A study from the Department of Molecular Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA shows that “Deubiquitinase DUBA is a post-translational brake on interleukin-17 production in T cells.” This study was published in the 19 February 2015 issue of Nature by Prof Dixit VM, Dr. Rutz, and others.
Significance: Based on the above study, Dr L Boominathan, Director-cum-chief Scientist of GBMD, suggests, for the first time, that DUBA, by decreasing the expression of its target gene, it may increase the stability and activity of tumor suppressor p53 homologue p73α. Thereby, it may inhibit tumorigenesis. Thus, pharmacological formulations encompassing “DUBA activators” can be used to inhibit the progression of human tumors, including p53-mutated human tumors.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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Citation: Boominathan, Molecular therapy for p53-mutated human cancers: Deubiquitnase DUBA increases the stability and activity of p73α and inhibits tumorigenesis via down regulation of its target gene, 26/January/2015, 22.02, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Amount: $ 500* * Research cooperation
Undisclosed information: How DUBA increases the stability and activity of p73α
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* Research cooperation