| Literature DB >> 33190592 |
Mohd Shariq1, Neha Quadir1,2, Javaid Ahmad Sheikh3, Alok Kumar Singh4, William R Bishai4, Nasreen Z Ehtesham1, Seyed E Hasnain2,5.
Abstract
Innate immune signaling and xenophagy are crucial innate defense strategies exploited by the host to counteract intracellular pathogens with ubiquitination as a critical regulator of these processes. These pathogens, including Mycobacterium tuberculosis (M. tb), co-opt the host ubiquitin machinery by utilizing secreted or cell surface effectors to dampen innate host defenses. Inversely, the host utilizes ubiquitin ligase-mediated ubiquitination of intracellular pathogens and recruits autophagy receptors to induce xenophagy. In the current article, we discuss the co-option of the ubiquitin pathway by the M. tb virulence effectors.Abbreviations: ANAPC2: anaphase promoting complex subunit 2; IL: interleukin; Lys: lysine (K); MAPK: mitogen-activated protein kinase; MAP3K7/TAK1; mitogen-activated protein kinase kinase kinase 7; M. tb: Mycobacterium tuberculosis; NFKB/NF-κB: nuclear factor kappa B subunit; PtpA: protein tyrosine phosphatase; SQSTM1/p62: sequestosome 1; V-ATPase: vacuolar-type H+-ATPase; UBA: a eukaryotic-like ubiquitin-associated domain.Entities:
Keywords: Autophagy; Mycobacterium tuberculosis; ubiquitination; virulence effectors; xenophagy
Mesh：
Year: 2020 PMID： 33190592 PMCID： PMC8032244 DOI： 10.1080/15548627.2020.1850009
Source DB: PubMed Journal: Autophagy ISSN： 1554-8627 Impact factor: 16.016