Actin-organizing protein palladin modulates C2C12 cell fate determination.

ABSTRACT:

Background

Cell confluency and serum deprivation promote the transition of C2C12 myoblasts into myocytes and subsequence fusion into myotubes. However, despite all myoblasts undergoing the same serum deprivation trigger, their responses vary: whether they become founder myocytes, remain proliferative, or evolve into fusion-competent myocytes remains unclear. We have previously shown that depletion of the scaffolding protein palladin in myoblasts inhibits cell migration and promotes premature muscle differentiation, pointing to its potential significance in muscle development and the necessity for a more in-depth examination of its function in cellular heterogeneity.

Methods and results

Here, we showed that the subcellular localization of palladin might contribute to founder-

SUBMITTER: Nguyen NUN 

PROVIDER: S-EPMC11255515 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature