@article{9aa5936f7f0c43058b494dd17a459e02,
title = "Post translational modifications in tuberculosis: ubiquitination paradox",
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.",
keywords = "Autophagy, Mycobacterium tuberculosis, ubiquitination, virulence effectors, xenophagy",
author = "Mohd Shariq and Neha Quadir and Sheikh, {Javaid Ahmad} and Singh, {Alok Kumar} and Bishai, {William R.} and Ehtesham, {Nasreen Z.} and Hasnain, {Seyed E.}",
note = "Funding Information: MS acknowledges fellowship support from Department of Science and Technology, Government of India under DST-SERB N-PDF programme. NQ is a DHR Young Scientist. JAS is supported by the Start-up Research Grant from UGC and DST-SERB. AKS and WRB gratefully acknowledge the support of NIH grant AI 143610. SEH and NZE are supported by the Centre of Excellence Grant BT/PR12817/COE/34/23/2015 and DBT North-East Grants BT/PR23099/NER/95/632/2017 and BT/PR23155/NER/95/634/2017 by Department of Biotechnology, Ministry of Science and Technology, Government of India. SEH is a JC Bose National Fellow, Department of Science and Technology, Government of India and Robert Koch Fellow, Robert Koch Institute, Germany. Funding Information: This work was supported by the Department of Biotechnology, Ministry of Science and Technology [BT/PR12817/COE/34/23/2015]; Department of Biotechnology, Ministry of Science and Technology [BT/PR23099/NER/95/632/2017]; Department of Biotechnology, Ministry of Science and Technology [BT/PR23155/NER/95/634/2017]; National Institutes of Health [AI 143610]. MS acknowledges fellowship support from Department of Science and Technology, Government of India under DST-SERB N-PDF programme. NQ is a DHR Young Scientist. JAS is supported by the Start-up Research Grant from UGC and DST-SERB. AKS and WRB gratefully acknowledge the support of NIH grant AI 143610. SEH and NZE are supported by the Centre of Excellence Grant BT/PR12817/COE/34/23/2015 and DBT North-East Grants BT/PR23099/NER/95/632/2017 and BT/PR23155/NER/95/634/2017 by Department of Biotechnology, Ministry of Science and Technology, Government of India. SEH is a JC Bose National Fellow, Department of Science and Technology, Government of India and Robert Koch Fellow, Robert Koch Institute, Germany. Publisher Copyright: {\textcopyright} 2020 Informa UK Limited, trading as Taylor & Francis Group.",
year = "2021",
doi = "10.1080/15548627.2020.1850009",
language = "English (US)",
volume = "17",
pages = "814--817",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Taylor and Francis Ltd.",
number = "3",
}