CYLD-mediated signaling and diseases.

Abstract

The conserved cylindromatosis (CYLD) codes for a deubiquitinating enzyme and is a crucial regulator of diverse cellular processes such as immune responses, inflammation, death, and proliferation. It directly regulates multiple key signaling cascades, such as the Nuclear Factor kappa B [NFkB] and the Mitogen-Activated Protein Kinase (MAPK) pathways, by its catalytic activity on polyubiquitinated key intermediates. Several lines of emerging evidence have linked CYLD to the pathogenesis of various maladies, including cancer, poor infection control, lung fibrosis, neural development, and now cardiovascular dysfunction. While CYLD-mediated signaling is cell type and stimuli specific, the activity of CYLD is tightly controlled by phosphorylation and other regulators such as Snail. This review explores a broad selection of current and past literature regarding CYLD's expression, function and regulation with emerging reports on its role in cardiovascular disease.

• Authors: Bryan J Mathis, Yimu Lai, Chen Qu, Joseph S Janicki, Taixing Cui
• Journal: Current drug targets (Curr Drug Targets) Vol. 16 Issue 4 Pg. 284-94 ( 2015) ISSN: 1873-5592 [Electronic] United Arab Emirates
• PMID: 25342597 (Publication Type: Journal Article, Review)

Chemical References

• Inflammation Mediators
• Tumor Suppressor Proteins
• CYLD protein, human
• Deubiquitinating Enzyme CYLD
• Ubiquitin-Specific Proteases

Topics

• Animals
• Autophagy
• Cardiovascular Diseases (enzymology, immunology, pathology, physiopathology)
• Cardiovascular System (enzymology, immunology, pathology, physiopathology)
• Cell Cycle
• Deubiquitinating Enzyme CYLD
• Humans
• Inflammation Mediators (immunology, metabolism)
• Signal Transduction
• Tumor Suppressor Proteins (immunology, metabolism)
• Ubiquitin-Specific Proteases (immunology, metabolism)