The p53 and Calcium Regulated Actin Rearrangement in Model Cells.

ABSTRACT: Long-term cellular stress maintains high intracellular Ca²⁺ concentrations which ultimately initiates apoptosis. Our interest is focused on how the gelsolin (GSN) and junctional mediating and regulating Y protein (JMY) play important roles in stress response. Both of these proteins can bind p53 and actin. We investigated using in vitro fluorescence spectroscopy and found that the p53 competes with actin in GSN to inhibit p53-JMY complex formation. A high Ca²⁺ level initializes p53 dimerization; the dimer competes with actin on JMY, which can lead to p53-JMY cotransport into the nucleus. Here we investigated how the motility and division rate of HeLa cells changes due to low-voltage electroporation of GSN or JMY in scratching assays. We revealed that JMY inhibits their

SUBMITTER: Hencz A 

PROVIDER: S-EPMC9408879 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature