Research Topics
Genomes and Genes | Shigeki MiyamotoSummaryAffiliation: University of Wisconsin Country: USA Publications
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Publications
Bone marrow stromal cells from multiple myeloma patients uniquely induce bortezomib resistant NF-kappaB activity in myeloma cellsStephanie Markovina
Program in Cellular and Molecular Biology and Medical Science Training Program, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53705, USA
Mol Cancer 9:176. 2010..The mediating factor(s) of this bortezomib-resistant NF-kappaB activity is induced by BMSCs is not currently understood...
Molecular linkage between the kinase ATM and NF-kappaB signaling in response to genotoxic stimuliZhao Hui Wu
Department of Pharmacology, University of Wisconsin Madison, 301 SMI, 1300 University Avenue, Madison, WI 53706, USA
Science 311:1141-6. 2006..Thus, regulated nuclear shuttling of NEMO links two signaling kinases, ATM and IKK, to activate NF-kappaB by genotoxic signals...- Bortezomib-resistant nuclear factor-kappaB activity in multiple myeloma cellsStephanie Markovina
Department of Pharmacology, University of Wisconsin, Madison, WI 53706, USA
Mol Cancer Res 6:1356-64. 2008..Further elucidation of the mechanism of PIR NF-kappaB regulation could lead to the identification of novel diagnostic biomarkers and/or therapeutic targets for MM treatment... - Calcium-dependent regulation of NEMO nuclear export in response to genotoxic stimuliCraig M Berchtold
Department of Pharmacology, 301 SMI, 1300 University Avenue, University of Wisconsin, Madison, WI 53706, USA
Mol Cell Biol 27:497-509. 2007.... - Inhibition of IkappaBalpha nuclear export as an approach to abrogate nuclear factor-kappaB-dependent cancer cell survivalShelby O'Connor
Program in Cellular and Molecular Biology, Department of Pharmacology, University of Wisconsin Madison, 3795 Medical Sciences Center, 1300 University Avenue, Madison, WI 53706, USA
Mol Cancer Res 3:42-9. 2005.... - PIASy mediates NEMO sumoylation and NF-kappaB activation in response to genotoxic stressAngela M Mabb
Program in Molecular and Cellular Pharmacology, Department of Pharmacology, University of Wisconsin, Madison, WI 53706, USA
Nat Cell Biol 8:986-93. 2006..Our findings demonstrate that PIASy is the first SUMO ligase for NEMO whose substrate specificity seems to be controlled by IKK interaction, subcellular targeting and oxidative stress conditions... - Induction of a pro-apoptotic ATM-NF-kappaB pathway and its repression by ATR in response to replication stressZhao Hui Wu
Department of Pharmacology, University of Wisconsin, Madison, WI 53706, USA
EMBO J 27:1963-73. 2008..Thus, replication stress and DSB inducers activate NF-kappaB through a conserved pathway with opposite biologic outcomes, and ATR antagonizes ATM function at least in part by competing for NEMO association... - Nuclear factor-kappaB dimer exchange promotes a p21(waf1/cip1) superinduction response in human T leukemic cellsPei-Yun Chang
Program in Molecular and Cellular Pharmacology, Department of Pharmacology, University of Wisconsin-Madison, 301 Medical Sciences Center, 1300 University Avenue, Madison, WI 53706, USA
Mol Cancer Res 4:101-12. 2006..Thus, we propose that low basal NFKB1 expression coupled with sequential NF-kappaB activation events can promote increased chemoresistance in certain T leukemic cells... - NF-κB induction of the SUMO protease SENP2: A negative feedback loop to attenuate cell survival response to genotoxic stressMoon Hee Lee
McArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin Madison, 6159 Wisconsin Institute for Medical Research, 1111 Highland Avenue, Madison, WI 53705, USA
Mol Cell 43:180-91. 2011..Our study establishes a self-attenuating feedback mechanism selective to DNA damage-induced signaling to limit NF-κB-dependent cell survival responses... 
A PAR-SUMOnious mechanism of NEMO activationKevin McCool
Molecular and Cellular Pharmacology Program, Medical Scientist Training Program, Department of Pharmacology, University of Wisconsin, Madison, 6159 Wisconsin Institute for Medical Research, Madison, WI 53705, USA
Mol Cell 36:349-50. 2009..In this issue of Molecular Cell, Stilmann et al. (2009) demonstrate a new mode of prosurvival NF-kappaB activation through the formation of a PARP-1-poly(ADP-ribose) signaling scaffold in response to DNA damage...- NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cellsPei Yun Chang
Program in Molecular and Cellular Pharmacology, Department of Pharmacology, University of Wisconsin Madison, Madison, Wisconsin 53706, USA
Cancer Res 66:6008-13. 2006..Thus, TAL1 modulates NFKB1 expression and an NF-kappaB-dependent transcriptional program in a subset of human T-cell leukemia cells... - Prevalence of bortezomib-resistant constitutive NF-kappaB activity in mantle cell lymphomaDavid T Yang
Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, USA
Mol Cancer 7:40. 2008..While MCL cells have been shown to harbor constitutive NF-kappaB activity, what fraction of this activity in primary MCL samples is sensitive or resistant to inhibition by bortezomib remains unclear... - Enhanced G2-M arrest by nuclear factor-{kappa}B-dependent p21waf1/cip1 inductionShelly M Wuerzberger-Davis
Department of Pharmacology, University of Wisconsin, 301 Service Memorial Institute, 1300 University Avenue, Madison, WI 53706, USA
Mol Cancer Res 3:345-53. 2005..Thus, cell cycle-coupled induction of p21waf1/cip1 by NF-kappaB represents a resistance mechanism in certain cancer cells... - Regulation of constitutive p50/c-Rel activity via proteasome inhibitor-resistant IkappaBalpha degradation in B cellsShelby O'Connor
Department of Pharmacology, University of Wisconsin, 301 SMI, 1300 University Ave, Madison, WI 53706, USA
Mol Cell Biol 24:4895-908. 2004..Thus, our findings suggest that nonconventional PIR degradation of IkappaBalpha may play a physiological role in the development of B cells in vivo... - RelA life and death decisionsShigeki Miyamoto
Department of Pharmacology, University of Wisconsin-Madison, 1300 University Avenue, Madison, WI 53706, USA
Mol Cell 13:763-4. 2004..However, in this issue of Molecular Cell, demonstrate that anticancer drugs turn RelA into an accomplice of apoptosis by instructing it to dominantly repress survival gene transcription... - PIDD: a switch hitterZhao-hui Wu
Department of Pharmacology, University of Wisconsin-Madison, 1300 University Avenue, Madison, WI 53706, USA
Cell 123:980-2. 2005..2005) demonstrate that, in response to such stress, PIDD forms a nuclear complex that enhances sumoylation of NEMO. This modification is important for the activation of the antiapoptotic transcription factor NF-kappaB... - DNA damage-dependent NF-κB activation: NEMO turns nuclear signaling inside outKevin W McCool
Medical Scientist Training Program, University of Wisconsin Madison, Madison, WI 53705, USA
Immunol Rev 246:311-26. 2012..Accumulating evidence suggests that DNA damage-dependent NF-κB activation may play significant biological roles, particularly during lymphocyte differentiation and progression of human malignancies... - Evidence for a phosphorylation-independent role for Ser 32 and 36 in proteasome inhibitor-resistant (PIR) IkappaBalpha degradation in B cellsStephanie Markovina
Program in Cellular and Molecular Biology, Department of Pharmacology, University of Wisconsin, 3795 Medical Sciences Center, 1300 University Avenue, Madison, WI 53706, USA
Exp Cell Res 307:15-25. 2005..These results suggest that B lineage cells can differentiate between PIR and canonical IkappaBalpha degradation through the absence or presence of dually phosphorylated IkappaBalpha... - Sequential modification of NEMO/IKKgamma by SUMO-1 and ubiquitin mediates NF-kappaB activation by genotoxic stressTony T Huang
Department of Pharmacology, University of Wisconsin Madison, 301 SMI, 1300 University Avenue, Madison, WI 53706, USA
Cell 115:565-76. 2003..These SUMO and ubiquitin modification pathways may serve as anticancer drug targets... - CYLD: a DUB with many talentsSara J S Simonson
Department of Pharmacology, University of Wisconsin Madison, 1300 University Avenue, Madison, WI 53706, USA
Dev Cell 13:601-3. 2007.... - TAK-ling IKK activation: "Ub" the judgeShelly M Wuerzberger-Davis
Department of Pharmacology, University of Wisconsin Madison, 6159 Wisconsin Institute for Medical Research, 1111 Highland Avenue, Madison, WI 53705, USA
Sci Signal 3:pe3. 2010..This study introduces a paradigm shift in the still-evolving mechanism of regulation of NF-kappaB... - Nuclear initiated NF-κB signaling: NEMO and ATM take center stageShigeki Miyamoto
Department of Pharmacology, University of Wisconsin Madison, 6159 Wisconsin Institute for Medical Research, 1111 Highland Avenue, Madison, WI 53705, USA
Cell Res 21:116-30. 2011..This review will summarize these new developments, while identifying significant unanswered questions and providing new hypotheses that may be addressed in future studies... - A mechanistic insight into a proteasome-independent constitutive inhibitor kappaBalpha (IkappaBalpha) degradation and nuclear factor kappaB (NF-kappaB) activation pathway in WEHI-231 B-cellsStuart D Shumway
Program in Cellular and Molecular Biology, Department of Pharmacology, University of Wisconsin, 3795 Medical Sciences Center, 1300 University Avenue, Madison, WI 53706, USA
Biochem J 380:173-80. 2004..These findings further support the notion that IkappaB instability governs the maintenance of constitutive p50-c-Rel activity in certain B-cells via a unique degradation pathway... - Nuclear export of the NF-κB inhibitor IκBα is required for proper B cell and secondary lymphoid tissue formationShelly M Wuerzberger-Davis
McArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin Carbone Cancer Center, University of Wisconsin Madison, 6159 Wisconsin Institute for Medical Research, 1111 Highland Avenue, Madison, WI 53705, USA
Immunity 34:188-200. 2011..Thus, IκBα nuclear export is essential to maintain constitutive, canonical, and noncanonical NF-κB activation potentials in mature B cells in vivo... - The zinc finger domain of NEMO is selectively required for NF-kappa B activation by UV radiation and topoisomerase inhibitorsTony T Huang
Program in Molecular and Cellular Pharmacology, Department of Pharmacology, University of Wisconsin Madison, Madison, Wisconsin 53706 1532, USA
Mol Cell Biol 22:5813-25. 2002..Thus, we suggest that the zinc finger domain of NEMO likely represents a point of convergence for signaling pathways initiated by slow and weak NF-kappa B-activating conditions...