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Ano6 regulates C2C12 myoblast proliferation and differentiation
Author(s) -
Zhao Piming,
Xu Li,
Mariano Andrew T.,
Han Renzhi
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.939.11
Subject(s) - c2c12 , myogenesis , myocyte , microbiology and biotechnology , skeletal muscle , biology , chemistry , endocrinology
Anocatamin 6 (Ano6) is a member of TMEM16, a conserved gene family predicted to code for eight transmembrane proteins with putative Ca2+‐activated chloride channel activity. Ano6 mutations lead to Scott syndrome (SCTS) in patients, a bleeding disorder caused by a defect in Ca2+‐activated Ano6‐mediated phosphatidylserine exposure in platelets and other blood cells. However, the function of ANO6 remains unknown in most other tissues including skeletal muscle. Here we show that Ano6 regulates muscle cell proliferation and differentiation using C2C12 cells as a model system. Ano6 is expressed in adult mouse skeletal muscle and C2C12 myocytes. To investigate the functions of Ano6 in muscle cells, we established Ano6 knockdown (KD) C2C12 cell line using lentiviral shRNA targeting Ano6. Ano6 KD significantly reduced C2C12 myoblast proliferation and promoted myoblast differentiation to form myotubes, suggesting that Ano6 plays an essential role in muscle growth. In the future, we will further define the mechanisms underlying the roles of Ano6 in muscle cells.