PE_PGRS62 promotes the survival of Mycobacterium smegmatis within macrophages via disrupting ER stress‐mediated apoptosis-Reference-Cited by-同舟云学术

PE_PGRS62 promotes the survival of Mycobacterium smegmatis within macrophages via disrupting ER stress‐mediated apoptosis

Published:2019-04 Issue:11 Volume:234 Page:19774-19784
ISSN:0021-9541
Container-title:Journal of Cellular Physiology
language:en
Short-container-title:J Cell Physiol

Author:

Long Quanxin¹,Xiang Xiaohong²,Yin Qingqin³,Li Shuangjiang⁴,Yang Wenmin⁵,Sun Hang¹,Liu Qi¹,Xie Jianping⁵,Deng Wanyan¹^ORCID

Affiliation:

1. Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases The Second Affiliated Hospital, Chongqing Medical University Chongqing People's Republic of China

2. School of Pharmacy Chongqing Medical and Pharmaceutical College Chongqing People's Republic of China

3. Department of Respiratory Medicine, China National Clinical Research Center for Respiratory Diseases Beijing Children's Hospital, Capital Medical University, National Center for Children's Health Beijing People's Republic of China

4. Department of Physical Examination Center The Second Affiliated Hospital, Chongqing Medical University Chongqing People's Republic of China

5. State Key Laboratory Breeding Base of Eco‐Environment and Bio‐Resource of the Three Gorges Area, Key Laboratory of Eco‐environments in Three Gorges Reservoir Region, Ministry of Education School of Life Sciences, Institute of Modern Biopharmaceuticals, Southwest University People's Republic of China

Funder

Chongqing Science and Technology Commission

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcp.28577

Reference57 articles.

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4. Are the PE-PGRS proteins of Mycobacterium tuberculosis variable surface antigens?

5. Execution of Macrophage Apoptosis by PE_PGRS33 of Mycobacterium tuberculosis Is Mediated by Toll-like Receptor 2-dependent Release of Tumor Necrosis Factor-α

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