ArticleMolecular biology reports2010
Apoptosis screening of human chromosome 21 proteins reveals novel cell death regulators.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- S-phase kinase-associated protein 2 knockdown blocks colorectal cancer growth via regulation of both p27 and p16 expression.Cancer gene therapy · 2013Article
- VEGF is essential for the growth and migration of human hepatocellular carcinoma cells.Molecular biology reports · 2012Article
- Identification of transcription factor E3 (TFE3) as a receptor-independent activator of Gα16: gene regulation by nuclear Gα subunit and its activator.The Journal of biological chemistry · 2011Article
- DLC-1 as a modulator of proliferation, apoptosis and migration in Burkitt's lymphoma cells.Molecular biology reports · 2011Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functional analysis of chromosome 21 (Chr21) proteins is of great medical relevance. This refers, in particular, to the trisomy of human Chr21, which results in Down's syndrome, a complex developmental and neurodegenerative disease. In a previous study we analyzed 89 human Chr21 genes for the subcellular localization of their encoded proteins using a transfected-cell array technique. In the present study, the results of the follow-up investigation are presented in which 52 human Chr21 genes were over-expressed in HEK cells using the transfected-cell array platform, and the effect of this protein over-expression on the induction of apoptosis has been analyzed. We found that the over-expression of two Chr21 proteins (claudin-14 and -8) induced cell death independent of the classic caspase-mediated apoptosis. Our results strongly suggest the functional involvement of claudins in the control of the cell cycle and regulation of the cell death induction mechanism.
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