Zobrazeno 1 - 10
of 75
pro vyhledávání: '"Jonathan J Miner"'
Autor:
Forrest C Walker, Ebrahim Hassan, Stefan T Peterson, Rachel Rodgers, Lawrence A Schriefer, Cassandra E Thompson, Yuhao Li, Gowri Kalugotla, Carla Blum-Johnston, Dylan Lawrence, Broc T McCune, Vincent R Graziano, Larissa Lushniak, Sanghyun Lee, Alexa N Roth, Stephanie M Karst, Timothy J Nice, Jonathan J Miner, Craig B Wilen, Megan T Baldridge
Publikováno v:
PLoS Pathogens, Vol 17, Iss 3, p e1009402 (2021)
Interferons (IFNs) are key controllers of viral replication, with intact IFN responses suppressing virus growth and spread. Using the murine norovirus (MNoV) system, we show that IFNs exert selective pressure to limit the pathogenic evolutionary pote
Externí odkaz:
https://doaj.org/article/90fb07bf8a2e40fb883cfc49c1867b66
Autor:
Samuel D. Chauvin, Shoichiro Ando, Joe A. Holley, Atsushi Sugie, Fang R. Zhao, Subhajit Poddar, Rei Kato, Cathrine A. Miner, Yohei Nitta, Siddharth R. Krishnamurthy, Rie Saito, Yue Ning, Yuya Hatano, Sho Kitahara, Shin Koide, W. Alexander Stinson, Jiayuan Fu, Nehalee Surve, Lindsay Kumble, Wei Qian, Oleksiy Polishchuk, Prabhakar S. Andhey, Cindy Chiang, Guanqun Liu, Ludovic Colombeau, Raphaël Rodriguez, Nicolas Manel, Akiyoshi Kakita, Maxim N. Artyomov, David C. Schultz, P. Toby Coates, Elisha D. O. Roberson, Yasmine Belkaid, Roger A. Greenberg, Sara Cherry, Michaela U. Gack, Tristan Hardy, Osamu Onodera, Taisuke Kato, Jonathan J. Miner
Publikováno v:
Nature Communications, Vol 15, Iss 1, Pp 1-23 (2024)
Abstract Age-related microangiopathy, also known as small vessel disease (SVD), causes damage to the brain, retina, liver, and kidney. Based on the DNA damage theory of aging, we reasoned that genomic instability may underlie an SVD caused by dominan
Externí odkaz:
https://doaj.org/article/ca3eac3b209b443bb4c3882b9c20a335
Autor:
Edward T Schmid, Iris K Pang, Eugenio A Carrera Silva, Lidia Bosurgi, Jonathan J Miner, Michael S Diamond, Akiko Iwasaki, Carla V Rothlin
Publikováno v:
eLife, Vol 5 (2016)
The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production through a negative feedback loop. Enhanced production of type I IFNs in Axl-/- dendritic cells (DCs) in vitro have led to speculati
Externí odkaz:
https://doaj.org/article/26ed936461cc4d648ecb813982f9941e
Autor:
W. Alexander Stinson, Cathrine A. Miner, Fang R. Zhao, Annena Jane Lundgren, Subhajit Poddar, Jonathan J. Miner
Publikováno v:
JCI Insight, Vol 7, Iss 17 (2022)
STING gain-of-function mutations cause STING-associated vasculopathy with onset in infancy (SAVI) in humans, a disease characterized by spontaneous lung inflammation and fibrosis. Mice with STING gain-of-function mutations (SAVI mice) develop αβ T
Externí odkaz:
https://doaj.org/article/a4c4e4bbfe444775954246d3e433d51c
Autor:
Pooja Khonde, Deyali Chatterjee, Madonna Bogacki, M. Kathryn Liszewski, Andria L. Ford, Jonathan J. Miner, John P. Atkinson, Elizabeth M. Brunt
Publikováno v:
Human Pathology. 135:22-34
Publikováno v:
Nature Reviews Rheumatology. 19:182-189
Autor:
Jung-Jin Lee, Peter C. Grayson, Ronald G. Collman, Brendan J Kelly, Antoine G. Sreih, Jiarui Lu, Peter A. Merkel, Noam A. Cohen, Kyle Bittinger, Sherry Chou, Hongzhe Lee, Rennie L. Rhee, Lisa M. Mattei, Jonathan J. Miner
Publikováno v:
Arthritis Rheumatol
OBJECTIVE Little is known about temporal changes in nasal bacteria in granulomatosis with polyangiitis (GPA). This study was undertaken to examine longitudinal changes in the nasal microbiome in association with relapse in GPA patients. METHODS Bacte
Publikováno v:
Journal of Biological Chemistry. :104866
Publikováno v:
Viral Immunol
Immune regulation at the maternal-fetal interface is complex due to conflicting immunological objectives: protection of the fetus from maternal pathogens and prevention of immune-mediated rejection of the semiallogeneic fetus and placenta. Interferon
Autor:
W. Alexander Stinson, Cathrine A. Miner, Fang R. Zhao, Annena Jane Lundgren, Subhajit Poddar, Jonathan J. Miner
Publikováno v:
JCI insight. 7(17)
STING gain-of-function mutations cause STING-associated vasculopathy with onset in infancy (SAVI) in humans, a disease characterized by spontaneous lung inflammation and fibrosis. Mice with STING gain-of-function mutations (SAVI mice) develop αβ T