مکس (ژن) - ویکیپدیا، دانشنامهٔ آزاد
مَـکس (انگلیسی: MAX) یا فاکتور ایکس مرتبط با Myc، یک ژن است که در انسان، پروتئین و فاکتور رونویسی MAX را کُدگذاری میکند.[۴][۵] این پروتئین دارای موتیفهای مارپیچ-حلقه-مارپیچ قلیایی و زیپ لوسین است و در نتیجه یکی از انواع bHLHZ محسوب میشود. این پروتئین در تزاید سلولی و آپوپتوز نقش دارد.[۶]
مَـکس با مولکولهای MSH2[۷] و N-Myc[۸][۹] تعامل پروتئین-پروتئین دارد.
اهمیت بالینی
[ویرایش]جهش در ژن مَـکس با بروز فئوکروموسیتومای ارثی در ارتباط است.[۱۰] اخیراً مشخص شده است که این ژن در سرطان ریه از نوع سلول غیرکوچک نیز غیرفعال میشود.
منابع
[ویرایش]- ↑ ۱٫۰ ۱٫۱ ۱٫۲ GRCm38: Ensembl release 89: ENSMUSG00000059436 - 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.
- ↑ Wagner AJ, Le Beau MM, Diaz MO, Hay N (May 1992). "Expression, regulation, and chromosomal localization of the Max gene". Proc Natl Acad Sci U S A. 89 (7): 3111–5. Bibcode:1992PNAS...89.3111W. doi:10.1073/pnas.89.7.3111. PMC 48814. PMID 1557420.
- ↑ "Entrez Gene: MAX MYC associated factor X".
- ↑ Amati B, Land H (February 1994). "Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death". Curr. Opin. Genet. Dev. 4 (1): 102–8. doi:10.1016/0959-437X(94)90098-1. PMID 8193530.
- ↑ Mac Partlin M, Homer E, Robinson H, McCormick CJ, Crouch DH, Durant ST, Matheson EC, Hall AG, Gillespie DA, Brown R (February 2003). "Interactions of the DNA mismatch repair proteins MLH1 and MSH2 with c-MYC and MAX". Oncogene. 22 (6): 819–25. doi:10.1038/sj.onc.1206252. PMID 12584560.
- ↑ Blackwood EM, Eisenman RN (Mar 1991). "Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc". Science. 251 (4998): 1211–7. Bibcode:1991Sci...251.1211B. doi:10.1126/science.2006410. ISSN 0036-8075. PMID 2006410.
- ↑ FitzGerald MJ, Arsura M, Bellas RE, Yang W, Wu M, Chin L, Mann KK, DePinho RA, Sonenshein GE (April 1999). "Differential effects of the widely expressed dMax splice variant of Max on E-box vs initiator element-mediated regulation by c-Myc". Oncogene. 18 (15): 2489–98. doi:10.1038/sj.onc.1202611. PMID 10229200.
- ↑ Comino-Méndez I, Gracia-Aznárez FJ, Schiavi F, Landa I, Leandro-García LJ, Letón R, Honrado E, Ramos-Medina R, Caronia D, Pita G, Gómez-Graña A, de Cubas AA, Inglada-Pérez L, Maliszewska A, Taschin E, Bobisse S, Pica G, Loli P, Hernández-Lavado R, Díaz JA, Gómez-Morales M, González-Neira A, Roncador G, Rodríguez-Antona C, Benítez J, Mannelli M, Opocher G, Robledo M, Cascón A (July 2011). "Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma". Nat. Genet. 43 (7): 663–7. doi:10.1038/ng.861. PMID 21685915. S2CID 205357831.
- مشارکتکنندگان ویکیپدیا. «MAX (gene)». در دانشنامهٔ ویکیپدیای انگلیسی، بازبینیشده در ۱۰ نوامبر ۲۰۲۱.
برای مطالعهٔ بیشتر
[ویرایش]- Grandori C, Cowley SM, James LP, Eisenman RN (2001). "The Myc/Max/Mad network and the transcriptional control of cell behavior". Annu. Rev. Cell Dev. Biol. 16: 653–99. doi:10.1146/annurev.cellbio.16.1.653. PMID 11031250.
- Lüscher B (2001). "Function and regulation of the transcription factors of the Myc/Max/Mad network". Gene. 277 (1–2): 1–14. doi:10.1016/S0378-1119(01)00697-7. PMID 11602341.
- Wechsler DS, Dang CV (1992). "Opposite orientations of DNA bending by c-Myc and Max". Proc. Natl. Acad. Sci. U.S.A. 89 (16): 7635–9. Bibcode:1992PNAS...89.7635W. doi:10.1073/pnas.89.16.7635. PMC 49765. PMID 1323849.
- Mäkelä TP, Koskinen PJ, Västrik I, Alitalo K (1992). "Alternative forms of Max as enhancers or suppressors of Myc-ras cotransformation". Science. 256 (5055): 373–7. Bibcode:1992Sci...256..373M. doi:10.1126/science.256.5055.373. PMID 1566084. S2CID 37558098.
- Gilladoga AD, Edelhoff S, Blackwood EM, Eisenman RN, Disteche CM (1992). "Mapping of MAX to human chromosome 14 and mouse chromosome 12 by in situ hybridization". Oncogene. 7 (6): 1249–51. PMID 1594250.
- Blackwood EM, Eisenman RN (1991). "Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc". Science. 251 (4998): 1211–7. Bibcode:1991Sci...251.1211B. doi:10.1126/science.2006410. PMID 2006410.
- Zervos AS, Faccio L, Gatto JP, Kyriakis JM, Brent R (1995). "Mxi2, a mitogen-activated protein kinase that recognizes and phosphorylates Max protein". Proc. Natl. Acad. Sci. U.S.A. 92 (23): 10531–4. Bibcode:1995PNAS...9210531Z. doi:10.1073/pnas.92.23.10531. PMC 40645. PMID 7479834.
- Bousset K, Henriksson M, Lüscher-Firzlaff JM, Litchfield DW, Lüscher B (1993). "Identification of casein kinase II phosphorylation sites in Max: effects on DNA-binding kinetics of Max homo- and Myc/Max heterodimers". Oncogene. 8 (12): 3211–20. PMID 8247525.
- Ayer DE, Kretzner L, Eisenman RN (1993). "Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity". Cell. 72 (2): 211–22. doi:10.1016/0092-8674(93)90661-9. PMID 8425218. S2CID 13317223.
- Västrik I, Koskinen PJ, Alitalo R, Mäkelä TP (1993). "Alternative mRNA forms and open reading frames of the max gene". Oncogene. 8 (2): 503–7. PMID 8426752.
- Ferré-D'Amaré AR, Prendergast GC, Ziff EB, Burley SK (1993). "Recognition by Max of its cognate DNA through a dimeric b/HLH/Z domain". Nature. 363 (6424): 38–45. Bibcode:1993Natur.363...38F. doi:10.1038/363038a0. PMID 8479534. S2CID 4304430.
- Hurlin PJ, Quéva C, Koskinen PJ, Steingrímsson E, Ayer DE, Copeland NG, Jenkins NA, Eisenman RN (1996). "Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation". EMBO J. 14 (22): 5646–59. doi:10.1002/j.1460-2075.1995.tb00252.x. PMC 394680. PMID 8521822.
- Grandori C, Mac J, Siëbelt F, Ayer DE, Eisenman RN (1996). "Myc-Max heterodimers activate a DEAD box gene and interact with multiple E box-related sites in vivo". EMBO J. 15 (16): 4344–57. doi:10.1002/j.1460-2075.1996.tb00808.x. PMC 452159. PMID 8861962.
- Brownlie P, Ceska T, Lamers M, Romier C, Stier G, Teo H, Suck D (1997). "The crystal structure of an intact human Max-DNA complex: new insights into mechanisms of transcriptional control". Structure. 5 (4): 509–20. doi:10.1016/S0969-2126(97)00207-4. PMID 9115440.
- Meroni G, Reymond A, Alcalay M, Borsani G, Tanigami A, Tonlorenzi R, Lo Nigro C, Messali S, Zollo M, Ledbetter DH, Brent R, Ballabio A, Carrozzo R (1997). "Rox, a novel bHLHZip protein expressed in quiescent cells that heterodimerizes with Max, binds a non-canonical E box and acts as a transcriptional repressor". EMBO J. 16 (10): 2892–906. doi:10.1093/emboj/16.10.2892. PMC 1169897. PMID 9184233.
- Gupta MP, Amin CS, Gupta M, Hay N, Zak R (1997). "Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein, Max, for positive regulation of cardiac alpha-myosin heavy-chain gene expression". Mol. Cell. Biol. 17 (7): 3924–36. doi:10.1128/mcb.17.7.3924. PMC 232245. PMID 9199327.
- Gupta K, Anand G, Yin X, Grove L, Prochownik EV (1998). "Mmip1: a novel leucine zipper protein that reverses the suppressive effects of Mad family members on c-myc". Oncogene. 16 (9): 1149–59. doi:10.1038/sj.onc.1201634. PMID 9528857.
- Lavigne P, Crump MP, Gagné SM, Hodges RS, Kay CM, Sykes BD (1998). "Insights into the mechanism of heterodimerization from the 1H-NMR solution structure of the c-Myc-Max heterodimeric leucine zipper". J. Mol. Biol. 281 (1): 165–81. doi:10.1006/jmbi.1998.1914. PMID 9680483.
- FitzGerald MJ, Arsura M, Bellas RE, Yang W, Wu M, Chin L, Mann KK, DePinho RA, Sonenshein GE (1999). "Differential effects of the widely expressed dMax splice variant of Max on E-box vs initiator element-mediated regulation by c-Myc". Oncogene. 18 (15): 2489–98. doi:10.1038/sj.onc.1202611. PMID 10229200.
پیوند به بیرون
[ویرایش]- MAX protein, human در سرعنوانهای موضوعی پزشکی (MeSH) در کتابخانهٔ ملی پزشکی ایالات متحدهٔ آمریکا
- Max در دانشنامهٔ اجزای دیانای