The NF- k B Family of Transcription Factors and Its Regulation
The NF- k B Family of Transcription Factors and Its Regulation
复制标题
NF-kB转录因子家族及其调控
DOI：
--
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
S. Ghosh
中科院分区：
文献类型：
--
作者：
Andrea Oeckinghaus;S. Ghosh
核因子- k B（nuclear factor- k B）是一组转录因子，在免疫、细胞增殖、分化和存活等方面发挥重要作用.可诱导的NF-κ B活化依赖于NF-κ B蛋白抑制剂（I k Bs）的磷酸化诱导的蛋白体降解，其在未刺激的细胞中的胞质溶胶中保留无活性的NF-κ B二聚体。导致NF-κ B活化的大多数不同的信号传导途径集中在I κ B激酶（IKK）复合物上，该复合物负责I κ B磷酸化并且对于信号转导至NF-κ B是必需的. NF-κ B活性的额外调节是通过NF-κ B信号通路核心组分的各种翻译后修饰实现的。除了IKK和I k B蛋白以及其他通路特异性介质的胞质修饰外，转录因子本身也被广泛修饰艾德。在过去的二十年里，在解开控制NF-κ B反应的复杂调控网络方面取得了巨大的进展。这使得NF-κ B途径成为理解信号转导和基因调控一般原理的范例。使用多种信号传导衔接子来参与IKK活性。IKK B对经典I k Bs信号应答区（SRR）丝氨酸残基的磷酸化导致I k B泛素化和随后的蛋白体降解。这导致NF-κ B二聚体的释放，然后其可以易位到细胞核并诱导靶基因的转录。非经典途径依赖于NIK（NF-kB诱导激酶）诱导的IKK α活化。IKK α磷酸化p100 NF-κ B亚基，导致p100蛋白体加工成p52.这导致p52-RelB二聚体的激活，其靶向特定的k B元件。
Nuclear factor- k B (NF- k B) consists of afamilyof transcription factorsthat play critical roles in inflammation, immunity, cell proliferation, differentiation, and survival. Inducible NF- k B activation depends on phosphorylation-induced proteosomal degradation of the inhibitor of NF- k B proteins (I k Bs), which retain inactive NF- k B dimers in the cytosol in unstimulated cells. The majority of the diverse signaling pathways that lead to NF- k B activation converge on the I k B kinase (IKK) complex, which is responsible for I k B phosphorylation and is essential for signal transduction to NF- k B. Additional regulation of NF- k B activity is achieved through various post-translational modifications of the core componentsof the NF- k B signaling pathways. In addition to cytosolic modifications of IKK and I k B proteins, as well as other pathway-specific mediators, the transcription factors are themselves extensively modified. Tremendous progress has been made over the last two decades in unraveling the elaborate regulatory networks that control the NF- k B response. This has made the NF- k B pathway a paradigm for understanding general principles of signal transduction and gene regulation. uses a large variety of signaling adaptors to engage IKK activity. Phosphorylation of serine residues in the signal responsive region (SRR) of classical I k Bs by IKK b leads to I k B ubiquitination and subsequent proteosomal degradation. This results in release of the NF- k B dimer, which can then translocate to the nucleus and induce transcription of target genes. The non-canonical pathway depends on NIK (NF-k B-inducing kinase) induced activation of IKK a . IKK a phosphorylates the p100 NF- k B subunit, which leads to proteosomal processing of p100 to p52. This results in the activation of p52-RelB dimers, which target specific k B elements.
登录
查看更多内容
DOI：
--
发表时间：
2004
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Jennifer Wessells;M. Baer;H. Young;E. Claudio;K. Brown;U. Siebenlist;P. Johnson
通讯作者：
Jennifer Wessells;M. Baer;H. Young;E. Claudio;K. Brown;U. Siebenlist;P. Johnson
影响因子：
11.4
作者：
NEUMANN, M;GRIESHAMMER, T;SERFLING, E
通讯作者：
SERFLING, E
影响因子：
16
作者：
Ryo, A;Suizu, F;Lu, KP
通讯作者：
Lu, KP
瞬时转染细胞中 NF-kappaB 蛋白对 p105 加工的抑制。
DOI：
--
发表时间：
1996
期刊：
Oncogene.
影响因子：
--
作者：
Harhaj,EW;Maggirwar,SB;Sun,SC
通讯作者：
Sun,SC
影响因子：
16
作者：
Zhong, HH;Voll, RE;Ghosh, S
通讯作者：
Ghosh, S