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bcl-2在细胞凋亡中的作用分析。

Analysis of the role of bcl-2 in apoptosis.

作者信息

Hawkins C J, Vaux D L

机构信息

Walter & Eliza Hall Institute for Medical Research, Victoria, Australia.

出版信息

Immunol Rev. 1994 Dec;142:127-39. doi: 10.1111/j.1600-065x.1994.tb00886.x.

Abstract

Cells undergo apoptosis in response to a wide range of stimuli, and this response may represent an ancient defence mechanism against pathogens. Bcl-2 is able to prevent apoptosis in many cases. Although blocking cell suicide is not directly oncogenic, enforced bcl-2 expression can lead to cancer by lengthening the life-span of cells, during which time secondary changes, such as activation of additional oncogenes like c-myc, can occur. Bcl-2 cannot block apoptosis of target cells by cytotoxic T lymphocytes. Thus cytotoxic T cells are able to fight viruses that carry anti-apoptosis genes that resemble bcl-2. Genes involved in the regulation of mammalian apoptosis are similar to those that mediate programmed cell death in C. elegans. By studying cell death genes in viruses and worms as well as mammals, we will learn more about this fascinating process.

摘要

细胞会对多种刺激产生凋亡反应,这种反应可能代表了一种对抗病原体的古老防御机制。在许多情况下,Bcl-2能够阻止细胞凋亡。虽然阻断细胞自杀并非直接致癌,但Bcl-2的强制表达可通过延长细胞寿命导致癌症,在此期间可能发生诸如激活额外的癌基因如c-myc等二次变化。Bcl-2无法阻止细胞毒性T淋巴细胞介导的靶细胞凋亡。因此,细胞毒性T细胞能够对抗携带类似Bcl-2的抗凋亡基因的病毒。参与哺乳动物细胞凋亡调控的基因与那些介导秀丽隐杆线虫程序性细胞死亡的基因相似。通过研究病毒、蠕虫以及哺乳动物中的细胞死亡基因,我们将更多地了解这一迷人的过程。

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