MSH2

MSH2
ساختارهای موجود
PDB	جستجوی هم‌ساخت‌شناسی: PDBe RCSB
فهرست شناسه‌های PDB
	2O8B, 2O8C, 2O8D, 2O8E, 2O8F, 3THW, 3THX, 3THY, 3THZ
معین‌کننده‌ها
نام‌های دیگر	MSH2, mutS homolog 2, COCA1, FCC1, HNPCC, HNPCC1, LCFS2, hMMRCS2, MSH-2
شناسه‌های بیرونی	OMIM: 609309 MGI: 101816 HomoloGene: 210 GeneCards: MSH2
موقعیت ژن (موش)
کروموزوم	کروموزوم ۱۷ (موش)
پایان	88,031,141 bp
الگوی گسترش RNA
	More reference expression data
هستی‌شناسی ژن
عملکرد ملکولی	• DNA binding; • nucleotide binding; • protein homodimerization activity; • mismatched DNA binding; • dinucleotide insertion or deletion binding; • ADP binding; • centromeric DNA binding; • oxidized purine DNA binding; • single-stranded DNA binding; • damaged DNA binding; • ATPase activity; • protein C-terminus binding; • GO:0001948، GO:0016582 پیوند پروتئینی; • single thymine insertion binding; • four-way junction DNA binding; • MutLalpha complex binding; • enzyme binding; • double-stranded DNA binding; • dinucleotide repeat insertion binding; • ATP binding; • protein kinase binding; • magnesium ion binding; • single guanine insertion binding; • guanine/thymine mispair binding; • Y-form DNA binding; • heteroduplex DNA loop binding; • double-strand/single-strand DNA junction binding; • ATP-dependent activity, acting on DNA; • chromatin binding;
ترکیبات سلولی	• MutSbeta complex; • membrane; • MutSalpha complex; • نوکلئوپلاسم; • mismatch repair complex; • هسته یاخته; • کروموزوم;
فرایند زیستی	• GO:1904089 negative regulation of neuron apoptotic process; • germ cell development; • male gonad development; • postreplication repair; • determination of adult lifespan; • in utero embryonic development; • cellular response to DNA damage stimulus; • فسفرگیری اکسایشی; • maintenance of DNA repeat elements; • positive regulation of helicase activity; • somatic recombination of immunoglobulin gene segments; • intrinsic apoptotic signaling pathway in response to DNA damage; • negative regulation of DNA recombination; • somatic recombination of immunoglobulin genes involved in immune response; • بازسازی نابرابر دی‌ان‌ای; • B cell differentiation; • B cell mediated immunity; • GO:0100026 بازسازی دی‌ان‌ای; • positive regulation of isotype switching to IgA isotypes; • positive regulation of isotype switching to IgG isotypes; • double-strand break repair; • meiotic gene conversion; • واکنش به اشعه ایکس; • response to UV-B; • somatic hypermutation of immunoglobulin genes; • mitotic intra-S DNA damage checkpoint signaling; • intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator; • negative regulation of reciprocal meiotic recombination; • isotype switching; • protein localization to chromatin; • DNA recombination;
	منابع: آمیگو / کوئیک‌گو
هم‌ساخت‌شناسی
	4436
	17685
	ENSG00000095002
	ENSMUSG00000024151
	P43246
	P43247
	NM_000251، NM_001258281، XM_005264332، XM_011532867، XR_001738747، XM_047444416 XR_939685، NM_000251، NM_001258281، XM_005264332، XM_011532867، XR_001738747، XM_047444416
	NM_008628
	NP_001245210، XP_005264389، XP_011531169 NP_000242، NP_001245210، XP_005264389، XP_011531169
	NP_032654
	ویکی‌داده
مشاهده/ویرایش انسان	مشاهده/ویرایش موش

پروتئین Msh2 ترمیم عدم تطابق دی‌ان‌ای (انگلیسی: DNA mismatch repair protein Msh2) که با نام اختصاری MSH2 شناخته می‌شود، یک پروتئین است که در انسان توسط ژن «MSH2» واقع بر کروموزوم ۲ کُدگذاری می‌شود. ژن «MSH2»، یک ژن سرکوب‌گر تومور و به‌طور مشخص یک «ژن محافظ» است که کارش ترمیم عدم تطابق جفت‌بازهای دی‌ان‌ای است. MSH2 می‌تواند با مولکول‌های MSH6 یا MSH3، یک ترکیب شیمیایی دوتایی بسازد که کارشان بازسازی دی‌ان‌ای، شاملِ «ترمیم بُرش نوکلئوتید»،^[۴] «نوترکیبی هم‌ساخت»^[۵] و «ترمیم برش جفت‌بازها» است.^[۶]

پروتئین MSH2 با مولکول‌های BRCA1^[۷] و پی۵۳^[۸] تعامل پروتئین-پروتئین دارد.

اهمیت بالینی[ویرایش]

آسیب به مولکول دی‌ان‌ای دلیل اصلی بروز سرطان است^[۹] و کمبود پروتئین‌هایی که در ترمیم آسیب‌های دی‌ان‌ای نقش دارند، زمینه‌ساز بروز سرطان‌هاست.^[۱۰]^[۱۱] آسیب به دی‌ان‌ای علاوه بر احتمال بروز جهش‌های ژنی بیشتر، به‌دلیلِ خطاهای به‌وجود آمده در ترمیم دی‌ان‌ای، سبب تغییرات اپی‌ژنتیک می‌گردد.^[۱۲]^[۱۳] یک چنین تغییرات اپی‌ژنتیکی، خود از دلایل دیگر بروز سرطان است.

جهش در ژن «MSH2» سبب ناپایداری ریزاَقماری (microsatellite instability) شده^[۱۴] و ممکن است از دلایل بروز «سرطان غیرپولیپی ارثی روده بزرگ» (HNPCC) یا سندرم لینچ باشد.^[۱۵] متیلاسیون ناحیهٔ پروموتر ژن «MSH2» و کمبود تولید این پروتئین در سرطان مری،^[۱۶] سرطان ریه از نوعِ غیر سلول کوچک^[۱۷]^[۱۸] و سرطان روده بزرگ^[۱۹] دیده شده‌است.

توالی متیلاسیون ناحیهٔ پروموتر ژن «*MSH2*» در سرطان‌های غیرارثی
سرطان	توالی متیلاسیون ناحیهٔ پروموتر ژن MSH2	منبع
لوسمی حاد لنفاوی	۴۳٪	^[۱۷]
لوسمی حاد لنفاوی عودکرده	۸۶٪	^[۲۰]
کارسینوم کلیه	۵۱–۵۵٪	^[۲۱]^[۲۲]
سرطان مری از نوع سلول سنگفرشی	۲۹–۴۸٪	^[۱۶]^[۲۳]
سرطان‌های سر و گردن از نوع سلول سنگفرشی	۲۷–۳۶٪	^[۲۴]^[۲۵]^[۲۶]
سرطان ریه از نوع سلول غیر کوچک	۲۹–۳۴٪	^[۱۷]^[۱۸]
سرطان کبد	۱۰–۲۹٪	^[۲۷]
سرطان روده بزرگ	۳–۲۴٪	^[۱۹]^[۲۸]^[۲۹]^[۳۰]
سارکوم بافت نرم	۸٪	^[۳۱]

منابع[ویرایش]

↑ ^۱٫۰ ^۱٫۱ ^۱٫۲ GRCm38: Ensembl release 89: ENSMUSG00000024151 - Ensembl, May 2017
↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑ Mellon I, Rajpal DK, Koi M, Boland CR, Champe GN (April 1996). "Transcription-coupled repair deficiency and mutations in human mismatch repair genes". Science. 272 (5261): 557–60. Bibcode:1996Sci...272..557M. doi:10.1126/science.272.5261.557. PMID 8614807. S2CID 13084965.
↑ de Wind N, Dekker M, Berns A, Radman M, te Riele H (July 1995). "Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer". Cell. 82 (2): 321–30. doi:10.1016/0092-8674(95)90319-4. PMID 7628020. S2CID 7954019.
↑ Pitsikas P, Lee D, Rainbow AJ (May 2007). "Reduced host cell reactivation of oxidative DNA damage in human cells deficient in the mismatch repair gene hMSH2". Mutagenesis. 22 (3): 235–43. doi:10.1093/mutage/gem008. PMID 17351251.
↑ Wang Y, Cortez D, Yazdi P, Neff N, Elledge SJ, Qin J (April 2000). "BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures". Genes Dev. 14 (8): 927–39. doi:10.1101/gad.14.8.927 (inactive 31 October 2021). PMC 316544. PMID 10783165.{{cite journal}}: CS1 maint: DOI inactive as of اکتبر 2021 (link)
↑ Scherer SJ, Welter C, Zang KD, Dooley S (April 1996). "Specific in vitro binding of p53 to the promoter region of the human mismatch repair gene hMSH2". Biochem. Biophys. Res. Commun. 221 (3): 722–8. doi:10.1006/bbrc.1996.0663. PMID 8630028.
↑ Kastan MB (April 2008). "DNA damage responses: mechanisms and roles in human disease: 2007 G.H.A. Clowes Memorial Award Lecture". Molecular Cancer Research. 6 (4): 517–24. doi:10.1158/1541-7786.MCR-08-0020. PMID 18403632.
↑ Harper JW, Elledge SJ (December 2007). "The DNA damage response: ten years after". Molecular Cell. 28 (5): 739–45. doi:10.1016/j.molcel.2007.11.015. PMID 18082599.
↑ Dietlein F, Reinhardt HC (December 2014). "Molecular pathways: exploiting tumor-specific molecular defects in DNA repair pathways for precision cancer therapy". Clinical Cancer Research. 20 (23): 5882–7. doi:10.1158/1078-0432.CCR-14-1165. PMID 25451105.
↑ O'Hagan HM, Mohammad HP, Baylin SB (2008). "Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island". PLOS Genetics. 4 (8): e1000155. doi:10.1371/journal.pgen.1000155. PMC 2491723. PMID 18704159.
↑ Cuozzo C, Porcellini A, Angrisano T, Morano A, Lee B, Di Pardo A, Messina S, Iuliano R, Fusco A, Santillo MR, Muller MT, Chiariotti L, Gottesman ME, Avvedimento EV (July 2007). "DNA damage, homology-directed repair, and DNA methylation". PLOS Genetics. 3 (7): e110. doi:10.1371/journal.pgen.0030110. PMC 1913100. PMID 17616978.
↑ Bonis PA, Trikalinos TA, Chung M, Chew P, Ip S, DeVine DA, Lau J (May 2007). "Hereditary nonpolyposis colorectal cancer: diagnostic strategies and their implications". Evid Rep Technol Assess (Full Rep) (150): 1–180. PMC 4781224. PMID 17764220.
↑ Müller A, Fishel R (2002). "Mismatch repair and the hereditary non-polyposis colorectal cancer syndrome (HNPCC)". Cancer Invest. 20 (1): 102–9. doi:10.1081/cnv-120000371. PMID 11852992. S2CID 3581304.
↑ ^۱۶٫۰ ^۱۶٫۱ Ling ZQ, Li P, Ge MH, Hu FJ, Fang XH, Dong ZM, Mao WM (2011). "Aberrant methylation of different DNA repair genes demonstrates distinct prognostic value for esophageal cancer". Dig. Dis. Sci. 56 (10): 2992–3004. doi:10.1007/s10620-011-1774-z. PMID 21674174. S2CID 22913110.
↑ ^۱۷٫۰ ^۱۷٫۱ ^۱۷٫۲ Wang YC, Lu YP, Tseng RC, Lin RK, Chang JW, Chen JT, Shih CM, Chen CY (2003). "Inactivation of hMLH1 and hMSH2 by promoter methylation in primary non-small cell lung tumors and matched sputum samples". J. Clin. Invest. 111 (6): 887–95. doi:10.1172/JCI15475. PMC 153761. PMID 12639995.
↑ ^۱۸٫۰ ^۱۸٫۱ Hsu HS, Wen CK, Tang YA, Lin RK, Li WY, Hsu WH, Wang YC (2005). "Promoter hypermethylation is the predominant mechanism in hMLH1 and hMSH2 deregulation and is a poor prognostic factor in nonsmoking lung cancer". Clin. Cancer Res. 11 (15): 5410–6. doi:10.1158/1078-0432.CCR-05-0601. PMID 16061855.
↑ ^۱۹٫۰ ^۱۹٫۱ Lee KH, Lee JS, Nam JH, Choi C, Lee MC, Park CS, Juhng SW, Lee JH (2011). "Promoter methylation status of hMLH1, hMSH2, and MGMT genes in colorectal cancer associated with adenoma-carcinoma sequence". Langenbecks Arch Surg. 396 (7): 1017–26. doi:10.1007/s00423-011-0812-9. PMID 21706233. S2CID 8069716.
↑ خطای یادکرد: خطای یادکرد:برچسب <ref>‎ غیرمجاز؛ متنی برای یادکردهای با نام WangCX وارد نشده است. (صفحهٔ راهنما را مطالعه کنید.).
↑ Stoehr C, Burger M, Stoehr R, Bertz S, Ruemmele P, Hofstaedter F, Denzinger S, Wieland WF, Hartmann A, Walter B (2012). "Mismatch repair proteins hMLH1 and hMSH2 are differently expressed in the three main subtypes of sporadic renal cell carcinoma" (PDF). Pathobiology. 79 (3): 162–8. doi:10.1159/000335642. PMID 22378480. S2CID 26687941.
↑ Yoo KH, Won KY, Lim SJ, Park YK, Chang SG (2014). "Deficiency of MSH2 expression is associated with clear cell renal cell carcinoma". Oncol Lett. 8 (5): 2135–2139. doi:10.3892/ol.2014.2482. PMC 4186615. PMID 25295100.
↑ Ling ZQ, Zhao Q, Zhou SL, Mao WM (2012). "MSH2 promoter hypermethylation in circulating tumor DNA is a valuable predictor of disease-free survival for patients with esophageal squamous cell carcinoma". Eur J Surg Oncol. 38 (4): 326–32. doi:10.1016/j.ejso.2012.01.008. PMID 22265839.
↑ Sengupta S, Chakrabarti S, Roy A, Panda CK, Roychoudhury S (2007). "Inactivation of human mutL homolog 1 and mutS homolog 2 genes in head and neck squamous cell carcinoma tumors and leukoplakia samples by promoter hypermethylation and its relation with microsatellite instability phenotype". Cancer. 109 (4): 703–12. doi:10.1002/cncr.22430. PMID 17219447. S2CID 20191692.
↑ Demokan S, Suoglu Y, Demir D, Gozeler M, Dalay N (2006). "Microsatellite instability and methylation of the DNA mismatch repair genes in head and neck cancer". Ann. Oncol. 17 (6): 995–9. doi:10.1093/annonc/mdl048. PMID 16569647.
↑ Czerninski R, Krichevsky S, Ashhab Y, Gazit D, Patel V, Ben-Yehuda D (2009). "Promoter hypermethylation of mismatch repair genes, hMLH1 and hMSH2 in oral squamous cell carcinoma". Oral Dis. 15 (3): 206–13. doi:10.1111/j.1601-0825.2008.01510.x. PMID 19207881.
↑ Hinrichsen I, Kemp M, Peveling-Oberhag J, Passmann S, Plotz G, Zeuzem S, Brieger A (2014). "Promoter methylation of MLH1, PMS2, MSH2 and p16 is a phenomenon of advanced-stage HCCs". PLOS ONE. 9 (1): e84453. Bibcode:2014PLoSO...984453H. doi:10.1371/journal.pone.0084453. PMC 3882222. PMID 24400091.
↑ Vlaykova T, Mitkova A, Stancheva G, Kadiyska T, Gulubova M, Yovchev Y, Cirovski G, Chilingirov P, Damyanov D, Kremensky I, Mitev V, Kaneva R (2011). "Microsatellite instability and promoter hypermethylation of MLH1 and MSH2 in patients with sporadic colorectal cancer". J BUON. 16 (2): 265–73. PMID 21766496.
↑ Malhotra P, Anwar M, Kochhar R, Ahmad S, Vaiphei K, Mahmood S (2014). "Promoter methylation and immunohistochemical expression of hMLH1 and hMSH2 in sporadic colorectal cancer: a study from India". Tumour Biol. 35 (4): 3679–87. doi:10.1007/s13277-013-1487-3. PMID 24317816. S2CID 10615946.
↑ Onrat S, Ceken I, Ellidokuz E, Kupelioğlu A (2011). "Alterations of copy number of methylation pattern in mismatch repair genes by methylation specific-multiplex ligation-dependent probe amplification in cases of colon cancer". Balkan J. Med. Genet. 14 (2): 25–34. doi:10.2478/v10034-011-0044-x. PMC 3776700. PMID 24052709.
↑ Kawaguchi K, Oda Y, Saito T, Yamamoto H, Takahira T, Kobayashi C, Tamiya S, Tateishi N, Iwamoto Y, Tsuneyoshi M (2006). "DNA hypermethylation status of multiple genes in soft tissue sarcomas". Mod. Pathol. 19 (1): 106–14. doi:10.1038/modpathol.3800502. PMID 16258501.

مشارکت‌کنندگان ویکی‌پدیا. «MSH2». در دانشنامهٔ ویکی‌پدیای انگلیسی، بازبینی‌شده در ۸ نوامبر ۲۰۲۱.

برای مطالعهٔ بیشتر[ویرایش]

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پیوند به بیرون[ویرایش]

MutS Homolog 2 Protein در سرعنوان‌های موضوعی پزشکی (MeSH) در کتابخانهٔ ملی پزشکی ایالات متحدهٔ آمریکا

[refGRCm38Ensembl-1] ۱٫۰ ^۱٫۱ ^۱٫۲ GRCm38: Ensembl release 89: ENSMUSG00000024151 - Ensembl, May 2017

[2] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[3] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[Mellon-4] Mellon I, Rajpal DK, Koi M, Boland CR, Champe GN (April 1996). "Transcription-coupled repair deficiency and mutations in human mismatch repair genes". Science. 272 (5261): 557–60. Bibcode:1996Sci...272..557M. doi:10.1126/science.272.5261.557. PMID 8614807. S2CID 13084965.

[Wind-5] Wind N, Dekker M, Berns A, Radman M, te Riele H (July 1995). "Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer". Cell. 82 (2): 321–30. doi:10.1016/0092-8674(95)90319-4. PMID 7628020. S2CID 7954019.

[Pitsikas-6] Pitsikas P, Lee D, Rainbow AJ (May 2007). "Reduced host cell reactivation of oxidative DNA damage in human cells deficient in the mismatch repair gene hMSH2". Mutagenesis. 22 (3): 235–43. doi:10.1093/mutage/gem008. PMID 17351251.

[pmid10783165-7] Wang Y, Cortez D, Yazdi P, Neff N, Elledge SJ, Qin J (April 2000). "BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures". Genes Dev. 14 (8): 927–39. doi:10.1101/gad.14.8.927 (inactive 31 October 2021). PMC 316544. PMID 10783165.{{cite journal}}: CS1 maint: DOI inactive as of اکتبر 2021 (link)

[pmid8630028-8] Scherer SJ, Welter C, Zang KD, Dooley S (April 1996). "Specific in vitro binding of p53 to the promoter region of the human mismatch repair gene hMSH2". Biochem. Biophys. Res. Commun. 221 (3): 722–8. doi:10.1006/bbrc.1996.0663. PMID 8630028.

[pmid18403632-9] Kastan MB (April 2008). "DNA damage responses: mechanisms and roles in human disease: 2007 G.H.A. Clowes Memorial Award Lecture". Molecular Cancer Research. 6 (4): 517–24. doi:10.1158/1541-7786.MCR-08-0020. PMID 18403632.

[pmid18082599-10] Harper JW, Elledge SJ (December 2007). "The DNA damage response: ten years after". Molecular Cell. 28 (5): 739–45. doi:10.1016/j.molcel.2007.11.015. PMID 18082599.

[pmid25451105-11] Dietlein F, Reinhardt HC (December 2014). "Molecular pathways: exploiting tumor-specific molecular defects in DNA repair pathways for precision cancer therapy". Clinical Cancer Research. 20 (23): 5882–7. doi:10.1158/1078-0432.CCR-14-1165. PMID 25451105.

[Hagan-12] O'Hagan HM, Mohammad HP, Baylin SB (2008). "Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island". PLOS Genetics. 4 (8): e1000155. doi:10.1371/journal.pgen.1000155. PMC 2491723. PMID 18704159.

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