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An Evolution-Guided Analysis Reveals a Multi-Signaling Regulation of Fas by Tyrosine Phosphorylation and its Implication in Human Cancers.一项进化引导分析揭示了酪氨酸磷酸化对Fas的多信号调节及其在人类癌症中的意义。
PLoS Biol. 2016 Mar 4;14(3):e1002401. doi: 10.1371/journal.pbio.1002401. eCollection 2016 Mar.
3
Structural Basis and Functional Role of Intramembrane Trimerization of the Fas/CD95 Death Receptor.Fas/CD95死亡受体膜内三聚化的结构基础及功能作用
Mol Cell. 2016 Feb 18;61(4):602-613. doi: 10.1016/j.molcel.2016.01.009. Epub 2016 Feb 4.
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γ-Secretase Activity Is Required for Regulated Intramembrane Proteolysis of Tumor Necrosis Factor (TNF) Receptor 1 and TNF-mediated Pro-apoptotic Signaling.γ-分泌酶活性是肿瘤坏死因子(TNF)受体1的调节性膜内蛋白水解和TNF介导的促凋亡信号传导所必需的。
J Biol Chem. 2016 Mar 11;291(11):5971-5985. doi: 10.1074/jbc.M115.679076. Epub 2016 Jan 11.
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The cybernetics of TNF: Old views and newer ones.肿瘤坏死因子的控制论:旧观点与新观点
Semin Cell Dev Biol. 2016 Feb;50:105-14. doi: 10.1016/j.semcdb.2015.10.014. Epub 2015 Oct 22.
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The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.肿瘤坏死因子家族细胞因子TL1A:从淋巴细胞共刺激因子到疾病共谋者。
J Leukoc Biol. 2015 Sep;98(3):333-45. doi: 10.1189/jlb.3RI0315-095R. Epub 2015 Jul 17.
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A set of NF-κB-regulated microRNAs induces acquired TRAIL resistance in lung cancer.一组由核因子κB调控的微小RNA可诱导肺癌产生获得性肿瘤坏死因子相关凋亡诱导配体耐药性。
Proc Natl Acad Sci U S A. 2015 Jun 30;112(26):E3355-64. doi: 10.1073/pnas.1504630112. Epub 2015 Jun 15.
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Involvement of the cytoplasmic cysteine-238 of CD40 in its up-regulation of CD23 expression and its enhancement of TLR4-triggered responses.
Int Immunol. 2015 Nov;27(11):555-65. doi: 10.1093/intimm/dxv030. Epub 2015 May 14.
9
Stoichiometry of Heteromeric BAFF and APRIL Cytokines Dictates Their Receptor Binding and Signaling Properties.异源三聚体BAFF和APRIL细胞因子的化学计量决定其受体结合和信号传导特性。
J Biol Chem. 2015 Jun 26;290(26):16330-42. doi: 10.1074/jbc.M115.661405. Epub 2015 May 7.
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Tumor necrosis factor receptor 2 (TNFR2)·interleukin-17 receptor D (IL-17RD) heteromerization reveals a novel mechanism for NF-κB activation.肿瘤坏死因子受体2(TNFR2)·白细胞介素-17受体D(IL-17RD)异源二聚化揭示了核因子κB激活的新机制。
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肿瘤坏死因子家族:家族惯例与个体差异。

The Tumor Necrosis Factor Family: Family Conventions and Private Idiosyncrasies.

机构信息

Department of Biomolecular Sciences, The Weizmann Institute of Science, 76100 Rehovot, Israel.

出版信息

Cold Spring Harb Perspect Biol. 2018 Oct 1;10(10):a028431. doi: 10.1101/cshperspect.a028431.

DOI:10.1101/cshperspect.a028431
PMID:28847899
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6169814/
Abstract

The tumor necrosis factor (TNF) cytokine family and the TNF/nerve growth factor (NGF) family of their cognate receptors together control numerous immune functions, as well as tissue-homeostatic and embryonic-development processes. These diverse functions are dictated by both shared and distinct features of family members, and by interactions of some members with nonfamily ligands and coreceptors. The spectra of their activities are further expanded by the occurrence of the ligands and receptors in both membrane-anchored and soluble forms, by "re-anchoring" of soluble forms to extracellular matrix components, and by signaling initiation via intracellular domains (IDs) of both receptors and ligands. Much has been learned about shared features of the receptors as well as of the ligands; however, we still have only limited knowledge of the mechanistic basis for their functional heterogeneity and for the differences between their functions and those of similarly acting cytokines of other families.

摘要

肿瘤坏死因子 (TNF) 细胞因子家族及其同源受体的 TNF/神经生长因子 (NGF) 家族共同控制着众多免疫功能,以及组织稳态和胚胎发育过程。这些不同的功能是由家族成员的共同和独特特征以及一些成员与非家族配体和共受体的相互作用决定的。它们的活性谱通过配体和受体以膜锚定和可溶性形式的存在、可溶性形式与细胞外基质成分的“再锚定”以及通过受体和配体的细胞内结构域 (IDs) 进行的信号转导起始进一步扩大。我们已经了解了受体以及配体的共同特征;然而,对于它们功能异质性的机制基础以及它们与其他家族中类似作用的细胞因子的功能差异,我们仍然知之甚少。