

17. Data suggest that CLIC4 is regulated by RhoA to be targeted to the plasma membrane, where it may function not as an inducible chloride channel but rather by displaying Cys-dependent transferase activity toward a yet unknown substrate.

18. CLIC4 functions to promote endothelial cell proliferation and to regulate endothelial morphogenesis, and is thus involved in multiple steps of in vitro angiogenesis.

19. CLIC4 is differentially regulated in fibroblasts and its expression contributes to a myofibroblast phenotype

20. CLIC4 has alternate cellular functions that are distinct from their proposed roles as chloride channels

Mouse (Murine) Chloride Intracellular Channel 4 (CLIC4) interaction partners

1. Results demonstrate that down-regulating CLIC4 inhibit the proliferation and promotes the apoptosis of mouse liver cancer Hca-F cell.

2. Results indicate CLICs (CLIC1, CLIC4 and CLIC5)-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.

3. Data, including data from studies in primary cells from knockout mice, suggest Clic1 and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 inflammasomes; in LPS macrophage activation, Clic1 and Clic4 are translocated to nucleus/cell membranes. (Clic1 = chloride intracellular channel 1; Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 = NLR family pyrin domain containing 3)

4. study reports an alternately-spliced form of Smad7, Smad7Delta, that is induced by TGF-beta and CLIC4, is a dominant inhibitor of Smad7 and enhances TGF-beta signaling

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

6. CLIC4 is not required for collaterogenesis but is essential for perinatal maturation of nascent collaterals through a mechanism that supports VEGF signaling.

7. However, the absence of CLIC4 has no significant impact on the extent of functional recovery or fibrosis following acute injury.

8. Data suggest that compartmentalized expression of chloride intracellular channel 4 (CLIC4) in specific adult tissues and cells provides a focus to explore potential functions of this protein.

9. Increased CLIC4 expression is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension.

10. These results indicate that CLIC4 participates in skin healing and corneal wound reepithelialization through enhancement of epithelial migration by a mechanism that may involve a compromised TGF-beta pathway.

11. Data suggest that iNOS-induced nuclear CLIC4 is an essential part of the macrophage deactivation program.

12. CLIC4 is required for an optimal macrophage response to diverse pathogens. CLIC4-null these findings suggest that CLIC4 is an LPS-induced product that can serve as a positive regulator of LPS signaling

13. S-nitrosylation governs CLIC4 structure, its association with protein partners, and thus its intracellular distribution

14. mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53.

15. mtCLIC is involved in mitochondrial membrane potential generation in mitochondrial DNA-depleted cells.

16. CLIC4 nuclear translocation is an integral part of the cellular response to stress and may contribute to the initiation of nuclear alterations that are associated with apoptosis.

17. CLIC4 plays a critical role in angiogenesis by supporting acidification of vacuoles along the cell-hollowing tubulogenic pathway.

18. These results newly identify Schnurri-2 and CLIC4 as modifiers of TGF-beta signalling through their stabilization of p-Smad2 and 3 in the nucleus.

19. CLIC4 specifies native collateral formation, exerting influences upstream of hypoxia-inducible factor-1alpha-VEGF signaling