The role of interferon regulatory factors in the interferon system and cell growth control

The role of interferon regulatory factors in the interferon system and cell growth control
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DOI:
10.1016/s0300-9084(99)80017-0
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发表时间:
1998-08-01
期刊:
影响因子:
3.9
通讯作者:
Tanaka, N
Tanaka, N
中科院分区:
生物学3区
文献类型:
--
作者:
Harada, H;Taniguchi, T;Tanaka, N

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复杂的细胞反应通常由遗传调控网络协调,其中给定的转录因子控制不同靶基因组的表达。干扰素调节因子(IRF)-1和IRF-2最初被分别鉴定为干扰素-β(IFN-β)以及IFN-诱导基因的转录激活因子和阻遏因子。然而,这些因子已经被证明不仅调节对IFN的细胞应答,而且调节细胞生长、对癌基因转化的易感性、细胞凋亡的诱导和T细胞免疫应答的发展。此外,证据表明,IRF-1基因的缺失和/或失活可能是某些人类造血系统肿瘤发生的关键步骤。随后,这些因子已被证明构成转录因子家族,称为IRF家族。最近的研究表明,其他IRF家族成员也参与IFN系统和细胞转化的调节。IRF家族可以是转录因子的实例,其可以根据细胞类型和/或细胞刺激物的性质选择性地调节几组基因,从而引起宿主针对感染和肿瘤发生的防御机制。(C)法国生物化学与分子生物学协会/爱思唯尔,巴黎。
Complex cellular responses are often coordinated by a genetic regulatory network in which a given transcription factor controls the expression of a diverse set of target genes. Interferon regulatory factor (IRF)-1 and IRF-2 have originally been identified as a transcriptional activator and repressor, respectively, of the interferon-beta (IFN-beta) as well as of IFN-inducible genes. However, these factors have since been shown to modulate not only the cellular response to IFNs, but also cell growth, susceptibility to transformation by oncogenes, induction of apoptosis, and development of the T cell immune response. Furthermore, the evidence suggests that deletion and/or inactivation of the IRF-1 gene may be a critical step in the development of some human hematopoietic neoplasms. Subsequently, these factors have been shown to constitute a family of transcription factors, termed the IRF-family. Recent studies indicate that other IRF family members also involve the regulation of the IFN system and cell transformation. The IRF-family may be examples of transcription factors which can selectively modulate several sets of genes depending on the cell type and/or nature of the cellular stimuli, so as to evoke host defense mechanisms against infection and oncogenesis. (C) Societe francaise de biochimie et biologie moleculaire/Elsevier, Paris.