Редактирование: TRPC1 (раздел)

==Publications==

{{medline-entry
|title=Ca  entry via [[TRPC1]] is essential for cellular differentiation and modulates secretion via the SNARE complex.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31182642
|abstract=Properties of adipocytes, including differentiation and adipokine secretion, are crucial factors in obesity-associated metabolic syndrome. Here, we provide evidence that Ca  influx in primary adipocytes, especially upon Ca  store depletion, plays an important role in adipocyte differentiation, functionality and subsequently metabolic regulation. The endogenous Ca  entry channel in both subcutaneous and visceral adipocytes was found to be dependent on [[TRPC1]]-[[STIM1]], and blocking Ca  entry with SKF96365 or using [[TRPC1]]  knockdown adipocytes inhibited adipocyte differentiation. Additionally, [[TRPC1]]  mice have decreased organ weight, but increased adipose deposition and reduced serum adiponectin and leptin concentrations, without affecting total adipokine expression. Mechanistically, [[TRPC1]]-mediated Ca  entry regulated SNARE complex formation, and agonist-mediated secretion of adipokine-loaded vesicles was inhibited in [[TRPC1]]  adipose. These results suggest an unequivocal role of [[TRPC1]] in adipocyte differentiation and adiponectin secretion, and that loss of [[TRPC1]] disturbs metabolic homeostasis.This article has an associated First Person interview with the first author of the paper.
|mesh-terms=* Adipocytes
* Adipogenesis
* Adiponectin
* Adiposity
* Aging
* Animals
* Calcium
* Cell Differentiation
* Male
* Mice
* Protein Isoforms
* SNARE Proteins
* Subcutaneous Fat
* TRPC Cation Channels
|keywords=* Adipocyte differentiation
* Adiponectin secretion
* Ca2  entry
* Metabolic homeostasis
* TRPC1
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6633397
}}