CLIC4/Arf6 Pathway.

ABSTRACT:

Rationale

Increased expression of CLIC4 (chloride intracellular channel 4) is a feature of endothelial dysfunction in pulmonary arterial hypertension, but its role in disease pathology is not fully understood.

Objective

To identify CLIC4 effectors and evaluate strategies targeting CLIC4 signaling in pulmonary hypertension.

Methods and results

Proteomic analysis of CLIC4-interacting proteins in human pulmonary artery endothelial cells identified regulators of endosomal trafficking, including Arf6 (ADP ribosylation factor 6) GTPase activating proteins and clathrin, while CLIC4 overexpression affected protein regulators of vesicular trafficking, lysosomal function, and inflammation. CLIC4 reduced BMPRII (bone morphogenetic protein receptor II) expression and signaling as

SUBMITTER: Abdul-Salam VB 

PROVIDER: S-EPMC6325770 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature