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本文引用的文献

1
NF-kappaB activation in T cells requires discrete control of IkappaB kinase alpha/beta (IKKalpha/beta) phosphorylation and IKKgamma ubiquitination by the ADAP adapter protein.T 细胞中 NF-κB 的激活需要 ADAP 衔接蛋白对 IKKα/β(IKKα/β)磷酸化和 IKKγ 泛素化的离散控制。
J Biol Chem. 2010 Apr 9;285(15):11100-5. doi: 10.1074/jbc.M109.068999. Epub 2010 Feb 17.
2
Pulsatile stimulation determines timing and specificity of NF-kappaB-dependent transcription.脉冲式刺激决定了NF-κB依赖性转录的时间和特异性。
Science. 2009 Apr 10;324(5924):242-6. doi: 10.1126/science.1164860.
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CARMA1-mediated NF-kappaB and JNK activation in lymphocytes.CARMA1介导淋巴细胞中的核因子κB和JNK激活。
Immunol Rev. 2009 Mar;228(1):199-211. doi: 10.1111/j.1600-065X.2008.00749.x.
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The structure, regulation, and function of ZAP-70.ZAP-70的结构、调控及功能。
Immunol Rev. 2009 Mar;228(1):41-57. doi: 10.1111/j.1600-065X.2008.00753.x.
5
T-cell receptor proximal signaling via the Src-family kinases, Lck and Fyn, influences T-cell activation, differentiation, and tolerance.通过Src家族激酶Lck和Fyn的T细胞受体近端信号传导影响T细胞的激活、分化和耐受性。
Immunol Rev. 2009 Mar;228(1):9-22. doi: 10.1111/j.1600-065X.2008.00745.x.
6
The kinase PDK1 integrates T cell antigen receptor and CD28 coreceptor signaling to induce NF-kappaB and activate T cells.激酶PDK1整合T细胞抗原受体和CD28共受体信号,以诱导核因子-κB并激活T细胞。
Nat Immunol. 2009 Feb;10(2):158-66. doi: 10.1038/ni.1687. Epub 2009 Jan 4.
7
Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival.酪蛋白激酶1α调控抗原受体诱导的核因子κB激活及人淋巴瘤细胞存活。
Nature. 2009 Mar 5;458(7234):92-6. doi: 10.1038/nature07613. Epub 2008 Dec 31.
8
The proteolytic activity of the paracaspase MALT1 is key in T cell activation.旁胱天蛋白酶MALT1的蛋白水解活性在T细胞活化中起关键作用。
Nat Immunol. 2008 Mar;9(3):272-81. doi: 10.1038/ni1568. Epub 2008 Feb 10.
9
IkappaB kinase beta-induced phosphorylation of CARMA1 contributes to CARMA1 Bcl10 MALT1 complex formation in B cells.IkappaB激酶β诱导的CARMA1磷酸化有助于B细胞中CARMA1、Bcl10和MALT1复合物的形成。
J Exp Med. 2007 Dec 24;204(13):3285-93. doi: 10.1084/jem.20070379. Epub 2007 Dec 17.
10
Malt1 ubiquitination triggers NF-kappaB signaling upon T-cell activation.麦芽凝集素1泛素化在T细胞活化时触发核因子κB信号传导。
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TCR/CD28 调控 NF-κB 的诱导

Regulation of NF-κB induction by TCR/CD28.

机构信息

Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

出版信息

Immunol Res. 2011 Aug;50(2-3):113-7. doi: 10.1007/s12026-011-8216-z.

DOI:10.1007/s12026-011-8216-z
PMID:21717079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4066383/
Abstract

NF-κB family transcription factors are a common downstream target for inducible transcription mediated by many different cell-surface receptors, especially those receptors involved in inflammation and adaptive immunity. It is now clear that different classes of receptors employ different proximal signaling strategies to activate the common NF-κB signaling components, such as the IKK complex. For antigen receptors expressed by T and B cells, this pathway requires a complex of proteins including the proteins Carma1, Bcl10, and Malt1. Here, we discuss some of what is known about regulation of these proteins downstream of TCR/CD3 and co-stimulatory CD28 signaling. We also discuss another unique aspect of TCR-mediated NF-κB activation, i.e., the spatial restriction imposed on signaling events by the formation of the immunological synapse between a T cell and antigen-presenting cell presenting specific peptide/MHC.

摘要

NF-κB 家族转录因子是许多不同细胞表面受体介导的诱导性转录的常见下游靶标,尤其是那些参与炎症和适应性免疫的受体。现在很清楚,不同类别的受体采用不同的近端信号策略来激活常见的 NF-κB 信号成分,如 IKK 复合物。对于 T 细胞和 B 细胞表达的抗原受体,该途径需要包括 Carma1、Bcl10 和 Malt1 在内的蛋白质复合物。在这里,我们讨论了 TCR/CD3 和共刺激 CD28 信号下游这些蛋白质调节的一些已知内容。我们还讨论了 TCR 介导的 NF-κB 激活的另一个独特方面,即 TCR 与呈递特定肽/MHC 的抗原呈递细胞之间形成免疫突触对信号事件施加的空间限制。