Jeffery S. Cox

ORCID: 0000-0002-5061-6618
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About
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Research Areas
  • Tuberculosis Research and Epidemiology
  • Mycobacterium research and diagnosis
  • Autophagy in Disease and Therapy
  • Antibiotic Resistance in Bacteria
  • interferon and immune responses
  • Immune Response and Inflammation
  • Bacterial Genetics and Biotechnology
  • RNA and protein synthesis mechanisms
  • Immune cells in cancer
  • Galectins and Cancer Biology
  • Endoplasmic Reticulum Stress and Disease
  • Bacteriophages and microbial interactions
  • Biochemical and Molecular Research
  • HIV Research and Treatment
  • Mosquito-borne diseases and control
  • Inflammasome and immune disorders
  • CRISPR and Genetic Engineering
  • Immune Cell Function and Interaction
  • RNA Interference and Gene Delivery
  • Diagnosis and treatment of tuberculosis
  • Cytokine Signaling Pathways and Interactions
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Vibrio bacteria research studies
  • Pharmacogenetics and Drug Metabolism
  • Infectious Diseases and Tuberculosis

University of California, Berkeley
2003-2024

University of California, San Francisco
2010-2020

University of San Francisco
2020

University of the Witwatersrand
2019

University of California System
2013

Howard Hughes Medical Institute
1992-2009

Albert Einstein College of Medicine
1999-2009

Rockefeller University
2009

Cornell University
2009

San Francisco Foundation
2002-2006

Circadian clocks have evolved to regulate physiologic and behavioral rhythms in anticipation of changes the environment. Although molecular clock is present innate immune cells, its role monocyte homeostasis remains unknown. Here, we report that Ly6C(hi) inflammatory monocytes exhibit diurnal variation, which controls their trafficking sites inflammation. This cyclic pattern confers protection against Listeria monocytogenes regulated by repressive activity circadian gene Bmal1. Accordingly,...

10.1126/science.1240636 article EN Science 2013-08-23

Although many bacterial pathogens use specialized secretion systems for virulence, no such have been described Mycobacterium tuberculosis , a major pathogen of humans that proliferates in host macrophages. In screen to identify genes required virulence M. we discovered three components and two substrates the first Sec-independent pathway which designate Snm pathway. Here demonstrate proteins Snm1, -2, -4 are ESAT-6 CFP-10, small previously identified as T cell antigens. Snm2, member AAA...

10.1073/pnas.2235593100 article EN Proceedings of the National Academy of Sciences 2003-10-13

Toxin-antitoxin (TA) systems, stress-responsive genetic elements ubiquitous in microbial genomes, are unusually abundant the major human pathogen Mycobacterium tuberculosis. Why M. tuberculosis has so many TA systems and what role they play unique biology of is unknown. To address these questions, we have taken a comprehensive approach to identify functionally characterize all encoded genome. Here show that 88 putative system candidates present tuberculosis, considerably more than previously...

10.1371/journal.pgen.1000767 article EN cc-by PLoS Genetics 2009-12-10

Abstract The ESX-1 secretion system is a major determinant of Mycobacterium tuberculosis virulence, although the pathogenic mechanisms resulting from ESX-1-mediated transport remain unclear. By global transcriptional profiling tissues mice infected with either wild-type or mutant bacilli, we found that host genes controlled by in vivo are predominantly IFN regulated. required for production type I IFNs during infection and macrophages vitro. macrophage signaling pathway leading to kinase...

10.4049/jimmunol.178.5.3143 article EN The Journal of Immunology 2007-03-01

The endoplasmic reticulum (ER) is a multifunctional organelle responsible for production of both lumenal and membrane components secretory pathway compartments. Secretory proteins are folded, processed, sorted in the ER lumen lipid synthesis occurs on itself. In yeast Saccharomyces cerevisiae, highly regulated: ER-resident by unfolded protein response inositol response. We demonstrate that these two responses intimately linked, forming different branches same pathway. Furthermore, we present...

10.1091/mbc.8.9.1805 article EN Molecular Biology of the Cell 1997-09-01

CITATION: Bitter, W., et al. 2009. Systematic genetic nomenclature for type VII secretion systems. PLoS Pathogens, 5(10): 1-6, doi: 10.1371/journal.ppat.1000507.

10.1371/journal.ppat.1000507 article EN cc-by PLoS Pathogens 2009-10-29

Abstract The Stimulator of Interferon Genes (STING) pathway initiates potent immune responses upon recognition DNA. To initiate signaling, serine 365 (S365) in the C-terminal tail (CTT) STING is phosphorylated, leading to induction type I interferons (IFNs). Additionally, evolutionary conserved such as autophagy also occur downstream STING, but their relative importance during vivo infections remains unclear. Here we report that mice harboring a 365-to-alanine (S365A) mutation are...

10.1038/s41467-020-17156-x article EN cc-by Nature Communications 2020-07-07

Summary Reactive nitrogen species (RNS) play an essential role in host defence against Mycobacterium tuberculosis (MTB) the mouse model of (TB), as evidenced by increased susceptibility mice deficient inducible isoform nitric oxide synthase (NOS2). In contrast, reactive oxygen (ROS) protection MTB is less clear, and defective ROS‐generating phagocyte NADPH oxidase (Phox) are relatively resistant. This suggests that might possess efficient mechanisms to evade or counter oxidative burst,...

10.1111/j.1365-2958.2004.04078.x article EN Molecular Microbiology 2004-04-30

Mycobacterium tuberculosis , the causative agent of human tuberculosis, is unique among bacterial pathogens in that it displays a wide array complex lipids and lipoglycans on its cell surface. One more remarkable sulfated glycolipid, termed sulfolipid-1 (SL-1), which thought to mediate specific host-pathogen interactions during infection. However, direct role for SL-1 M. virulence has not been established. Here we show MmpL8, member large family predicted lipid transporters required...

10.1073/pnas.1030024100 article EN Proceedings of the National Academy of Sciences 2003-04-30
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