anti-Chloride Intracellular Channel 1 (CLIC1) Anticorps

Human Chloride Intracellular Channel 1 (CLIC1) interaction partners

1. We demonstrate that CLIC1 is able to modulate cyclic AMP-induced chloride currents and suggest that CLIC1 modulation could be important for chloride homeostasis in this cell type.

2. High CLIC1 expression is associated with Merkel cell polyomavirus positive Merkel cell carcinoma.

3. After CLIC1 knockdown, the expression levels of ITGalpha3, ITGalphav, ITGbeta1 and Bcl-2 mRNA and protein were decreased significantly in gastric cancer cells, as well as AKT-phosphorylation, ERK-phosphorylation and p38-phosphorylation, were reduced in vivo.

4. The current study provides the first statistically convincing evidence that downregulation of miR-372 may occur in gallbladder cancer tissues, which may be associated with aggressive and progressive tumor behavior by affecting CLIC1 expression.

5. The CLIC1-mediated drug resistance is achieved through positive regulation of MRP1 in choriocarcinoma.CLIC1 is highly expressed in chemoresistant choriocarcinoma.

6. Proteomic analysis indicates that CLIC1 promotes tumorgenesis in epithelial ovarian cancer.

7. CLIC1 is a possible tumor marker for ovarian cancer. Dendritic cells pulsed with MtHsp70-CLIC1 can enhance antitumor immunity against ovarian cancer, providing a novel immune therapeutic strategy.

8. Either dysfunction or downregulation of CLIC1 can partially decrease the antineoplastic effects of metformin.

9. The expression of CLIC1 might be closely related to the carcinogenesis, clinical biological behaviors, and prognosis of pancreatic ductal adenocarcinomas.

10. Extracellular vesicle-mediated transfer of CLIC1 protein is a novel mechanism for the regulation of glioblastoma growth.

11. Results indicate that CLIC1 is an important contributor to tumor invasion, metastasis, and angiogenesis.

12. CLIC1 acts as a putative oncogene in pancreatic cancer.

13. Data show that glutamate 85 and glutamate 228 are pH-sensor residues of chloride intracellular channel protein CLIC1 and contribute to the pH-response stability in different ways.

14. 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)

15. CLIC1 may be a potential sensitive and specific molecular biomarker for early diagnose for serous epithelial ovarian cancers metastasis.

16. It participates in migration and invasion of hepatocellular carcinoma by targeting maspin.

17. The expression of CLIC1 is closely related to the progression of gall bladder cancer and may be used as an effective marker for predicting the prognosis of this disease.

18. Data indicate the chloride channel protein CLIC1 as the most penetrant receptor.

19. Results indicate that CLIC1 could regulate prostate cancer cell proliferation and migration by regulating the(MAPK)/ERK pathway.

20. CLIC1 protein is involved in the metastasis of colon cancer LOVO cells via regulating the ROS/ERK pathway in the hypoxia-reoxygenation process

Mouse (Murine) Chloride Intracellular Channel 1 (CLIC1) interaction partners

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

2. We conclude that the role of CLIC1 in macrophage superoxide production is to support redistribution of NADPH oxidase to the plasma membrane, and not through major effects on ERM cytoskeleton or by acting as a plasma membrane chloride channel.

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. This study demonstrates for the first time that CLIC1 is overexpressed during AS development both in vitro and in vivo and can regulate the accumulation of inflammatory cytokines and production of oxidative stress.

5. Results indicate that CLIC1 is an important contributor to tumor invasion, metastasis, and angiogenesis.

6. Clic1 have a role in migration and invasion in hepatocarcinoma maybe via modulating the expression of Annexin A7 and Gelsolin.

7. These data all point to an important role for CLIC1 in regulating macrophage function through its ion channel activity.

8. The down-regulation of CLIC1 enhanced proliferative activity.

9. CLIC1 may play an important role in tumor metastasis.

10. CLIC1 is essential for the proliferation and invasion of hepatocellular carcinoma cells.

11. CLIC1 may play a role in the regulation of osteoblastic differentiation from mesenchymal progenitors, although its physiologic role in osteoblasts remains to be determined.

12. Ischemia augmented CLIC1 and CLIC4 expression similarly in wild-type mice. However, CLIC1 increased 3-fold more in Clic4(-/-) mice, suggesting compensation.