SMAD3
همساخت ۳ مادران مخالف دکپنتاپلجیک (انگلیسی: Mothers against decapentaplegic homolog 3) یک پروتئین است که در انسان توسط ژن «SMAD3» واقع بر بازوی بلند کروموزوم ۱۵ کُدگذاری میشود.[۵][۶]
این پروتئین عضوی از خانواده بزرگ SMAD است که این نیز به نوبهٔ خود، جزئی از اَبَرخانوادهٔ فاکتور رشد تغییردهنده بتا است.
نقش این پروتئین، تعدیل پیامهایی است که توسط فاکتور رشد تغییردهنده بتا آغاز میشود و در تزاید، تمایز و مرگ سلول نقش دارد.[۷][۸]
اهمیت بالینی
افزایش فعالیت SMAD3 در بیماریزایی اسکلرودرمی نقش دارد. مولکول SMAD3 همچنین یک تنظیمکنندهٔ چندکاره در فیزیولوژی چربی است و با بروز چاقی و دیابت نوع ۲ مرتبط است.
این پروتئین همچنین در سرطان پروستات،[۹][۱۰] سرطان روده بزرگ،[۱۱][۱۲][۱۳] سرطان پستان[۱۴] و فیبروز کلیهها[۱۵] نقش دارد.
جستارهای وابسته
منابع
- ↑ ۱٫۰ ۱٫۱ ۱٫۲ GRCh38: Ensembl release 89: ENSG00000166949 – Ensembl, May 2017
- ↑ ۲٫۰ ۲٫۱ ۲٫۲ GRCm38: Ensembl release 89: ENSMUSG00000032402 – 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.
- ↑ "Entrez Gene: SMAD3 SMAD family member 3".
- ↑ Zhang Y, Feng X, We R, Derynck R (September 1996). "Receptor-associated Mad homologues synergize as effectors of the TGF-beta response". Nature. 383 (6596): 168–72. doi:10.1038/383168a0. PMID 8774881.
- ↑ Massagué J (1998). "TGF-beta signal transduction". Annual Review of Biochemistry. 67 (1): 753–91. doi:10.1146/annurev.biochem.67.1.753. PMID 9759503.
- ↑ Moustakas A, Souchelnytskyi S, Heldin CH (December 2001). "Smad regulation in TGF-beta signal transduction". Journal of Cell Science. 114 (Pt 24): 4359–69. PMID 11792802.
- ↑ Huang S, Liao Q, Li L, Xin D (July 2014). "PTTG1 inhibits SMAD3 in prostate cancer cells to promote their proliferation". Tumour Biology. 35 (7): 6265–70. doi:10.1007/s13277-014-1818-z. PMID 24627133.
- ↑ Lu S, Lee J, Revelo M, Wang X, Lu S, Dong Z (October 2007). "Smad3 is overexpressed in advanced human prostate cancer and necessary for progressive growth of prostate cancer cells in nude mice". Clinical Cancer Research. 13 (19): 5692–702. doi:10.1158/1078-0432.CCR-07-1078. PMID 17908958.
- ↑ Hachimine D, Uchida K, Asada M, Nishio A, Kawamata S, Sekimoto G, Murata M, Yamagata H, Yoshida K, Mori S, Tahashi Y, Matsuzaki K, Okazaki K (June 2008). "Involvement of Smad3 phosphoisoform-mediated signaling in the development of colonic cancer in IL-10-deficient mice". International Journal of Oncology. 32 (6): 1221–6. doi:10.3892/ijo.32.6.1221. PMID 18497983.
- ↑ Seamons A, Treuting PM, Brabb T, Maggio-Price L (2013). "Characterization of dextran sodium sulfate-induced inflammation and colonic tumorigenesis in Smad3(-/-) mice with dysregulated TGFβ". PLOS ONE. 8 (11): e79182. doi:10.1371/journal.pone.0079182. PMC 3823566. PMID 24244446.
{{cite journal}}: نگهداری یادکرد:doi رایگان بینشان (رده) نگهداری یادکرد:شماره مقاله بهجای شماره صفحه (رده) - ↑ Kawamata S, Matsuzaki K, Murata M, Seki T, Matsuoka K, Iwao Y, Hibi T, Okazaki K (March 2011). "Oncogenic Smad3 signaling induced by chronic inflammation is an early event in ulcerative colitis-associated carcinogenesis". Inflammatory Bowel Diseases. 17 (3): 683–95. doi:10.1002/ibd.21395. PMID 20602465.
- ↑ Petersen M, Pardali E, van der Horst G, Cheung H, van den Hoogen C, van der Pluijm G, Ten Dijke P (March 2010). "Smad2 and Smad3 have opposing roles in breast cancer bone metastasis by differentially affecting tumor angiogenesis". Oncogene. 29 (9): 1351–61. doi:10.1038/onc.2009.426. PMID 20010874.
- ↑ Meng XM, Chung AC, Lan HY (February 2013). "Role of the TGF-β/BMP-7/Smad pathways in renal diseases". Clinical Science. 124 (4): 243–54. doi:10.1042/CS20120252. PMID 23126427.
- مشارکتکنندگان ویکیپدیا. «Mothers against decapentaplegic homolog 3». در دانشنامهٔ ویکیپدیای انگلیسی، بازبینیشده در ۱۵ مارس ۲۰۲۰.
برای مطالعهٔ بیشتر
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