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

Citation data:

Molecular cancer, ISSN: 1476-4598, Vol: 5, Issue: 1, Page: 52

Publication Year:
2006
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Citations 30
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Repository URL:
https://jdc.jefferson.edu/pacbfp/46
PMID:
17081288
DOI:
10.1186/1476-4598-5-52
PMCID:
PMC1636066
Author(s):
Ghiselli, Giancarlo
Publisher(s):
Springer Nature
Tags:
Biochemistry, Genetics and Molecular Biology; Medicine; Thomas Jefferson University; Department of Pathology and Cell Biology; Amino Acid Sequence; Animals; Genetically Modified; Apoptosis; Cell Cycle Proteins; Cells; Cultured; Chromosomal Proteins; Non-Histone; Chromosome Mapping; Cloning; Molecular; Embryo; Mammalian; Nonmammalian; Embryonic Development; Gene Expression Regulation; Developmental; Genomic Instability; HCT116 Cells; Humans; Molecular Sequence Data; Proteochondroitin Sulfates; RNA; Messenger; Stored; Sequence Homology; Amino Acid; Transfection; Tumor Suppressor Protein p53; Zebrafish; Zygote; Biological Phenomena, Cell Phenomena, and Immunity; Medical Cell Biology
article description
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.