By a News Reporter-Staff News Editor at Genomics & Genetics Weekly -- Research findings on Oncology are discussed in a new report. According to news reporting out of New York City, New York, by NewsRx editors, research stated, "The prostate tumor suppressor NKX3.1 augments response to DNA damage and enhances survival after DNA damage. Within minutes of DNA damage, NKX3.1 undergoes phosphorylation at tyrosine 222, which is required for a functional interaction with ataxia telangiectasia mutated (ATM) kinase."
Our news journalists obtained a quote from the research from Columbia University, "NKX3.1 binds to the N-terminal region of ATM, accelerates ATM activation, and hastens the formation of ?histone2AX. NKX3.1 enhances DNA-dependent ATM kinase activation by both the MRN complex and H2O2 in a DNA-damage-independent manner. ATM, bound to the NKX3.1 homeodomain, phosphorylates NKX3.1, leading to ubiquitination and degradation. Thus, NKX3.1 and ATM have a functional interaction leading to ATM activation and then NKX3.1 degradation in a tightly regulated DNA damage response specific to prostate epithelial cells."
According to the news editors, the research concluded: "These findings demonstrate a mechanism for the tumor-suppressor properties of NKX3.1, demonstrate how NKX3.1 may enhance DNA integrity in prostate stem cells and may help to explain how cells differ in their sensitivity to DNA damage."
For more information on this research see: Functional activation of ATM by the prostate cancer suppressor NKX3.1. Cell Reports, 2013;4(3):516-29. (Elsevier - www.elsevier.com; Cell Reports - www.elsevier.com/wps/product/cws_home/727006)
Our news journalists report that additional information may be obtained by contacting C. Bowen, Dept. of Medicine, Herbert Irving Comprehensive Cancer Center, Columbia University, 177 Fort Washington Avenue, MHB 6N-435, New York, NY 10032, United States. Additional authors for this research include J.H. Ju, J.H. Lee, T.T. Paull and E.P Gelmann (see also Oncology).
Keywords for this news article include: Genetics, Oncology, DNA Damage, Proteomics, DNA Research, New York City, United States, Prostate Cancer, Prostatic Neoplasms, Deoxyribonucleic Acid, North and Central America.
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