anti-Chloride Intracellular Channel 1 (CLIC1) Anticorps

Human Chloride Intracellular Channel 1 (CLIC1) interaction partners

1. After CLIC1 knockdown, the expression levels of ITGalpha3, ITGalphav, ITGbeta1 and Bcl-2 (Montrer BCL2 Anticorps) mRNA and protein were decreased significantly in gastric cancer cells, as well as AKT (Montrer AKT1 Anticorps)-phosphorylation, ERK (Montrer EPHB2 Anticorps)-phosphorylation and p38 (Montrer CRK Anticorps)-phosphorylation, were reduced in vivo.

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

3. The CLIC1-mediated drug resistance is achieved through positive regulation of MRP1 (Montrer MDM4 Anticorps) in choriocarcinoma.CLIC1 is highly expressed in chemoresistant choriocarcinoma.

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

5. CLIC1 is a possible tumor marker for ovarian cancer. Dendritic cells pulsed with MtHsp70 (Montrer HSPA9 Anticorps)-CLIC1 can enhance antitumor immunity against ovarian cancer, providing a novel immune therapeutic strategy.

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

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

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

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

10. CLIC1 acts as a putative oncogene (Montrer RAB1A Anticorps) in pancreatic cancer.

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

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

2. We conclude that the role of CLIC1 in macrophage superoxide production is to support redistribution of NADPH oxidase (Montrer NOX1 Anticorps) to the plasma membrane, and not through major effects on ERM (Montrer ETV5 Anticorps) cytoskeleton or by acting as a plasma membrane chloride channel (Montrer CLCA1 Anticorps).

3. Data, including data from studies in primary cells from knockout mice, suggest Clic1 and Clic4 (Montrer CLIC4 Anticorps) participate in signaling interleukin 1beta secretion and in activation of Nlrp3 (Montrer NLRP3 Anticorps) inflammasomes; in LPS (Montrer TLR4 Anticorps) macrophage activation, Clic1 and Clic4 (Montrer CLIC4 Anticorps) are translocated to nucleus/cell membranes. (Clic1 = chloride intracellular channel 1; Clic4 (Montrer CLIC4 Anticorps) = chloride intracellular channel 4 (Montrer CLIC4 Anticorps), mitochondrial; Nlrp3 (Montrer NLRP3 Anticorps) = NLR family pyrin domain containing 3 (Montrer NLRP3 Anticorps))

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 (Montrer ANXA7 Anticorps) and Gelsolin (Montrer GSN Anticorps).

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.