On the footsteps of Triadin and its role in skeletal muscle

• 作者: Claudio F Perez
• 来源期刊: 世界生物化学杂志：英文版（电子版）
• 学科: 生物学
• 关键词: Excitation-contraction coupling Triadin-null CALCIUM release RYANODINE receptor FKBP12 RESTING CALCIUM
• 年，卷（期）: 2011,（8）
• 页码范围: 177-183
• 页数: 7页
• 分类号: Q593.3

摘要

Calcium is a crucial element for striated muscle function. As such, myoplasmic free Ca2+ concentration is delicately regulated through the concerted action of multiple Ca2+ pathways that relay excitation of the plasma membrane to the intracellular contractile machinery. In skeletal muscle, one of these major Ca2+ pathways is Ca2+ release from intracellular Ca2+ stores through type-1 ryanodine receptor/Ca2+ release channels (RyR1), which positions RyR1 in a strategic cross point to regulate Ca2+ homeostasis. This major Ca2+ traff ic point appears to be highly sensitive to the intracellular environment, which senses through a plethora of chemical and protein-protein interactions. Among these modulators, perhaps one of the most elusive is Triadin, a musclespecif ic protein that is involved in many crucial aspect of muscle function. This family of proteins mediates complex interactions with various Ca2+ modulators and seems poised to be a relevant modulator of Ca2+ signaling in cardiac and skeletal muscles. The purpose of this review is to examine the most recent evidence and current understanding of the role of Triadin in muscle function, in general, with particular emphasis on its contribution to Ca2+ homeostasis.