Zobrazeno 1 - 10
of 25
pro vyhledávání: '"John P. Pribis"'
Publikováno v:
mBio, Vol 13, Iss 3 (2022)
ABSTRACT Mechanisms of evolution and evolution of antibiotic resistance are both fundamental and world health problems. Stress-induced mutagenesis defines mechanisms of mutagenesis upregulated by stress responses, which drive adaptation when cells ar
Externí odkaz:
https://doaj.org/article/08449f6d585a4eefad9f76f7706d6fd2
Autor:
Sodam Kim, Sun Young Kim, John P. Pribis, Michael Lotze, Kevin P. Mollen, Richard Shapiro, Patricia Loughran, Melanie J. Scott, Timothy R. Billiar
Publikováno v:
Molecular Medicine, Vol 19, Iss 1, Pp 88-98 (2013)
Abstract High mobility group box 1 (HMGB1) is a DNA-binding protein that possesses cytokinelike, proinflammatory properties when released extracellularly in the C23–C45 disulfide form. HMGB1 also plays a key role as a mediator of acute and chronic
Externí odkaz:
https://doaj.org/article/92b9e541abc146bfb6c6222a91fe8dca
Autor:
Yin Zhai, P.J. Minnick, John P. Pribis, Libertad Garcia-Villada, P.J. Hastings, Christophe Herman, Susan M. Rosenberg
Publikováno v:
Mol Cell
SUMMARYAntibiotics can induce mutations that cause antibiotic resistance, triggered by stress responses. The identities of the stress-response activators reveal environmental cues that elicit mutagenesis, and are weak links in mutagenesis networks, i
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c5aadf3bba733393d7f196ea7c5a3239
https://doi.org/10.1101/2022.07.06.499071
https://doi.org/10.1101/2022.07.06.499071
Autor:
Heyuan Li, Yin Zhai, Susan M. Rosenberg, John P. Pribis, Jacob Paiano, P. J. Hastings, Jingjing Liu, Devon M. Fitzgerald, Ralf B. Nehring, Jun Xia, Qian Mei, André Nussenzweig
Publikováno v:
Science Advances
Caught in the act, DNA reaction intermediates in bacterial genomes may illuminate disease-driving regions in human chromosomes.
Chromosomal fragile sites are implicated in promoting genome instability, which drives cancers and neurological disea
Chromosomal fragile sites are implicated in promoting genome instability, which drives cancers and neurological disea
Autor:
Domokos Gerö, Petra Szoleczky, Katalin Módis, John P Pribis, Yousef Al-Abed, Huan Yang, Sangeeta Chevan, Timothy R Billiar, Kevin J Tracey, Csaba Szabo
Publikováno v:
PLoS ONE, Vol 8, Iss 6, p e65994 (2013)
High mobility group box 1 (HMGB1), a highly conserved, ubiquitous protein, is released into the circulation during sterile inflammation (e.g. arthritis, trauma) and circulatory shock. It participates in the pathogenesis of delayed inflammatory respon
Externí odkaz:
https://doaj.org/article/d0277f57b73a44e88b9a0c0a2be63b84
Autor:
Susan M. Rosenberg, Jingjing Liu, P. J. Hastings, Jun Xia, David Bates, Ohad Lewin-Epstein, Qian Mei, Christophe Herman, Julia Bos, Devon M. Fitzgerald, Anthony Z. Wang, Robert H. Austin, John P. Pribis, Lilach Hadany, Libertad García-Villada, Yin Zhai
Publikováno v:
Molecular Cell
Molecular Cell, Elsevier, 2019, 74 (4), pp.785-800.e7. ⟨10.1016/j.molcel.2019.02.037⟩
Mol Cell
Molecular Cell, Elsevier, 2019, 74 (4), pp.785-800.e7. ⟨10.1016/j.molcel.2019.02.037⟩
Mol Cell
We tested the in vivo potential of a MHC class I-restricted blocking peptide to sufficiently lower an anti-viral CTL response for preventing virus-induced CTL-mediated autoimmune diabetes (insulin-dependent diabetes mellitus (IDDM)) in vivo without a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbb03673e5d876440440359b782e7c90
https://doi.org/10.1101/493015
https://doi.org/10.1101/493015
Autor:
Yousef Al-Abed, Wei Long, Kevin J. Tracey, Sangeeta S. Chavan, Ulf Andersson, Sergio I. Valdés-Ferrer, Doug T. Golenbock, Timothy R. Billiar, Helena Erlandsson Harris, Jianmin Meng, Zhongliang Ju, Csaba Szabó, John P. Pribis, Ben Lu, Huan Yang, Jesse Roth, Ahmed A. Ragab, Haichao Wang, Daniel J. Antoine, Domokos Gero, Peter Lundbäck, Jianhua Li, Mingzhu He
Publikováno v:
The Journal of Experimental Medicine
JOURNAL OF EXPERIMENTAL MEDICINE
JOURNAL OF EXPERIMENTAL MEDICINE
Yang et al. show that a disulfide isoform of HMGB1, with a role in TLR4 signaling, physically interacts with and binds MD-2. MD-2 deficiency in macrophage cell lines or in primary mouse macrophages stimulated with HMGB1 implicates MD-2 in TLR4 signal
Autor:
Sangeeta S. Chavan, Yousef Al-Abed, Sodam Kim, Hongbo Xu, Timothy R. Billiar, Petra Szoleczky, Eileen M. Bauer, Csaba Szabó, John P. Pribis, Huan Yang, Domokos Gero, Marcelo F. Montenegro, Changchun Cai, Tunliang Li, Kevin J. Tracey
Publikováno v:
Molecular Medicine. 21:749-757
Extracellular high-mobility group box 1 (HMGB1) (disulfide form), via activation of toll-like receptor 4 (TLR4)-dependent signaling, is a strong driver of pathologic inflammation in both acute and chronic conditions. Identification of selective inhib
Autor:
Xinmei Zhu, Sidney M. Morris, Paulo C. Rodriguez, Juan B. Ochoa, Timothy R. Billiar, Yoram Vodovotz, John P. Pribis
Publikováno v:
Annals of Surgery. 259:171-178
Objective To explore the hypothesis that decreased arginine availability by myeloid-derived suppressor cells (MDSCs) is a cause of T-cell dysfunction after physical injury (PI). Background Arginine is an essential amino acid for normal T-cell functio
Autor:
John P. Pribis, Susan G. Hilsenbeck, Alfred M. Lentzsch, Chenyue W. Hu, María Angélica Bravo Núñez, Mohan C. Joshi, Cristian Coarfa, Jun Xia, James C. Hu, Mercedes Perez, Reid T. Powell, Ali Jalali, Sandra A. LaBonte, Deborah A. Siegele, Megan Richters, Devon M. Fitzgerald, Yumeng Wang, P. J. Hastings, Christophe Herman, Susan M. Rosenberg, Kenneth L. Scott, David Bates, Christine Queitsch, Meztli L. Matadamas Guzmán, Adam T. Szafran, Yin Zhai, Ralf B. Nehring, Janet L. Gibson, Kyle M. Miller, Michael A. Mancini, Ryan L. Frisch, Qian Mei, Li-Ya Chiu, Han Liang
Publikováno v:
Cell. 176:127-143.e24
SUMMARYDNA damage provokes mutations and cancer, and results from external carcinogens or endogenous cellular processes. Yet, the intrinsic instigators of DNA damage are poorly understood. Here we identify proteins that promote endogenous DNA damage