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SWI/SNF：修订间差异

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== 作用机理 ==
== 作用机理 ==
人们发现酵母中的SWI/SNF复合体能使[[DNA]]在不同的位置与[[组蛋白]]结合成[[核小体]]<ref name="pmid10466730">{{cite journal | author = Whitehouse I, Flaus A, Cairns BR, White MF, Workman JL, Owen-Hughes T | title = Nucleosome mobilization catalysed by the yeast SWI/SNF complex | journal = Nature | volume = 400 | issue = 6746 | pages = 784–7 |date=August 1999 | pmid = 10466730 | doi = 10.1038/23506 | url = }}</ref>。目前已提出两种SWI/SNF重塑核小体的机制<ref name="pmid12897850">{{cite journal | author = van Holde K, Yager T | title = Models for chromatin remodeling: a critical comparison | journal = Biochem. Cell Biol. | volume = 81 | issue = 3 | pages = 169–72 | year = 2003 | pmid = 12897850 | doi = 10.1139/o03-038 }}</ref>。一种认为核小体DNA中的扭转缺陷发生单向扩散，使DNA从进入核小体的地方开始贴着组蛋白八聚体的表面螺旋状地传播。另一种机制叫做“突起”或“环再捕获”。
人们发现酵母中的SWI/SNF复合体能使[[DNA]]在不同的位置与[[组蛋白]]结合成[[核小体]]<ref name="pmid10466730">{{cite journal | author = Whitehouse I, Flaus A, Cairns BR, White MF, Workman JL, Owen-Hughes T | title = Nucleosome mobilization catalysed by the yeast SWI/SNF complex | journal = Nature | volume = 400 | issue = 6746 | pages = 784–7 |date=August 1999 | pmid = 10466730 | doi = 10.1038/23506 | url = }}</ref>。目前已提出两种SWI/SNF重塑核小体的机制<ref name="pmid12897850">{{cite journal | author = van Holde K, Yager T | title = Models for chromatin remodeling: a critical comparison | journal = Biochem. Cell Biol. | volume = 81 | issue = 3 | pages = 169–72 | year = 2003 | pmid = 12897850 | doi = 10.1139/o03-038 }}</ref>。一种机制叫做“扭转扩散”，认为核小体DNA中的扭转缺陷发生单向扩散，使DNA从进入核小体的地方开始贴着组蛋白八聚体的表面螺旋状地传播。另一种机制叫做“突起”或“环再捕获”，意即DNA在核小体边缘与之分离，形成一环状突起。环状突起在组蛋白八聚体表面像波浪般传播，最后在核小体内部重新与之结合。这样DNA就在和组蛋白接触点数量不变的情况下完成位移<ref name="pmid12666181">{{cite journal | author = Flaus A, Owen-Hughes T | title = Mechanisms for nucleosome mobilization | journal = Biopolymers | volume = 68 | issue = 4 | pages = 563–78 | year = 2003 | pmid = 12666181 | doi = 10.1002/bip.10323 }}</ref>。最新研究提出了与“扭转扩散”机制相抵触的有力证据，增加了“环再捕获”模型的说服力<ref name="pmid16518397">{{cite journal | author = Zofall M, Persinger J, Kassabov SR, Bartholomew B | title = Chromatin remodeling by ISW2 and SWI/SNF requires DNA translocation inside the nucleosome | journal = Nat. Struct. Mol. Biol. | volume = 13 | issue = 4 | pages = 339–46 | year = 2006 | pmid = 16518397 | doi = 10.1038/nsmb1071 }}</ref>。

== 肿瘤抑制作用 ==
人类的SWI/SNF复合体（mSWI/SNF）对很多人类恶性肿瘤有抑制作用。1998年首先发现它能抑制横纹肌样瘤（一种罕见的儿童恶性肿瘤）ref name="pmid9671307">{{cite journal | author = Versteege I, Sévenet N, Lange J, Rousseau-Merck MF, Ambros P, Handgretinger R, Aurias A, Delattre O | title = Truncating mutations of hSNF5/INI1 in aggressive paediatric cancer | journal = Nature | volume = 394 | issue = 6689 | pages = 203–6 |date=July 1998 | pmid = 9671307 | doi = 10.1038/28212 }}</ref>。随着[[DNA测序]]成本逐渐降低，2010年左右许多肿瘤首次得到测序。其中数项研究表明SWI/SNF对多种恶性肿瘤有抑制作用<ref name="pmid20942669">{{cite journal | author = Wiegand KC, Shah SP, Al-Agha OM, Zhao Y, Tse K, Zeng T, Senz J, McConechy MK, Anglesio MS, Kalloger SE, Yang W, Heravi-Moussavi A, Giuliany R, Chow C, Fee J, Zayed A, Prentice L, Melnyk N, Turashvili G, Delaney AD, Madore J, Yip S, McPherson AW, Ha G, Bell L, Fereday S, Tam A, Galletta L, Tonin PN, Provencher D, Miller D, Jones SJ, Moore RA, Morin GB, Oloumi A, Boyd N, Aparicio SA, Shih IeM, Mes-Masson AM, Bowtell DD, Hirst M, Gilks B, Marra MA, Huntsman DG | title = ARID1A mutations in endometriosis-associated ovarian carcinomas | journal = N. Engl. J. Med. | volume = 363 | issue = 16 | pages = 1532–43 |date=October 2010 | pmid = 20942669 | pmc = 2976679 | doi = 10.1056/NEJMoa1008433 }}</ref><ref name="pmid21822264">{{cite journal | author = Li M, Zhao H, Zhang X, Wood LD, Anders RA, Choti MA, Pawlik TM, Daniel HD, Kannangai R, Offerhaus GJ, Velculescu VE, Wang L, Zhou S, Vogelstein B, Hruban RH, Papadopoulos N, Cai J, Torbenson MS, Kinzler KW | title = Inactivating mutations of the chromatin remodeling gene ARID2 in hepatocellular carcinoma | journal = Nat. Genet. | volume = 43 | issue = 9 | pages = 828–9 |date=September 2011 | pmid = 21822264 | pmc = 3163746 | doi = 10.1038/ng.903 }}</ref><ref name="pmid22233809">{{cite journal | author = Shain AH, Giacomini CP, Matsukuma K, Karikari CA, Bashyam MD, Hidalgo M, Maitra A, Pollack JR | title = Convergent structural alterations define SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeler as a central tumor suppressive complex in pancreatic cancer | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 109 | issue = 5 | pages = E252–9 |date=January 2012 | pmid = 22233809 | pmc = 3277150 | doi = 10.1073/pnas.1114817109 }}</ref><ref name="pmid21248752">{{cite journal | author = Varela I, Tarpey P, Raine K, Huang D, Ong CK, Stephens P, Davies H, Jones D, Lin ML, Teague J, Bignell G, Butler A, Cho J, Dalgliesh GL, Galappaththige D, Greenman C, Hardy C, Jia M, Latimer C, Lau KW, Marshall J, McLaren S, Menzies A, Mudie L, Stebbings L, Largaespada DA, Wessels LF, Richard S, Kahnoski RJ, Anema J, Tuveson DA, Perez-Mancera PA, Mustonen V, Fischer A, Adams DJ, Rust A, Chan-on W, Subimerb C, Dykema K, Furge K, Campbell PJ, Teh BT, Stratton MR, Futreal PA | title = Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma | journal = Nature | volume = 469 | issue = 7331 | pages = 539–42 |date=January 2011 | pmid = 21248752 | pmc = 3030920 | doi = 10.1038/nature09639 }}</ref>。对多个测序研究结果的荟萃分析表明，大约20%的人类恶性肿瘤中SWI/SNF存在变异<ref name="pmid23355908">{{cite journal | author = Shain AH, Pollack JR | title = The spectrum of SWI/SNF mutations, ubiquitous in human cancers | journal = PLoS ONE | volume = 8 | issue = 1 | pages = e55119 | year = 2013 | pmid = 23355908 | pmc = 3552954 | doi = 10.1371/journal.pone.0055119 }}</ref>。


== 另见 ==
== 另见 ==

2016年5月9日 (一) 07:09的版本

SWIB
拟南芥假定蛋白AT5G14170的SWIB/MDM2结构域的解析结构
鑑定
標誌SWIB
PfamPF02201（旧版）
InterPro（英语：InterPro）IPR003121
SMART（英语：Simple Modular Architecture Research Tool）SWIB
SCOP（英语：Structural Classification of Proteins）1ycr / SUPFAM

在分子生物学领域，SWI/SNF（英語：SWItch/Sucrose NonFermentable）[1][2]是同时存在于真核生物及原核生物中的一种核小体重塑复合物。简而言之，它们是一群与重塑DNA包装方式有关的蛋白质。SWI/SNF由多种蛋白构成，这些蛋白往往是SWI及SNF基因（SWI1、SWI2/SNF2、SWI3、SWI5、SWI6）的产物以及一些其它多肽[3]。SWI/SNF受DNA刺激后表现出ATP酶活性，在ATP催化放能的情况下可以破坏重构核小体的组蛋白和DNA之间交互作用的稳定性，不过这种结构改变的精确性质仍未明确。

人体中与SWI/SNF相似的蛋白是BAF（与SWI/SNF-A相似）和PBAF（与SWI/SNF-B相似）。BAF表示“BRG1（英语：SMARCA4）或HRBM（英语：SMARCA2）相关因子”，PBAF则表示“聚溴相关的BAF”[4]。

作用机理

人们发现酵母中的SWI/SNF复合体能使DNA在不同的位置与组蛋白结合成核小体[5]。目前已提出两种SWI/SNF重塑核小体的机制[6]。一种机制叫做“扭转扩散”，认为核小体DNA中的扭转缺陷发生单向扩散，使DNA从进入核小体的地方开始贴着组蛋白八聚体的表面螺旋状地传播。另一种机制叫做“突起”或“环再捕获”，意即DNA在核小体边缘与之分离，形成一环状突起。环状突起在组蛋白八聚体表面像波浪般传播，最后在核小体内部重新与之结合。这样DNA就在和组蛋白接触点数量不变的情况下完成位移[7]。最新研究提出了与“扭转扩散”机制相抵触的有力证据，增加了“环再捕获”模型的说服力[8]。

肿瘤抑制作用

人类的SWI/SNF复合体（mSWI/SNF）对很多人类恶性肿瘤有抑制作用。1998年首先发现它能抑制横纹肌样瘤（一种罕见的儿童恶性肿瘤）ref name="pmid9671307">Versteege I, Sévenet N, Lange J, Rousseau-Merck MF, Ambros P, Handgretinger R, Aurias A, Delattre O. Truncating mutations of hSNF5/INI1 in aggressive paediatric cancer. Nature. July 1998, 394 (6689): 203–6. PMID 9671307. doi:10.1038/28212. </ref>。随着DNA测序成本逐渐降低，2010年左右许多肿瘤首次得到测序。其中数项研究表明SWI/SNF对多种恶性肿瘤有抑制作用[9][10][11][12]。对多个测序研究结果的荟萃分析表明，大约20%的人类恶性肿瘤中SWI/SNF存在变异[13]。

另见

参考文献 s

  1. ^ Neigeborn L, Carlson M. Genes Affecting the Regulation of SUC2 Gene Expression by Glucose Repression in SACCHAROMYCES CEREVISIAE. Genetics. 1984, 108 (4): 845–58. PMC 1224269 可免费查阅. PMID 6392017. 
  2. ^ Stern M, Jensen R, Herskowitz I. Five SWI genes are required for expression of the HO gene in yeast. J. Mol. Biol. 1984, 178 (4): 853–68. PMID 6436497. doi:10.1016/0022-2836(84)90315-2. 
  3. ^ Pazin MJ, Kadonaga JT. SWI2/SNF2 and related proteins: ATP-driven motors that disrupt protein-DNA interactions?. Cell. 1997, 88 (6): 737–40. PMID 9118215. doi:10.1016/S0092-8674(00)81918-2. 
  4. ^ Nie Z, Yan Z, Chen EH, Sechi S, Ling C, Zhou S, Xue Y, Yang D, Murray D, Kanakubo E, Cleary ML, Wang W. Novel SWI/SNF chromatin-remodeling complexes contain a mixed-lineage leukemia chromosomal translocation partner. Mol. Cell. Biol. April 2003, 23 (8): 2942–52. PMC 152562 可免费查阅. PMID 12665591. doi:10.1128/MCB.23.8.2942-2952.2003. 
  5. ^ Whitehouse I, Flaus A, Cairns BR, White MF, Workman JL, Owen-Hughes T. Nucleosome mobilization catalysed by the yeast SWI/SNF complex. Nature. August 1999, 400 (6746): 784–7. PMID 10466730. doi:10.1038/23506. 
  6. ^ van Holde K, Yager T. Models for chromatin remodeling: a critical comparison. Biochem. Cell Biol. 2003, 81 (3): 169–72. PMID 12897850. doi:10.1139/o03-038. 
  7. ^ Flaus A, Owen-Hughes T. Mechanisms for nucleosome mobilization. Biopolymers. 2003, 68 (4): 563–78. PMID 12666181. doi:10.1002/bip.10323. 
  8. ^ Zofall M, Persinger J, Kassabov SR, Bartholomew B. Chromatin remodeling by ISW2 and SWI/SNF requires DNA translocation inside the nucleosome. Nat. Struct. Mol. Biol. 2006, 13 (4): 339–46. PMID 16518397. doi:10.1038/nsmb1071. 
  9. ^ Wiegand KC, Shah SP, Al-Agha OM, Zhao Y, Tse K, Zeng T, Senz J, McConechy MK, Anglesio MS, Kalloger SE, Yang W, Heravi-Moussavi A, Giuliany R, Chow C, Fee J, Zayed A, Prentice L, Melnyk N, Turashvili G, Delaney AD, Madore J, Yip S, McPherson AW, Ha G, Bell L, Fereday S, Tam A, Galletta L, Tonin PN, Provencher D, Miller D, Jones SJ, Moore RA, Morin GB, Oloumi A, Boyd N, Aparicio SA, Shih IeM, Mes-Masson AM, Bowtell DD, Hirst M, Gilks B, Marra MA, Huntsman DG. ARID1A mutations in endometriosis-associated ovarian carcinomas. N. Engl. J. Med. October 2010, 363 (16): 1532–43. PMC 2976679 可免费查阅. PMID 20942669. doi:10.1056/NEJMoa1008433. 
  10. ^ Li M, Zhao H, Zhang X, Wood LD, Anders RA, Choti MA, Pawlik TM, Daniel HD, Kannangai R, Offerhaus GJ, Velculescu VE, Wang L, Zhou S, Vogelstein B, Hruban RH, Papadopoulos N, Cai J, Torbenson MS, Kinzler KW. Inactivating mutations of the chromatin remodeling gene ARID2 in hepatocellular carcinoma. Nat. Genet. September 2011, 43 (9): 828–9. PMC 3163746 可免费查阅. PMID 21822264. doi:10.1038/ng.903. 
  11. ^ Shain AH, Giacomini CP, Matsukuma K, Karikari CA, Bashyam MD, Hidalgo M, Maitra A, Pollack JR. Convergent structural alterations define SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeler as a central tumor suppressive complex in pancreatic cancer. Proc. Natl. Acad. Sci. U.S.A. January 2012, 109 (5): E252–9. PMC 3277150 可免费查阅. PMID 22233809. doi:10.1073/pnas.1114817109. 
  12. ^ Varela I, Tarpey P, Raine K, Huang D, Ong CK, Stephens P, Davies H, Jones D, Lin ML, Teague J, Bignell G, Butler A, Cho J, Dalgliesh GL, Galappaththige D, Greenman C, Hardy C, Jia M, Latimer C, Lau KW, Marshall J, McLaren S, Menzies A, Mudie L, Stebbings L, Largaespada DA, Wessels LF, Richard S, Kahnoski RJ, Anema J, Tuveson DA, Perez-Mancera PA, Mustonen V, Fischer A, Adams DJ, Rust A, Chan-on W, Subimerb C, Dykema K, Furge K, Campbell PJ, Teh BT, Stratton MR, Futreal PA. Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma. Nature. January 2011, 469 (7331): 539–42. PMC 3030920 可免费查阅. PMID 21248752. doi:10.1038/nature09639. 
  13. ^ Shain AH, Pollack JR. The spectrum of SWI/SNF mutations, ubiquitous in human cancers. PLoS ONE. 2013, 8 (1): e55119. PMC 3552954 可免费查阅. PMID 23355908. doi:10.1371/journal.pone.0055119. 

外部链接

共激活因子（英语：Coactivators）
共阻遏因子（英语：Corepressors）
ATP-依賴性重塑因子
遗传学索引
描述
疾病
取自“https://zh.wikipedia.org/w/index.php?title=SWI/SNF&oldid=40052109”