Mutual regulation between glycosylation and transforming growth factor-β isoforms signaling pathway

Abstract

Transforming growth factor-beta (TGF-β) superfamily members orchestrate a wide breadth of biological processes. Through Sma and Mad (Smad)-related dependent or noncanonical pathways, TGF-β members involve in the occurrence and development of many diseases such as cancers, fibrosis, autoimmune diseases, cardiovascular diseases and brain diseases. Glycosylation is one kind of the most common posttranslational modifications on proteins or lipids. Abnormal protein glycosylation can lead to protein malfunction and biological process disorder, thereby causing serious diseases. Previously, researchers commonly make comprehensive systematic overviews on the roles of TGF-β signaling in a specific disease or biological process. In recent years, more and more evidences associate glycosylation modification with TGF-β signaling pathway, and we can no longer disengage and ignore the roles of glycosylation from TGF-β signaling to make investigation. In this review, we provide an overview of current findings involved in glycosylation within TGF-βs and theirs receptors, and the interaction effects between glycosylation and TGF-β subfamily signaling, concluding that there is an intricate mutual regulation between glycosylation and TGF-β signaling, hoping to present the glycosylation regulatory patterns that concealed in TGF-βs signaling pathways.

Keywords: Glycoprotein; Glycosylation; Transforming growth factor-beta (TGF-β) superfamily.