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更新于：2025-05-07

CLIC3

更新于：2025-05-07

基本信息

别名

chloride intracellular channel 3、Chloride intracellular channel protein 3、CLIC3

简介

In the soluble state, catalyzes glutaredoxin-like thiol disulfide exchange reactions with reduced glutathione as electron donor (PubMed:28198360, PubMed:37759794). Reduced in a glutathione-dependent way and secreted into the extracellular matrix where it activates TGM2 and promotes blood vessel growth during tissue remodeling as occurs in tumorigenesis. Can reduce specific cysteines in TGM2 and regulate cofactor binding (PubMed:28198360). Can insert into membranes and form outwardly rectifying chloride ion channels. May participate in cellular growth control.

关联

项与 CLIC3 相关的药物

HA-22-31

靶点

CLIC3

作用机制

CLIC3 blockers

在研机构

University of Saskatchewan

原研机构

University of Saskatchewan

在研适应症

转移性乳腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CLIC3 相关的临床结果

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100 项与 CLIC3 相关的转化医学

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0 项与 CLIC3 相关的专利（医药）

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项与 CLIC3 相关的文献（医药）

2025-04-01·Biophysical Journal

Biophysical characterization of anion channels in mitochondrion-endoplasmic-reticulum contact sites

Article

作者: Loyo-Celis, Veronica ; Davis, Jonathan ; Dyta, Mayukha ; Singh, Aryan ; Singh, Harpreet ; Thuma, Jenna ; Raut, Satish K ; Bhachu, Harmeet Rireika ; Gururaja Rao, Shubha ; Ponnalagu, Devasena ; Gopalan, Ajay ; Sanghvi, Shridhar Kiran ; Gabrilovich, Denis

The mitochondrion-endoplasmic reticulum (ER) contact sites (MERCs, also known as mitochondrial-associated membranes [MAMs]) are specialized regions of the ER that are in close proximity to the mitochondrion. These organelle structures play essential roles in a variety of processes, such as calcium signaling, lipid metabolism, renin-angiotensin-aldosterone system control, the unfolded protein response, and autophagy. MERCs are known to actively participate in ion transport between the ER and mitochondria. Although active calcium channels in MERCs have been detected, limited studies have been carried out to identify or characterize functional anion channels. Here, we tested whether functional anion channels are present in MERCs. We isolated MERCs from mouse organs (heart and brain) and reconstituted them in planar bilayers. The single-channel properties were recorded in the presence of various anion channel blockers or antagonists (IAA-94, DIDS, A9C, and NPPB). We corroborated the presence of anion channels targeted by these drugs using immunoblotting and immunocytochemistry. Biochemical analysis and immunocytochemistry corroborate that CLIC4, CLIC3, and VDACs are present in MERCs. Our results indicate that anion channels are active in MERCs, which could play a pertinent role in intracellular organelle communication.

2024-05-15·Die Pharmazie

Neurite outgrowth promotion in PC12 cells by 24(R)-ethyllophenol from Morus alba.

Article

作者: Honma, S. ; Takei, S. ; Handa, K. ; Tanaka, G ; Yoshida, M. ; Tanaka, G. ; Watanabe, K. ; Mitsumata, R. ; Shimada, D.

We examined the mechanism by which 24(R)-ethyllophenol (MAB28) isolated from the branches of Morus alba caused neurite outgrowth in rat pheochromocytoma cells (PC12). MAB28 significantly promoted neurite outgrowth to a similar degree as the positive control, nerve growth factor (NGF). After incubation with MAB28 in PC12 cells, phosphorylation of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and cyclic AMP response element-binding protein was detected, but the time course of phosphorylation was different from that induced by NGF. The expression of chloride intracellular channel protein 3 (CLIC3) was significantly decreased by MAB28. 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), an outward rectifying chloride channel inhibitor, significantly promoted neurite outgrowth in PC12 cells. These data suggested that MAB28 could induce neurite outgrowth by downregulating CLIC3 expression.

2023-08-17·Microbiology spectrum

Integration of Metabolomics and Transcriptomics Reveals Major Metabolic Pathways and Potential Biomarkers Involved in Pulmonary Tuberculosis and Pulmonary Tuberculosis-Complicated Diabetes.

Article

作者: He, Xinxin ; Wang, Yunguang ; Jin, Juan ; Sun, Lifang ; Zheng, Danna ; He, Qiang

Pulmonary tuberculosis (PTB) and diabetes mellitus (DM) are common chronic diseases that threaten human health. Patients with DM are susceptible to PTB, an important factor that aggravates the complications of diabetes. However, the molecular regulatory mechanism underlying the susceptibility of patients with DM to PTB infection remains unknown. In this study, healthy subjects, patients with primary PTB, and patients with primary PTB complicated by DM were recruited according to inclusion and exclusion criteria. Peripheral whole blood was collected, and alteration profiles and potential molecular mechanisms were further analyzed using integrated bioinformatics analysis of metabolomics and transcriptomics. Transcriptional data revealed that lipocalin 2 (LCN2), defensin alpha 1 (DEFA1), peptidoglycan recognition protein 1 (PGLYRP1), and integrin subunit alpha 2b (ITGA2B) were significantly upregulated, while chloride intracellular channel 3 (CLIC3) was significantly downregulated in the group with PTB and DM (PTB_DM) in contrast to the healthy control (HC) group. Additionally, the interleukin 17 (IL-17), phosphatidylinositol 3-kinase (PI3K)-AKT, and peroxisome proliferator-activated receptor (PPAR) signaling pathways are important for PTB infection and regulation of PTB-complicated diabetes. Metabolomic data showed that glycerophospholipid metabolism, carbon metabolism, and fat digestion and absorption processes were enriched in the differential metabolic analysis. Finally, integrated analysis of both metabolomic and transcriptomic data indicated that the NOTCH1/JAK/STAT signaling pathway is important in PTB complicated by DM. In conclusion, PTB infection altered the transcriptional and metabolic profiles of patients with DM. Metabolomic and transcriptomic changes were highly correlated in PTB patients with DM. Peripheral metabolite levels may be used as biomarkers for PTB management in patients with DM. IMPORTANCE The comorbidity of diabetes mellitus (DM) significantly increases the risk of tuberculosis infection and adverse tuberculosis treatment outcomes. Most previous studies have focused on the relationship between the effect of blood glucose control and the outcome of antituberculosis treatment in pulmonary tuberculosis (PTB) with DM (PTB_DM); however, early prediction and the underlying molecular mechanism of susceptibility to PTB infection in patients with DM remain unclear. In this study, transcriptome sequencing and untargeted metabolomics were performed to elucidate the key molecules and signaling pathways involved in PTB infection and the susceptibility of patients with diabetes to PTB. Our findings contribute to the development of vital diagnostic biomarkers for PTB or PTB_DM and provide a comprehensive understanding of molecular regulation during disease progression.

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