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The Two‐pore channel 2 (TPC2) mediates autophagy in skeletal muscles
Author(s) -
Lin peihui,
Komazaki Shinji,
Zhu hua,
Park ki ho,
Pan zui,
Duann pu,
Ma jianjie
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb86
Subject(s) - autophagy , skeletal muscle , microbiology and biotechnology , western blot , biology , flux (metallurgy) , regulator , chemistry , biochemistry , anatomy , apoptosis , gene , organic chemistry
Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca2+‐mobilizing messenger that in many cells releases Ca2+ from the endolysosomal system. Recent studies have shown that NAADP‐induced Ca2+ mobilization is mediated by the two‐pore channels (TPCs). The objective of this study is to test whether TPC2 is involved in autophagy in skeletal muscle. Methods Wild type or TPC2 null animals were subjected to autophagy induction to compare the autophagy fluxes in the animals. In some experiments, isolated neonatal myoblasts were used. Detection methods include LC3 western blot and electron micrographs. Summary of results and conclusions: Our data provide evidence that TPC2 is involved in regulating autophagy flux in skeletal muscle. TPC2 mutant demonstrated defective autophagy to maintain tissue homeostasis. Summary of funding: There is no NIH funding to support this research project yet.