• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

组蛋白去乙酰化酶相关的 Sin3B 蛋白抑制 DREAM 复合物靶标，并与 APC/C 合作促进静止。

The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence.

机构信息

Department of Biochemistry and Molecular Pharmacology, NYU Langone Medical Center, New York, NY 10016, USA.

Department of Internal Medicine and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.

出版信息

Cell Rep. 2018 Dec 4;25(10):2797-2807.e8. doi: 10.1016/j.celrep.2018.11.024.

DOI:10.1016/j.celrep.2018.11.024
PMID:30517867
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6324198/
Abstract

The mammalian DREAM complex is responsible for the transcriptional repression of hundreds of cell-cycle-related genes in quiescence. How the DREAM complex recruits chromatin-modifying entities to aid in its repression remains unknown. Using unbiased proteomics analysis, we have uncovered a robust association between the chromatin-associated Sin3B protein and the DREAM complex. We have determined that genetic inactivation of Sin3B results in the de-repression of DREAM target genes during quiescence but is insufficient to allow quiescent cells to resume proliferation. However, inactivation of APC/C was sufficient for Sin3B cells, but not parental cells, to re-enter the cell cycle. These studies identify Sin3B as a transcriptional corepressor associated with the DREAM complex in quiescence and reveals a functional cooperation between E2F target repression and APC/C in the negative regulation of cell-cycle progression.

摘要

哺乳动物的 DREAM 复合物负责在静止期转录抑制数百个细胞周期相关基因。DREAM 复合物如何招募染色质修饰因子来帮助其抑制仍然未知。使用无偏proteomics 分析，我们已经发现染色质相关的 Sin3B 蛋白与 DREAM 复合物之间存在强大的关联。我们已经确定，Sin3B 的遗传失活导致静止期 DREAM 靶基因的去抑制，但不足以使静止细胞重新开始增殖。然而，APC/C 的失活足以使 Sin3B 细胞而不是亲本细胞重新进入细胞周期。这些研究表明 Sin3B 是静止期与 DREAM 复合物相关的转录共抑制因子，并揭示了 E2F 靶基因抑制与 APC/C 在细胞周期进程负调控中的功能合作。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/beff73f9e76a/nihms-1516646-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/e2646b314794/nihms-1516646-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/7742ffe5cf59/nihms-1516646-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/15fa7400f2ee/nihms-1516646-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/3223839ee2de/nihms-1516646-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/beff73f9e76a/nihms-1516646-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/e2646b314794/nihms-1516646-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/7742ffe5cf59/nihms-1516646-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/15fa7400f2ee/nihms-1516646-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/3223839ee2de/nihms-1516646-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9f9/6324198/beff73f9e76a/nihms-1516646-f0006.jpg

相似文献

1
The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence.组蛋白去乙酰化酶相关的 Sin3B 蛋白抑制 DREAM 复合物靶标，并与 APC/C 合作促进静止。
Cell Rep. 2018 Dec 4;25(10):2797-2807.e8. doi: 10.1016/j.celrep.2018.11.024.
2
HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.组蛋白去乙酰化酶（HDAC）活性对于 DREAM 和 E2F:RB 复合物抑制细胞周期基因的表达是可有可无的。
Nat Commun. 2024 May 24;15(1):4450. doi: 10.1038/s41467-024-48724-0.
3
HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.组蛋白去乙酰化酶（HDAC）活性对于DREAM和E2F:RB复合物抑制细胞周期基因而言并非必需。
bioRxiv. 2023 Oct 28:2023.10.28.564489. doi: 10.1101/2023.10.28.564489.
4
Loss of the Caenorhabditis elegans pocket protein LIN-35 reveals MuvB's innate function as the repressor of DREAM target genes.秀丽隐杆线虫口袋蛋白LIN-35的缺失揭示了MuvB作为DREAM靶基因阻遏物的固有功能。
PLoS Genet. 2017 Nov 1;13(11):e1007088. doi: 10.1371/journal.pgen.1007088. eCollection 2017 Nov.
5
Haploinsufficiency of the Sin3/HDAC corepressor complex member SIN3B causes a syndromic intellectual disability/autism spectrum disorder.Sin3/HDAC 核心抑制复合物成员 SIN3B 的杂合性缺失导致综合征性智力障碍/自闭症谱系障碍。
Am J Hum Genet. 2021 May 6;108(5):929-941. doi: 10.1016/j.ajhg.2021.03.017. Epub 2021 Apr 2.
6
Myt1 family recruits histone deacetylase to regulate neural transcription.Myt1家族募集组蛋白去乙酰化酶以调节神经转录。
J Neurochem. 2005 Jun;93(6):1444-53. doi: 10.1111/j.1471-4159.2005.03131.x.
7
Sin3B: an essential regulator of chromatin modifications at E2F target promoters during cell cycle withdrawal.Sin3B：细胞周期退出过程中E2F靶基因启动子处染色质修饰的关键调节因子。
Cell Cycle. 2008 Jun 1;7(11):1550-4. doi: 10.4161/cc.7.11.6052. Epub 2008 Apr 1.
8
The potential of targeting Sin3B and its associated complexes for cancer therapy.将Sin3B及其相关复合物作为癌症治疗靶点的潜力。
Expert Opin Ther Targets. 2017 Nov;21(11):1051-1061. doi: 10.1080/14728222.2017.1386655. Epub 2017 Oct 9.
9
Cyclin-dependent kinase-mediated phosphorylation of RBP1 and pRb promotes their dissociation to mediate release of the SAP30·mSin3·HDAC transcriptional repressor complex.周期蛋白依赖性激酶介导的 RBP1 和 pRb 的磷酸化促进它们的解离，以介导 SAP30·mSin3·HDAC 转录抑制复合物的释放。
J Biol Chem. 2011 Feb 18;286(7):5108-18. doi: 10.1074/jbc.M110.198473. Epub 2010 Dec 9.
10
Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes.应激介导的Sin3B激活导致p53靶基因子集的负调控。
Biosci Rep. 2015 Jun 25;35(4):e00234. doi: 10.1042/BSR20150122.

引用本文的文献

1
Emerging Role of the DREAM Complex in Cancer and Therapeutic Opportunities.DREAM复合物在癌症中的新作用及治疗机会
Int J Mol Sci. 2025 Jan 1;26(1):322. doi: 10.3390/ijms26010322.
2
miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress.miR-96-5p 的表达足以在没有应激的情况下诱导和维持衰老细胞状态。
Proc Natl Acad Sci U S A. 2024 Oct;121(40):e2321182121. doi: 10.1073/pnas.2321182121. Epub 2024 Sep 26.
3
SIN3B Loss Heats up Cold Tumor Microenvironment to Boost Immunotherapy in Pancreatic Cancer.

本文引用的文献

1
Timing of transcription during the cell cycle: Protein complexes binding to E2F, E2F/CLE, CDE/CHR, or CHR promoter elements define early and late cell cycle gene expression.细胞周期中的转录时机：与E2F、E2F/CLE、CDE/CHR或CHR启动子元件结合的蛋白质复合物决定了细胞周期早期和晚期基因的表达。
Oncotarget. 2016 Jul 28;8(58):97736-97748. doi: 10.18632/oncotarget.10888. eCollection 2017 Nov 17.
2
The DREAM complex through its subunit Lin37 cooperates with Rb to initiate quiescence.DREAM 复合物通过其亚基 Lin37 与 Rb 合作启动静止。
Elife. 2017 Sep 18;6:e26876. doi: 10.7554/eLife.26876.
3
Chromatin-Associated Protein SIN3B Prevents Prostate Cancer Progression by Inducing Senescence.
SIN3B 缺失使冷肿瘤微环境升温，从而增强胰腺癌的免疫治疗效果。
Adv Sci (Weinh). 2024 Nov;11(43):e2402244. doi: 10.1002/advs.202402244. Epub 2024 Sep 24.
4
Expression Proteomics and Histone Analysis Reveal Extensive Chromatin Network Changes and a Role for Histone Tail Trimming during Cellular Differentiation.表达蛋白质组学和组蛋白分析揭示了广泛的染色质网络变化，以及组蛋白尾部修剪在细胞分化过程中的作用。
Biomolecules. 2024 Jun 24;14(7):747. doi: 10.3390/biom14070747.
5
APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.后期促进复合物/细胞周期体（APC/C）可防止细胞周期蛋白/细胞周期蛋白依赖性激酶（cyclin/CDK）活性出现非经典顺序，以维持CDK4/6抑制剂诱导的细胞停滞。
Proc Natl Acad Sci U S A. 2024 Jul 23;121(30):e2319574121. doi: 10.1073/pnas.2319574121. Epub 2024 Jul 18.
6
HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.组蛋白去乙酰化酶（HDAC）活性对于 DREAM 和 E2F:RB 复合物抑制细胞周期基因的表达是可有可无的。
Nat Commun. 2024 May 24;15(1):4450. doi: 10.1038/s41467-024-48724-0.
7
Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells.染色质可及性和细胞周期进程受小鼠造血干细胞中与组蛋白去乙酰化酶相关的 Sin3B 蛋白的控制。
Epigenetics Chromatin. 2024 Jan 23;17(1):2. doi: 10.1186/s13072-024-00526-w.
8
APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.后期促进复合物/细胞周期体（APC/C）可防止细胞周期蛋白/细胞周期蛋白依赖性激酶（cyclin/CDK）活性的非经典顺序，以维持CDK4/6抑制剂诱导的细胞停滞。
bioRxiv. 2023 Nov 9:2023.11.09.566394. doi: 10.1101/2023.11.09.566394.
9
HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.组蛋白去乙酰化酶（HDAC）活性对于DREAM和E2F:RB复合物抑制细胞周期基因而言并非必需。
bioRxiv. 2023 Oct 28:2023.10.28.564489. doi: 10.1101/2023.10.28.564489.
10
Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice.染色质相关 SIN3B 保护癌细胞免受致凋亡的遗传毒性应激，并决定 DNA 损伤修复途径的选择。
Mol Cancer Res. 2023 Sep 1;21(9):947-957. doi: 10.1158/1541-7786.MCR-22-0466.
染色质相关蛋白SIN3B通过诱导衰老来阻止前列腺癌进展。
Cancer Res. 2017 Oct 1;77(19):5339-5348. doi: 10.1158/0008-5472.CAN-16-3410. Epub 2017 Aug 14.
4
The Chromatin-Associated Phf12 Protein Maintains Nucleolar Integrity and Prevents Premature Cellular Senescence.与染色质相关的Phf12蛋白维持核仁完整性并防止细胞过早衰老。
Mol Cell Biol. 2017 Feb 15;37(5). doi: 10.1128/MCB.00522-16. Print 2017 Mar 1.
5
Proteomic Landscape of Tissue-Specific Cyclin E Functions in Vivo.体内组织特异性细胞周期蛋白E功能的蛋白质组学全景
PLoS Genet. 2016 Nov 9;12(11):e1006429. doi: 10.1371/journal.pgen.1006429. eCollection 2016 Nov.
6
The chromatin-associated Sin3B protein is required for hematopoietic stem cell functions in mice.染色质相关的Sin3B蛋白对于小鼠造血干细胞功能是必需的。
Blood. 2017 Jan 5;129(1):60-70. doi: 10.1182/blood-2016-06-721746. Epub 2016 Nov 2.
7
Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.TP53、DREAM、MMB-FOXM1和RB-E2F靶基因分析的整合确定了细胞周期基因调控网络。
Nucleic Acids Res. 2016 Jul 27;44(13):6070-86. doi: 10.1093/nar/gkw523. Epub 2016 Jun 8.
8
Enrichr: a comprehensive gene set enrichment analysis web server 2016 update.Enrichr：一个全面的基因集富集分析网络服务器2016年更新版。
Nucleic Acids Res. 2016 Jul 8;44(W1):W90-7. doi: 10.1093/nar/gkw377. Epub 2016 May 3.
9
Emerging Roles of Epigenetic Regulator Sin3 in Cancer.表观遗传调节因子Sin3在癌症中的新作用
Adv Cancer Res. 2016;130:113-35. doi: 10.1016/bs.acr.2016.01.006. Epub 2016 Mar 2.
10
Structural mechanisms of DREAM complex assembly and regulation.DREAM复合物组装与调控的结构机制。
Genes Dev. 2015 May 1;29(9):961-74. doi: 10.1101/gad.257568.114. Epub 2015 Apr 27.