지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2015.9
- 수록면
- 215 - 227 (13page)
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Apoptosis is an important host defense mechanism against mycobacterial infection. Recent reports suggest that links between apoptosis and endoplasmic reticulum (ER) stress are critical for the regulation of mycobacterial survival; however, the exact regulatory mechanisms are not well known. In this study, we isolated 20 Mycobacterium tuberculosis (Mtb) clinical strains from Korean patients and examined ER stress-mediated apoptosis in Mtb-infected macrophages. Most Mtb strains increased the rates of apoptosis and production of ER stress-sensing molecules in mouse macrophages, similar to Mtb H37Rv infection. Moreover, the intracellular survival of Mtb clinical isolates in macrophages was similar to that of H37Rv. Our data suggest that infection with Mtb downregulated MCP-1 and MCPIP. The regulation of MCPIP may decrease ROS production, leading to a reduction in ER stress-mediated apoptosis.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2016-475-001942014