M
Marty W. Mayo
Researcher at University of Virginia
Publications - 44
Citations - 15265
Marty W. Mayo is an academic researcher from University of Virginia. The author has contributed to research in topics: Transcription factor & Cancer. The author has an hindex of 29, co-authored 40 publications receiving 14518 citations. Previous affiliations of Marty W. Mayo include University of North Carolina at Chapel Hill & University of Michigan.
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Journal ArticleDOI
NF-κB Antiapoptosis: Induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to Suppress Caspase-8 Activation
TL;DR: Tumor necrosis factor alpha binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism.
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB
TL;DR: The activation of the transcription factor nuclear factor-kappa B by tumor necrosis factor, ionizing radiation, or daunorubicin, was found to protect from cell killing, providing a mechanism of cellular resistance to killing by some apoptotic reagents.
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Modulation of NF-κB-dependent transcription and cell survival by the SIRT1 deacetylase
Fan Yeung,Jamie E. Hoberg,Catherine S. Ramsey,Michael D Keller,David R. Jones,Roy A. Frye,Marty W. Mayo +6 more
TL;DR: It is demonstrated that SIRT1, a nicotinamide adenosine dinucleotide‐dependent histone deacetylase, regulates the transcriptional activity of NF‐κB and activity augments apoptosis in response to TNFα.
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NF-κB-Induced Loss of MyoD Messenger RNA: Possible Role in Muscle Decay and Cachexia
TL;DR: The role of NF-kappaB in cytokine-induced muscle degeneration was explored and its expression was down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo, elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.
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Akt Stimulates the Transactivation Potential of the RelA/p65 Subunit of NF-κB through Utilization of the IκB Kinase and Activation of the Mitogen-activated Protein Kinase p38
TL;DR: It is demonstrated that Akt, functioning through IκB kinase and p38, induces the transcription function of NF-κB by stimulating the RelA/p65 transactivation subunit of NF -κB.