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Retardation of cell cycle progression of macrophages from G1 to S phase by ICAM-L from Leishmania.

作者信息

Kuzmenok Oleg I, Chiang Su-Chi, Lin Yi-Chun, Lee Sho Tone

机构信息

Division of Infectious Diseases, Institute of Biomedical Sciences, Academia Sinica, IBMS, No.128, Academia Road Sec.2, Nan-Kang, Taipei 11529, Taiwan, ROC.

出版信息

Int J Parasitol. 2005 Dec;35(14):1547-55. doi: 10.1016/j.ijpara.2005.08.006. Epub 2005 Sep 13.

DOI:10.1016/j.ijpara.2005.08.006
PMID:16188262
Abstract

Leishmania, an obligate intracellular parasite of host macrophages, infects the macrophage through receptor-mediated phagocytosis that either activates or deactivates macrophages to eliminate the parasite or allow the parasite to grow intracellularly. ICAM-L, an intercellular adhesion molecule from L. amazonensis, results in lower MTT tests and proliferative responses of macrophages when incubated in vitro. The inhibition of cell proliferation, however, results from temporary retardation of the cell cycle progression at the G1 to S phase transition rather than cell death. The retardation is due to the upregulation of two CKI proteins, p21 and p27, in a p53-independent manner which, control the G(1) to S phase transition checkpoint.

摘要

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