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Roles of Herp in mycobacterial infected antigen presenting cells
Sang-Hun Son1,2, Ji-Ae Choi1,2, Junghwan Lee1,2, Soo-Na Cho1,2 , Nguyen Tam Doan1,2, Seongahn Lee1,2 and Chang-Hwa Song1,2,3
1 Department of Medical Science, 2 Department of Microbiology and 3 Translational immunology institute, College of Medicine, Chungnam National University,
Daejeon 35015, South Korea
BACKGROUND AIM
Endoplasmic reticulum (ER) stress plays an important role in the We found that herp was strongly increased in macrophage by
pathogenesis of tuberculosis. The homocysteine-inducible ER Mycobacterium tuberculosis (Mtb) H37Ra infection. ER stress
regulates Herp production during Mtb infection. Herp depletion
stress protein (Herp), part of the ER-associated protein increases reactive oxygen species production via ER stress
degradation (ERAD) pathway molecules, has not been known as regulation. Inhibition of Herp expression by using specific siRNA
a anti-mycobacterial factor. induced the LC3 and decreased p62, resulting in decrement of
intracellular survival of Mtb.
METHODS
To explore the role of Herp in tuberculosis, we compared suppressive effect of mycobacterial growth between Herp knockout
Raw264.7 cells and wild type control after mycobacterial infection.
RESULTS
CONCLUSION REFERENCES ACKNOWLEDGEMENTS
These results suggest that Herp plays an 1. Thuong manh Le. et al. (2016) Deletion of Herpud1 Enhances Heme 1. Herp is increased in macrophage during H37Ra infection.
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ER stress responses are increased in Herp knockout Raw264.7
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important role in regulation of intracellular Article ID 6163934, 9 pages. 3. cells compared to wild-type control during Mtb infection.
Herp depletion increased ROS production in Mtb-infected
survival of mycobacteria. These results 2. Yiman Li. et al. (2018) ER-localized protein-Herpud1 is a new mediator of IL- 4. macrophages.
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Herp depletion increased autophagy in Mtb-infected macrophages.
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apoptosis in M1-polarized macrophages during mycobacterial infections. 9. Our findings might provide new insight of host-derived therapy to
Scientific Reports, 6(1). doi:10.1038/srep37211 treat TB patients.
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