SMC3 knockdown triggers genomic instability and p53-dependent apoptosis in human and zebrafish cells.

ABSTRACT:

Background

The structural maintenance of chromosome 3 (SMC3) protein is a constituent of a number of nuclear multimeric protein complexes that are involved in DNA recombination and repair in addition to chromosomal segregation. Overexpression of SMC3 activates a tumorigenic cascade through which mammalian cells acquire a transformed phenotype. This has led us to examine in depth how SMC3 level affects cell growth and genomic stability. In this paper the effect of SMC3 knockdown has been investigated.

Results

Mammalian cells that are SMC3 deficient fail to expand in a clonal population. In order to shed light on the underlying mechanism, experiments were conducted in zebrafish embryos in which cell competence to undergo apoptosis is acquired at specific stages of development

SUBMITTER: Ghiselli G 

PROVIDER: S-EPMC1636066 | biostudies-literature | 2006 Nov

REPOSITORIES: biostudies-literature