BRCA1: Perbedaan antara revisi
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== Fungsi dan mekanisme ==
BRCA1 adalah bagian dari kompleks protein yang berfungsi memperbaiki [[Perbaikan DNA|kerusakan untai ganda]] pada DNA. Ketika DNA mengalami kerusakan, untaian pada DNA tersebut akan terputus. Terkadang hanya satu untai yang putus, terkadang kedua untai putus secara bersamaan. Agen pengikat silang DNA (''DNA'' ''cross-linking agent'') adalah salah satu penyebab utama dari kerusakan kromosom dan DNA. Pemutusan untai ganda (''double strand breaks'') terjadi sebagai intermediet setelah ikatan silang ini dihilangkan. Mutasi bialelik pada ''BRCA1'' telah diidentifikasi bertanggung jawab atas [[Anemia Fanconi]], Complementation Group S (FA-S), penyakit genetik yang terkait dengan hipersensitivitas terhadap agen pengikat silang DNA.<ref>{{Cite journal|last=Sawyer|first=Sarah L.|last2=Tian|first2=Lei|last3=Kähkönen|first3=Marketta|last4=Schwartzentruber|first4=Jeremy|last5=Kircher|first5=Martin|last6=University of Washington Centre for Mendelian Genomics|last7=FORGE Canada Consortium|last8=Majewski|first8=Jacek|last9=Dyment|first9=David A.|date=2015-02-01|title=Biallelic Mutations in BRCA1 Cause a New Fanconi Anemia Subtype|url=https://aacrjournals.org/cancerdiscovery/article/5/2/135/4638/Biallelic-Mutations-in-BRCA1-Cause-a-New-Fanconi|journal=Cancer Discovery|language=en|volume=5|issue=2|pages=135–142|doi=10.1158/2159-8290.CD-14-1156|issn=2159-8274|pmc=PMC4320660|pmid=25472942}}</ref>
[[Berkas:DsDNA break repair pathways.svg|jmpl|344x344px|Jenis-jenis perbaikan DNA untai ganda (''dsDNA repair'')]]
BRCA1 adalah bagian dari kompleks protein yang memperbaiki DNA ketika kedua untaiannya rusak. Ketika hal ini terjadi, sulit bagi mekanisme perbaikan untuk "mengetahui" cara mengganti urutan DNA yang benar. Ditambah lagi, terdapat berbagai mekanisme perbaikan DNA yang dapat dicoba. Mekanisme perbaikan untai ganda yang melibatkan BRCA1 adalah perbaikan yang diarahkan oleh homologi (''homology-directed repair''), di mana protein perbaikan menyalin urutan yang identik dari kromatid saudara (''sister chromatid'') yang masih utuh.<ref>{{Cite journal|last=Domchek|first=Susan M.|last2=Tang|first2=Jiangbo|last3=Stopfer|first3=Jill|last4=Lilli|first4=Dana R.|last5=Hamel|first5=Nancy|last6=Tischkowitz|first6=Marc|last7=Monteiro|first7=Alvaro N.A.|last8=Messick|first8=Troy E.|last9=Powers|first9=Jacquelyn|date=2013-04-01|title=Biallelic Deleterious BRCA1 Mutations in a Woman with Early-Onset Ovarian Cancer|url=https://aacrjournals.org/cancerdiscovery/article/3/4/399/4072/Biallelic-Deleterious-BRCA1-Mutations-in-a-Woman|journal=Cancer Discovery|language=en|volume=3|issue=4|pages=399–405|doi=10.1158/2159-8290.CD-12-0421|issn=2159-8274|pmc=PMC3625496|pmid=23269703}}</ref>
Di dalam nukleus dari berbagai jenis sel normal, protein BRCA1 berinteraksi dengan RAD51 selama perbaikan kerusakan untai ganda DNA.<ref>{{Cite journal|last=Boulton|first=S.J.|date=2006-10-01|title=Cellular functions of the BRCA tumour-suppressor proteins|url=https://portlandpress.com/biochemsoctrans/article/34/5/633/65958/Cellular-functions-of-the-BRCA-tumour-suppressor|journal=Biochemical Society Transactions|language=en|volume=34|issue=5|pages=633–645|doi=10.1042/BST0340633|issn=0300-5127}}</ref> Selain karena radiasi alami atau paparan yang lain, kerusakan ini dapat juga disebabkan ketika kromosom bertukar materi genetik, seperti pada proses rekombinasi homolog (contohnya, ''crossing over'' dalam pembelah meiosis). Protein BRCA2, yang memiliki fungsi yang mirip dengan BRCA1, juga berinteraksi dengan protein RAD51. Karena berperan dalam proses perbaikan kerusakan DNA, ketiga protein ini berperan penting dalam menjaga stabilitas genom manusia.<ref>{{Cite journal|last=Roy|first=Rohini|last2=Chun|first2=Jarin|last3=Powell|first3=Simon N.|date=2012-01|title=BRCA1 and BRCA2: different roles in a common pathway of genome protection|url=https://www.nature.com/articles/nrc3181|journal=Nature Reviews Cancer|language=en|volume=12|issue=1|pages=68–78|doi=10.1038/nrc3181|issn=1474-175X|pmc=PMC4972490|pmid=22193408}}</ref>
[[Berkas:Non homologous end joining and microhomology mediated end joining.png|kiri|jmpl|415x415px|''Non homogous end joining'' (NHEJ)]]
BRCA1 juga terlibat dalam jenis perbaikan DNA lainnya, yang disebut perbaikan ''mismatch''. BRCA1 berinteraksi dengan protein perbaikan ''mismatch'' DNA MSH2.<ref>{{Cite journal|last=Wang|first=Qiang|last2=Zhang|first2=Hongtao|last3=Guerrette|first3=Shawn|last4=Chen|first4=Jinqiu|last5=Mazurek|first5=Anthony|last6=Wilson|first6=Teresa|last7=Slupianek|first7=Artur|last8=Skorski|first8=Tomasz|last9=Fishel|first9=Richard|date=2001-08-02|title=Adenosine nucleotide modulates the physical interaction between hMSH2 and BRCA1|url=https://www.nature.com/articles/1204625|journal=Oncogene|language=en|volume=20|issue=34|pages=4640–4649|doi=10.1038/sj.onc.1204625|issn=0950-9232}}</ref> Eksperesi MSH2, MSH6, PARP, dan beberapa protein lain yang terlibat dalam perbaikan untai tunggal diketahui meningkat pada tumor payudara yang memiliki defisiensi BRCA1.<ref>{{Cite journal|last=Warmoes|first=Marc|last2=Jaspers|first2=Janneke E.|last3=Pham|first3=Thang V.|last4=Piersma|first4=Sander R.|last5=Oudgenoeg|first5=Gideon|last6=Massink|first6=Maarten P.G.|last7=Waisfisz|first7=Quinten|last8=Rottenberg|first8=Sven|last9=Boven|first9=Epie|date=2012-07|title=Proteomics of Mouse BRCA1-deficient Mammary Tumors Identifies DNA Repair Proteins with Potential Diagnostic and Prognostic Value in Human Breast Cancer|url=https://linkinghub.elsevier.com/retrieve/pii/S1535947620330061|journal=Molecular & Cellular Proteomics|language=en|volume=11|issue=7|pages=M111.013334–1–M111.013334-19|doi=10.1074/mcp.M111.013334|pmc=PMC3394939|pmid=22366898}}</ref>
BRCA1 dapat secara langsung berikatan dengan DNA, dengan afinitas yang lebih tinggi untuk struktur DNA yang bercabang (''branched structure''). Kemampuan untuk mengikat DNA ini berperan pada kemampuan BRCA1 dalam menghambat aktivitas nuklease kompleks MRN, juga aktivitas nuklease Mre11.<ref>{{Cite journal|last=Paull|first=Tanya T.|last2=Cortez|first2=David|last3=Bowers|first3=Blair|last4=Elledge|first4=Stephen J.|last5=Gellert|first5=Martin|date=2001-05-22|title=Direct DNA binding by Brca1|url=https://pnas.org/doi/full/10.1073/pnas.111125998|journal=Proceedings of the National Academy of Sciences|language=en|volume=98|issue=11|pages=6086–6091|doi=10.1073/pnas.111125998|issn=0027-8424|pmc=PMC33426|pmid=11353843}}</ref> Hal ini dapat menjelaskan peran BRCA1 untuk memfasilitasi perbaikan DNA dengan ketepatan yang lebih rendah melalui penggabungan ujung non-homolog (''non-homologous end joining'', NHEJ).<ref>{{Cite journal|last=Durant|first=Stephen T.|last2=Nickoloff|first2=Jac A|date=2005-09-22|title=Good Timing in the Cell Cycle for Precise DNA Repair by BRCA1|url=https://www.tandfonline.com/doi/full/10.4161/cc.4.9.2027|journal=Cell Cycle|language=en|volume=4|issue=9|pages=1216–1222|doi=10.4161/cc.4.9.2027|issn=1538-4101}}</ref> BRCA1 juga berkolokalisasi dengan γ-H2AX (histon H2AX terfosforilasi pada serine-139) dalam perbaikan kerusakan untai ganda DNA, yang mengindikasikan bahwa BRCA1 juga berperan dalam merekrut faktor-faktor perbaikan DNA.<ref>{{Cite journal|last=Starita|first=L|date=2003-06|title=The multiple nuclear functions of BRCA1: transcription, ubiquitination and DNA repair|url=https://linkinghub.elsevier.com/retrieve/pii/S0955067403000425|journal=Current Opinion in Cell Biology|language=en|volume=15|issue=3|pages=345–350|doi=10.1016/S0955-0674(03)00042-5}}</ref>
== Ekspresi ''BRCA1'' yang rendah pada kanker payudara
[[Berkas:Breast cancer ductal carcinoma in situ.jpg|jmpl|Kanker payudara berjenis duktal karsinoma ''in situ'']]
Ekspresi ''BRCA1'' berkurang atau tidak terdeteksi pada sebagian besar kanker payudara duktal tingkat tinggi (''high grade ductal breast cancers'').<ref>{{Cite journal|last=Wilson|first=Cindy A.|last2=Ramos|first2=Lillian|last3=Villaseñor|first3=Maria R.|last4=Anders|first4=Karl H.|last5=Press|first5=Michael F.|last6=Clarke|first6=Kathy|last7=Karlan|first7=Beth|last8=Chen|first8=Jun-Jie|last9=Scully|first9=Ralph|date=1999-02|title=Localization of human BRCA1 and its loss in high-grade, non-inherited breast carcinomas|url=https://www.nature.com/articles/ng0299_236|journal=Nature Genetics|language=en|volume=21|issue=2|pages=236–240|doi=10.1038/6029|issn=1061-4036}}</ref> Telah lama diketahui bahwa hilangnya aktivitas BRCA1, baik karena mutasi ''germ-line'' maupun karena penurunan regulasi ekspresi gen, menyebabkan pembentukan tumor pada jaringan-jaringan tertentu. Secara khusus, penurunan ekspresi ''BRCA1'' berkontribusi pada perkembangan tumor payudara sporadis (tidak diwariskan, terjadi secara spontan) dan yang diwariskan.<ref>{{Cite journal|last=Mueller|first=Christopher R|last2=Roskelley|first2=Calvin D|date=2002-02|title=Regulation of BRCA1 expression and its relationship to sporadic breast cancer|url=http://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr557|journal=Breast Cancer Research|language=en|volume=5|issue=1|doi=10.1186/bcr557|issn=1465-542X|pmc=PMC154136|pmid=12559046}}</ref> Ekspresi ''BRCA1'' yang menurun bersifat tumorigenik, karena penurunan ekspresi ini memaikan peran penting dalam perbaikan kerusakan DNA, terutama pemutusan untai ganda, melalui jalur rekombinasi homolog yang berpotensi bebas dari kesalahan.<ref name=":4">{{Cite journal|last=Jacinto|first=F. V.|last2=Esteller|first2=M.|date=2007-07-01|title=Mutator pathways unleashed by epigenetic silencing in human cancer|url=https://academic.oup.com/mutage/article-lookup/doi/10.1093/mutage/gem009|journal=Mutagenesis|language=en|volume=22|issue=4|pages=247–253|doi=10.1093/mutage/gem009|issn=0267-8357}}</ref> Karena sel yang kekurangan protein BRCA1 cenderung memperbaiki kerusakan DNA dengan mekanisme alternatif yang lebih rentan terhadap kesalahan, penurunan atau penonaktifan protein ini menghasilkan mutasi dan penataan ulang kromosom (''chromosomal rearrangemen)'' yang dapat menyebabkan progresi kanker payudara.<ref name=":4" />
== Interaksi Protein ==
BRCA1 telah terbukti berinteraksi dengan protein-protein berikut:
* [[Abl gene|ABL1]]<ref name="pmid12024016">{{cite journal | vauthors = Foray N, Marot D, Randrianarison V, Venezia ND, Picard D, Perricaudet M, Favaudon V, Jeggo P | title = Constitutive association of BRCA1 and c-Abl and its ATM-dependent disruption after irradiation | journal = Mol. Cell. Biol. | volume = 22 | issue = 12 | pages = 4020–32 | date = June 2002 | pmid = 12024016 | pmc = 133860 | doi = 10.1128/MCB.22.12.4020-4032.2002 }}</ref>
* [[AKT1]]<ref name="pmid10542266">{{cite journal | vauthors = Altiok S, Batt D, Altiok N, Papautsky A, Downward J, Roberts TM, Avraham H | title = Heregulin induces phosphorylation of BRCA1 through phosphatidylinositol 3-Kinase/AKT in breast cancer cells | journal = J. Biol. Chem. | volume = 274 | issue = 45 | pages = 32274–8 | date = November 1999 | pmid = 10542266 | doi = 10.1074/jbc.274.45.32274 | doi-access = free }}</ref><ref name="pmid19074868">{{cite journal | vauthors = Xiang T, Ohashi A, Huang Y, Pandita TK, Ludwig T, Powell SN, Yang Q | title = Negative Regulation of AKT Activation by BRCA1 | journal = Cancer Res. | volume = 68 | issue = 24 | pages = 10040–4 | date = December 2008 | pmid = 19074868 | pmc = 2605656 | doi = 10.1158/0008-5472.CAN-08-3009 }}</ref>
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* [[FANCD2]]<ref name="pmid14499622">{{cite journal | vauthors = Reuter TY, Medhurst AL, Waisfisz Q, Zhi Y, Herterich S, Hoehn H, Gross HJ, Joenje H, Hoatlin ME, Mathew CG, Huber PA | title = Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport | journal = Exp. Cell Res. | volume = 289 | issue = 2 | pages = 211–21 | date = October 2003 | pmid = 14499622 | doi = 10.1016/S0014-4827(03)00261-1 }}</ref>
* [[FHL2]]<ref name="pmid14550570">{{cite journal | vauthors = Yan J, Zhu J, Zhong H, Lu Q, Huang C, Ye Q | title = BRCA1 interacts with FHL2 and enhances FHL2 transactivation function | journal = FEBS Lett. | volume = 553 | issue = 1–2 | pages = 183–9 | date = October 2003 | pmid = 14550570 | doi = 10.1016/S0014-5793(03)00978-5 | s2cid = 31566004 | doi-access = free }}</ref><ref name="pmid14986435">{{cite journal | vauthors = Yan JH, Ye QN, Zhu JH, Zhong HJ, Zheng HY, Huang CF | title = [Isolation and characterization of a BRCA1-interacting protein] | language = zh | journal = Yi Chuan Xue Bao | volume = 30 | issue = 12 | pages = 1161–6 | date = December 2003 | pmid = 14986435 }}</ref>
* [[H2AFX]]<ref name="pmid10959836">{{cite journal | vauthors = Paull TT, Rogakou EP, Yamazaki V, Kirchgessner CU, Gellert M, Bonner WM | title = A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage | journal = Curr. Biol. | volume = 10 | issue = 15 | pages = 886–95 | year = 2000 | pmid = 10959836 | doi = 10.1016/S0960-9822(00)00610-2 | doi-access = free }}</ref>
* [[JUNB]]<ref name=pmid12080089/>
* [[JunD]]<ref name="pmid12080089">{{cite journal | vauthors = Hu YF, Li R | title = JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction | journal = Genes Dev. | volume = 16 | issue = 12 | pages = 1509–17 | date = June 2002 | pmid = 12080089 | pmc = 186344 | doi = 10.1101/gad.995502 }}</ref>
* [[LMO4]]<ref name="pmid12925972">{{cite journal | vauthors = Sutherland KD, Visvader JE, Choong DY, Sum EY, Lindeman GJ, Campbell IG | title = Mutational analysis of the LMO4 gene, encoding a BRCA1-interacting protein, in breast carcinomas | journal = Int. J. Cancer | volume = 107 | issue = 1 | pages = 155–8 | date = October 2003 | pmid = 12925972 | doi = 10.1002/ijc.11343 | s2cid = 20908722 | doi-access = free }}</ref><ref name="pmid11751867">{{cite journal | vauthors = Sum EY, Peng B, Yu X, Chen J, Byrne J, Lindeman GJ, Visvader JE | title = The LIM domain protein LMO4 interacts with the cofactor CtIP and the tumor suppressor BRCA1 and inhibits BRCA1 activity | journal = J. Biol. Chem. | volume = 277 | issue = 10 | pages = 7849–56 | date = March 2002 | pmid = 11751867 | doi = 10.1074/jbc.M110603200 | doi-access = free }}</ref>
* [[MAP3K3]]<ref name="pmid15205325">{{cite journal | vauthors = Gilmore PM, McCabe N, Quinn JE, Kennedy RD, Gorski JJ, Andrews HN, McWilliams S, Carty M, Mullan PB, Duprex WP, Liu ET, Johnston PG, Harkin DP | title = BRCA1 interacts with and is required for paclitaxel-induced activation of mitogen-activated protein kinase kinase kinase 3 | journal = Cancer Res. | volume = 64 | issue = 12 | pages = 4148–54 | date = June 2004 | pmid = 15205325 | doi = 10.1158/0008-5472.CAN-03-4080 | doi-access = free }}</ref>
* [[MED1]]<ref name="pmid15208681">{{cite journal | vauthors = Wada O, Oishi H, Takada I, Yanagisawa J, Yano T, Kato S | title = BRCA1 function mediates a TRAP/DRIP complex through direct interaction with TRAP220 | journal = Oncogene | volume = 23 | issue = 35 | pages = 6000–5 | date = August 2004 | pmid = 15208681 | doi = 10.1038/sj.onc.1207786 | doi-access = free }}</ref>
* [[MED17]]<ref name="pmid11504724">{{cite journal | vauthors = Chiba N, Parvin JD | title = Redistribution of BRCA1 among four different protein complexes following replication blockage | journal = J. Biol. Chem. | volume = 276 | issue = 42 | pages = 38549–54 | date = October 2001 | pmid = 11504724 | doi = 10.1074/jbc.M105227200 | doi-access = free }}</ref><ref name=pmid15208681/><ref name="pmid12154023">{{cite journal | vauthors = Chiba N, Parvin JD | title = The BRCA1 and BARD1 association with the RNA polymerase II holoenzyme | journal = Cancer Res. | volume = 62 | issue = 15 | pages = 4222–8 | date = August 2002 | pmid = 12154023 }}</ref>
* [[MED21]]<ref name="pmid9159119">{{cite journal | vauthors = Scully R, Anderson SF, Chao DM, Wei W, Ye L, Young RA, Livingston DM, Parvin JD | title = BRCA1 is a component of the RNA polymerase II holoenzyme | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 94 | issue = 11 | pages = 5605–10 | date = May 1997 | pmid = 9159119 | pmc = 20825 | doi = 10.1073/pnas.94.11.5605 | bibcode = 1997PNAS...94.5605S | doi-access = free }}</ref>
* [[MED24]]<ref name=pmid15208681/>
* [[MRE11A]]<ref name=pmid10783165/><ref name=pmid11504724/><ref name=pmid10426999/><ref name="pmid11353843">{{cite journal | vauthors = Paull TT, Cortez D, Bowers B, Elledge SJ, Gellert M | title = Direct DNA binding by Brca1 | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 98 | issue = 11 | pages = 6086–91 | date = May 2001 | pmid = 11353843 | pmc = 33426 | doi = 10.1073/pnas.111125998 | doi-access = free }}</ref>
* [[MSH2]]<ref name="pmid10783165">{{cite journal | vauthors = Wang Y, Cortez D, Yazdi P, Neff N, Elledge SJ, Qin J | title = BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures | journal = Genes Dev. | volume = 14 | issue = 8 | pages = 927–39 | date = April 2000 | pmid = 10783165 | pmc = 316544 | doi = 10.1101/gad.14.8.927}}</ref>
* [[MSH3]]<ref name="pmid14578343">{{cite journal | vauthors = Rodriguez M, Yu X, Chen J, Songyang Z | title = Phosphopeptide binding specificities of BRCA1 COOH-terminal (BRCT) domains | journal = J. Biol. Chem. | volume = 278 | issue = 52 | pages = 52914–8 | date = December 2003 | pmid = 14578343 | doi = 10.1074/jbc.C300407200 | doi-access = free }}</ref>
* [[MSH6]]<ref name=pmid10783165/>
* [[Myc]]<ref name=pmid11916966/><ref name="pmid14612409">{{cite journal | vauthors = Xiong J, Fan S, Meng Q, Schramm L, Wang C, Bouzahza B, Zhou J, Zafonte B, Goldberg ID, Haddad BR, Pestell RG, Rosen EM | title = BRCA1 inhibition of telomerase activity in cultured cells | journal = Mol. Cell. Biol. | volume = 23 | issue = 23 | pages = 8668–90 | date = December 2003 | pmid = 14612409 | pmc = 262673 | doi = 10.1128/MCB.23.23.8668-8690.2003 }}</ref><ref name="pmid12646176">{{cite journal | vauthors = Zhou C, Liu J | title = Inhibition of human telomerase reverse transcriptase gene expression by BRCA1 in human ovarian cancer cells | journal = Biochem. Biophys. Res. Commun. | volume = 303 | issue = 1 | pages = 130–6 | date = March 2003 | pmid = 12646176 | doi = 10.1016/S0006-291X(03)00318-8 }}</ref>
* [[Nibrin|NBN]]<ref name=pmid10783165/><ref name=pmid11504724/><ref name=pmid10426999/>
* [[N-myc-interactor|NMI]]<ref name="pmid11916966">{{cite journal | vauthors = Li H, Lee TH, Avraham H | title = A novel tricomplex of BRCA1, Nmi, and c-Myc inhibits c-Myc-induced human telomerase reverse transcriptase gene (hTERT) promoter activity in breast cancer | journal = J. Biol. Chem. | volume = 277 | issue = 23 | pages = 20965–73 | date = June 2002 | pmid = 11916966 | doi = 10.1074/jbc.M112231200 | doi-access = free }}</ref>
* [[NPM1]]
* [[Nuclear receptor coactivator 2|NCOA2]]<ref name="pmid11085509">{{cite journal | vauthors = Park JJ, Irvine RA, Buchanan G, Koh SS, Park JM, Tilley WD, Stallcup MR, Press MF, Coetzee GA | title = Breast cancer susceptibility gene 1 (BRCAI) is a coactivator of the androgen receptor | journal = Cancer Res. | volume = 60 | issue = 21 | pages = 5946–9 | date = November 2000 | pmid = 11085509 }}</ref>
* [[NUFIP1]]<ref name="pmid15107825">{{cite journal | vauthors = Cabart P, Chew HK, Murphy S | title = BRCA1 cooperates with NUFIP and P-TEFb to activate transcription by RNA polymerase II | journal = Oncogene | volume = 23 | issue = 31 | pages = 5316–29 | date = July 2004 | pmid = 15107825 | doi = 10.1038/sj.onc.1207684 | doi-access = free }}</ref>
* [[P53]]<ref name=pmid9926942/><ref name="pmid14710355">{{cite journal | vauthors = Abramovitch S, Werner H | title = Functional and physical interactions between BRCA1 and p53 in transcriptional regulation of the IGF-IR gene | journal = Horm. Metab. Res. | volume = 35 | issue = 11–12 | pages = 758–62 | year = 2003 | pmid = 14710355 | doi = 10.1055/s-2004-814154 | s2cid = 20898175 }}</ref><ref name="pmid9482880">{{cite journal | vauthors = Ouchi T, Monteiro AN, August A, Aaronson SA, Hanafusa H | title = BRCA1 regulates p53-dependent gene expression | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 95 | issue = 5 | pages = 2302–6 | date = March 1998 | pmid = 9482880 | pmc = 19327 | doi = 10.1073/pnas.95.5.2302 | bibcode = 1998PNAS...95.2302O | doi-access = free }}</ref><ref name="pmid9582019">{{cite journal | vauthors = Zhang H, Somasundaram K, Peng Y, Tian H, Zhang H, Bi D, Weber BL, El-Deiry WS | title = BRCA1 physically associates with p53 and stimulates its transcriptional activity | journal = Oncogene | volume = 16 | issue = 13 | pages = 1713–21 | date = April 1998 | pmid = 9582019 | doi = 10.1038/sj.onc.1201932 | doi-access = free }}</ref>
* [[PALB2]]<ref name="pmid19369211">{{cite journal | vauthors = Sy SM, Huen MS, Chen J | title = PALB2 is an integral component of the BRCA complex required for homologous recombination repair | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 106 | issue = 17 | pages = 7155–60 | date = April 2009 | pmid = 19369211 | pmc = 2678481 | doi = 10.1073/pnas.0811159106 | bibcode = 2009PNAS..106.7155S | doi-access = free }}</ref>
* [[POLR2A]]<ref name=pmid11504724/><ref name=pmid9159119/><ref name="pmid14506230">{{cite journal | vauthors = Krum SA, Miranda GA, Lin C, Lane TF | title = BRCA1 associates with processive RNA polymerase II | journal = J. Biol. Chem. | volume = 278 | issue = 52 | pages = 52012–20 | date = December 2003 | pmid = 14506230 | doi = 10.1074/jbc.M308418200 | doi-access = free }}</ref><ref name="pmid12955082">{{cite journal | vauthors = Krum SA, Womack JE, Lane TF | title = Bovine BRCA1 shows classic responses to genotoxic stress but low in vitro transcriptional activation activity | journal = Oncogene | volume = 22 | issue = 38 | pages = 6032–44 | date = September 2003 | pmid = 12955082 | doi = 10.1038/sj.onc.1206515 | doi-access = free }}</ref>
* [[PPP1CA]]<ref name="pmid12438214">{{cite journal | vauthors = Liu Y, Virshup DM, White RL, Hsu LC | title = Regulation of BRCA1 phosphorylation by interaction with protein phosphatase 1alpha | journal = Cancer Res. | volume = 62 | issue = 22 | pages = 6357–61 | date = November 2002 | pmid = 12438214 }}</ref>
* [[Rad50]]<ref name=pmid10783165/><ref name=pmid11504724/><ref name="pmid10426999">{{cite journal | vauthors = Zhong Q, Chen CF, Li S, Chen Y, Wang CC, Xiao J, Chen PL, Sharp ZD, Lee WH | title = Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response | journal = Science | volume = 285 | issue = 5428 | pages = 747–50 | date = July 1999 | pmid = 10426999 | doi = 10.1126/science.285.5428.747 }}</ref>
* [[RAD51]]<ref name="pmid9774970">{{cite journal | vauthors = Chen J, Silver DP, Walpita D, Cantor SB, Gazdar AF, Tomlinson G, Couch FJ, Weber BL, Ashley T, Livingston DM, Scully R | title = Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells | journal = Mol. Cell | volume = 2 | issue = 3 | pages = 317–28 | date = September 1998 | pmid = 9774970 | doi = 10.1016/S1097-2765(00)80276-2 | doi-access = free }}</ref><ref name="pmid9008167">{{cite journal | vauthors = Scully R, Chen J, Plug A, Xiao Y, Weaver D, Feunteun J, Ashley T, Livingston DM | title = Association of BRCA1 with Rad51 in mitotic and meiotic cells | journal = Cell | volume = 88 | issue = 2 | pages = 265–75 | date = January 1997 | pmid = 9008167 | doi = 10.1016/S0092-8674(00)81847-4 | doi-access = free }}</ref>
* [[RBBP4]]
== Referensi ==
<references />
==External links==
{{Commons category|BRCA1}}
* {{MeshName|BRCA1+Protein|3=BRCA1 Protein}}
* {{MeshName|Genes,+BRCA1|3=Genes, BRCA1}}
* [https://www.ebi.ac.uk/pdbe/pdbe-kb/proteins/P38398 PDBe-KB] memberikan gambaran umum tentang semua informasi struktur yang tersedia dalam PDB untuk protein BRCA1 manusia.
[[Kategori: Gen penekan tumor]]
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