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{{PBB|geneid=6774}}
'''信号转导及转录激活蛋白3'''（{{langx|en|Signal transducer and activator of transcription 3}}，'''STAT3'''）是一种由人类[[基因]]''STAT3'' 编码的[[转录因子]]<ref name="pmid7512451">{{cite journal | author = Akira S, Nishio Y, Inoue M, Wang XJ, Wei S, Matsusaka T, Yoshida K, Sudo T, Naruto M, Kishimoto T | title = Molecular cloning of APRF, a novel IFN-stimulated gene factor 3 p91-related transcription factor involved in the gp130-mediated signaling pathway | journal = Cell | volume = 77 | issue = 1 | pages = 63–71 |date=April 1994 | pmid = 7512451 | doi = 10.1016/0092-8674(94)90235-6| url = | issn = }}</ref>。

== 功能 ==
STAT3是[[信号转导及转录激活蛋白|STAT蛋白家族]]的成员。受到[[细胞因子]]和[[生长因子]]的调节，STAT3被受体相关的[[JAK激酶|Janus激酶]]（JAK）磷酸化，形成同源或异源二聚体，并转移到细胞核，在那里它们起转录激活剂的作用。具体而言，[[干扰素]]，[[表皮生长因子]]（EGF），[[白细胞介素]]（[[白细胞介素-5|IL-5]]和[[白细胞介素-6|IL-6]]）等配体作用于受体，导致酪氨酸705磷酸化后，STAT3被激活。此外，STAT3可能通过[[丝裂原活化蛋白激酶]]（MAPK）<ref>{{Cite journal|title=p42/p44 MAPK-mediated Stat3Ser727 phosphorylation is required for progestin-induced full activation of Stat3 and breast cancer growth|url=https://www.ncbi.nlm.nih.gov/pubmed/23329648|last=Tkach|first=Mercedes|last2=Rosemblit|first2=Cinthia|date=April 2013|journal=Endocrine-Related Cancer|issue=2|doi=10.1530/ERC-12-0194|volume=20|pages=197–212|issn=1479-6821|pmid=23329648|last3=Rivas|first3=Martín A.|last4=Proietti|first4=Cecilia J.|last5=Díaz Flaqué|first5=María Celeste|last6=Mercogliano|first6=María Florencia|last7=Beguelin|first7=Wendy|last8=Maronna|first8=Esteban|last9=Guzmán|first9=Pablo|access-date=2018-02-11|archive-date=2018-02-18|archive-url=https://web.archive.org/web/20180218214639/https://www.ncbi.nlm.nih.gov/pubmed/23329648|dead-url=no}}</ref>和[[c-src]][[非受体酪氨酸激酶]]磷酸化丝氨酸727而激活。<ref>{{Cite journal|title=Role of STATs as downstream signal transducers in Src family kinase-mediated tumorigenesis|url=https://www.ncbi.nlm.nih.gov/pubmed/15489919|last=Silva|first=Corinne M.|date=2004-10-18|journal=Oncogene|issue=48|doi=10.1038/sj.onc.1208159|volume=23|pages=8017–8023|issn=0950-9232|pmid=15489919|access-date=2018-02-11|archive-date=2018-02-18|archive-url=https://web.archive.org/web/20180218214632/https://www.ncbi.nlm.nih.gov/pubmed/15489919|dead-url=no}}</ref><ref>{{Cite journal|title=Structure, function, and regulation of STAT proteins|url=https://www.ncbi.nlm.nih.gov/pubmed/17216035|last=Lim|first=Cheh Peng|last2=Cao|first2=Xinmin|date=November 2006|journal=Molecular bioSystems|issue=11|doi=10.1039/b606246f|volume=2|pages=536–550|issn=1742-206X|pmid=17216035|access-date=2018-02-11|archive-date=2018-02-18|archive-url=https://web.archive.org/web/20180218214603/https://www.ncbi.nlm.nih.gov/pubmed/17216035|dead-url=no}}</ref>STAT3介导响应细胞刺激的各种基因的表达，因此在许多细胞过程如细胞生长和细胞凋亡中起关键作用。<ref>{{Cite journal|title=Central role of the threonine residue within the p+1 loop of receptor tyrosine kinase in STAT3 constitutive phosphorylation in metastatic cancer cells|url=https://www.ncbi.nlm.nih.gov/pubmed/15485908|last=Yuan|first=Zheng-Long|last2=Guan|first2=Ying-Jie|date=November 2004|journal=Molecular and Cellular Biology|issue=21|doi=10.1128/MCB.24.21.9390-9400.2004|volume=24|pages=9390–9400|issn=0270-7306|pmid=15485908|last3=Wang|first3=Lijuan|last4=Wei|first4=Wenyi|last5=Kane|first5=Agnes B.|last6=Chin|first6=Y. Eugene|access-date=2018-02-11|archive-date=2018-02-18|archive-url=https://web.archive.org/web/20180218214620/https://www.ncbi.nlm.nih.gov/pubmed/15485908|dead-url=no}}</ref>

当原肠胚形成开始时，STAT3缺陷的小鼠胚胎不能在胚胎发育第7天以后发育。<ref>{{Cite journal|title=Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality|url=https://www.ncbi.nlm.nih.gov/pubmed/9108058|last=Takeda|first=K.|last2=Noguchi|first2=K.|date=1997-04-15|journal=Proceedings of the National Academy of Sciences of the United States of America|issue=8|volume=94|pages=3801–3804|issn=0027-8424|pmid=9108058|last3=Shi|first3=W.|last4=Tanaka|first4=T.|last5=Matsumoto|first5=M.|last6=Yoshida|first6=N.|last7=Kishimoto|first7=T.|last8=Akira|first8=S.|access-date=2018-02-11|archive-date=2018-07-24|archive-url=https://web.archive.org/web/20180724002748/https://www.ncbi.nlm.nih.gov/pubmed/9108058|dead-url=no}}</ref>看来在这些发育的早期阶段，STAT3激活是胚胎干细胞（ESC）自我更新所必需的。事实上，如果STAT3通过其他方式被激活，LIF可以被省略，该LIF被提供给小鼠ESC培养物以保持其未分化状态。<ref>{{Cite journal|title=STAT3 activation is sufficient to maintain an undifferentiated state of mouse embryonic stem cells.|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1171502/|last=Matsuda|first=T|last2=Nakamura|first2=T|date=1999-08-02|journal=The EMBO Journal|issue=15|doi=10.1093/emboj/18.15.4261|volume=18|pages=4261–4269|issn=0261-4189|pmc=1171502|pmid=10428964|last3=Nakao|first3=K|last4=Arai|first4=T|last5=Katsuki|first5=M|last6=Heike|first6=T|last7=Yokota|first7=T}}</ref>

STAT3对于TH17辅助性T细胞的分化至关重要，TH17辅助性T细胞已涉及多种自體免疫性疾病。<ref>{{Cite journal|title=STAT3 regulates cytokine-mediated generation of inflammatory helper T cells|url=https://www.ncbi.nlm.nih.gov/pubmed/17277312|last=Yang|first=Xuexian O.|last2=Panopoulos|first2=Athanasia D.|date=2007-03-30|journal=The Journal of Biological Chemistry|issue=13|doi=10.1074/jbc.C600321200|volume=282|pages=9358–9363|issn=0021-9258|pmid=17277312|last3=Nurieva|first3=Roza|last4=Chang|first4=Seon Hee|last5=Wang|first5=Demin|last6=Watowich|first6=Stephanie S.|last7=Dong|first7=Chen|access-date=2018-02-11|archive-date=2018-07-23|archive-url=https://web.archive.org/web/20180723190217/https://www.ncbi.nlm.nih.gov/pubmed/17277312|dead-url=no}}</ref>在病毒感染期间，缺乏T细胞中STAT3的小鼠显示产生T-滤泡辅助（Tfh）细胞的能力受损，并且不能维持基于抗体的免疫性。<ref>{{Cite journal|title=T-cell STAT3 is required for the maintenance of humoral immunity to LCMV|url=https://www.ncbi.nlm.nih.gov/pubmed/25393615|last=McIlwain|first=David R.|last2=Grusdat|first2=Melanie|date=February 2015|journal=European Journal of Immunology|issue=2|doi=10.1002/eji.201445060|volume=45|pages=418–427|issn=1521-4141|pmc=4383653|pmid=25393615|last3=Pozdeev|first3=Vitaly I.|last4=Xu|first4=Haifeng C.|last5=Shinde|first5=Prashant|last6=Reardon|first6=Colin|last7=Hao|first7=Zhenyue|last8=Beyer|first8=Marc|last9=Bergthaler|first9=Andreas|access-date=2018-02-11|archive-date=2018-07-23|archive-url=https://web.archive.org/web/20180723222614/https://www.ncbi.nlm.nih.gov/pubmed/25393615|dead-url=no}}</ref>

==临床意义==

==在癌症中的双重作用==

==相互作用==
STAT3能与下列蛋白質发生[[蛋白質交互作用|交互作用]]：
{{div col|colwidth=20em}}
* [[雄激素受体|AR]]<ref name = pmid11751884/><ref name = pmid11322786>{{cite journal | author = Matsuda T, Junicho A, Yamamoto T, Kishi H, Korkmaz K, Saatcioglu F, Fuse H, Muraguchi A | title = Cross-talk between signal transducer and activator of transcription 3 and androgen receptor signaling in prostate carcinoma cells | journal = Biochem. Biophys. Res. Commun. | volume = 283 | issue = 1 | pages = 179–87 | year = 2001 | pmid = 11322786 | doi = 10.1006/bbrc.2001.4758 }}</ref>
* [[ELP2]]<ref name = pmid10954736>{{cite journal | author = Collum RG, Brutsaert S, Lee G, Schindler C | title = A Stat3-interacting protein (StIP1) regulates cytokine signal transduction | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 97 | issue = 18 | pages = 10120–5 | year = 2000 | pmid = 10954736 | pmc = 27739 | doi = 10.1073/pnas.170192197 }}</ref>
* [[EP300]]<ref name = pmid10205054>{{cite journal | author = Nakashima K, Yanagisawa M, Arakawa H, Kimura N, Hisatsune T, Kawabata M, Miyazono K, Taga T | title = Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300 | url = https://archive.org/details/sim_science_1999-04-16_284_5413/page/478 | journal = Science | volume = 284 | issue = 5413 | pages = 479–82 | year = 1999 | pmid = 10205054 | doi = 10.1126/science.284.5413.479}}</ref>
* [[表皮生长因子受体|EGFR]]<ref name = pmid15485908/><ref name = pmid10358079>{{cite journal | author = Olayioye MA, Beuvink I, Horsch K, Daly JM, Hynes NE | title = ErbB receptor-induced activation of stat transcription factors is mediated by Src tyrosine kinases | url = https://archive.org/details/sim_journal-of-biological-chemistry_1999-06-11_274_24/page/17208 | journal = J. Biol. Chem. | volume = 274 | issue = 24 | pages = 17209–18 | year = 1999 | pmid = 10358079 | doi = 10.1074/jbc.274.24.17209}}</ref>
* [[HIF1A]]<ref name = pmid18985005>{{cite journal | author = Jung JE, Kim HS, Lee CS, Shin YJ, Kim YN, Kang GH, Kim TY, Juhnn YS, Kim SJ, Park JW, Ye SK, Chung MH | title = STAT3 inhibits the degradation of HIF-1alpha by pVHL-mediated ubiquitination | journal = Exp. Mol. Med. | volume = 40 | issue = 5 | pages = 479–85 | year = 2008 | pmid = 18985005 | pmc = 2679355 | doi = 10.3858/emm.2008.40.5.479 }}</ref>
* [[JAK激酶1|JAK1]]<ref name = pmid11751884>{{cite journal | author = Ueda T, Bruchovsky N, Sadar MD | title = Activation of the androgen receptor N-terminal domain by interleukin-6 via MAPK and STAT3 signal transduction pathways | url = https://archive.org/details/sim_journal-of-biological-chemistry_2002-03-01_277_9/page/7076 | journal = J. Biol. Chem. | volume = 277 | issue = 9 | pages = 7076–85 | year = 2002 | pmid = 11751884 | doi = 10.1074/jbc.M108255200 }}</ref><ref name = pmid11722592>{{cite journal | author = Spiekermann K, Biethahn S, Wilde S, Hiddemann W, Alves F | title = Constitutive activation of STAT transcription factors in acute myelogenous leukemia | journal = Eur. J. Haematol. | volume = 67 | issue = 2 | pages = 63–71 | year = 2001 | pmid = 11722592 | doi = }}</ref>
* [[C-jun|JUN]]<ref name = pmid10490649>{{cite journal | author = Zhang X, Wrzeszczynska MH, Horvath CM, Darnell JE | title = Interacting regions in Stat3 and c-Jun that participate in cooperative transcriptional activation | url = https://archive.org/details/sim_molecular-and-cellular-biology_1999-10_19_10/page/7138 | journal = Mol. Cell. Biol. | volume = 19 | issue = 10 | pages = 7138–46 | year = 1999 | pmid = 10490649 | pmc = 84707 | doi = }}</ref>
* [[KHDRBS1]]<ref name = pmid11585385>{{cite journal | author = Sanchez-Margalet V, Martin-Romero C | title = Human leptin signaling in human peripheral blood mononuclear cells: activation of the JAK-STAT pathway | journal = Cell. Immunol. | volume = 211 | issue = 1 | pages = 30–6 | year = 2001 | pmid = 11585385 | doi = 10.1006/cimm.2001.1815 }}</ref>
* [[Mammalian target of rapamycin|MTOR]]<ref name = pmid10660304>{{cite journal | author = Yokogami K, Wakisaka S, Avruch J, Reeves SA | title = Serine phosphorylation and maximal activation of STAT3 during CNTF signaling is mediated by the rapamycin target mTOR | journal = Curr. Biol. | volume = 10 | issue = 1 | pages = 47–50 | year = 2000 | pmid = 10660304 | doi = 10.1016/S0960-9822(99)00268-7}}</ref><ref name = pmid15522880>{{cite journal | author = Kusaba H, Ghosh P, Derin R, Buchholz M, Sasaki C, Madara K, Longo DL | title = Interleukin-12-induced interferon-gamma production by human peripheral blood T cells is regulated by mammalian target of rapamycin (mTOR) | url = https://archive.org/details/sim_journal-of-biological-chemistry_2005-01-14_280_2/page/1036 | journal = J. Biol. Chem. | volume = 280 | issue = 2 | pages = 1037–43 | year = 2005 | pmid = 15522880 | doi = 10.1074/jbc.M405204200 }}</ref>
* [[MyoD|MYOD1]]<ref name = pmid12947115>{{cite journal | author = Kataoka Y, Matsumura I, Ezoe S, Nakata S, Takigawa E, Sato Y, Kawasaki A, Yokota T, Nakajima K, Felsani A, Kanakura Y | title = Reciprocal inhibition between MyoD and STAT3 in the regulation of growth and differentiation of myoblasts | url = https://archive.org/details/sim_journal-of-biological-chemistry_2003-11-07_278_45/page/44178 | journal = J. Biol. Chem. | volume = 278 | issue = 45 | pages = 44178–87 | year = 2003 | pmid = 12947115 | doi = 10.1074/jbc.M304884200 }}</ref>
* [[NDUFA13]]<ref name = pmid12867595>{{cite journal | author = Zhang J, Yang J, Roy SK, Tininini S, Hu J, Bromberg JF, Poli V, Stark GR, Kalvakolanu DV | title = The cell death regulator GRIM-19 is an inhibitor of signal transducer and activator of transcription 3 | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 100 | issue = 16 | pages = 9342–7 | year = 2003 | pmid = 12867595 | pmc = 170920 | doi = 10.1073/pnas.1633516100 }}</ref>
* [[NFKB1]]<ref name = pmid12057007/>
* [[Glucocorticoid receptor|NR3C1]]<ref name = pmid14522952>{{cite journal | author = Lerner L, Henriksen MA, Zhang X, Darnell JE | title = STAT3-dependent enhanceosome assembly and disassembly: synergy with GR for full transcriptional increase of the alpha 2-macroglobulin gene | url = https://archive.org/details/sim_genes-development_2003-10-15_17_20/page/2564 | journal = Genes Dev. | volume = 17 | issue = 20 | pages = 2564–77 | year = 2003 | pmid = 14522952 | pmc = 218150 | doi = 10.1101/gad.1135003 }}</ref><ref name = pmid9388192>{{cite journal | author = Zhang Z, Jones S, Hagood JS, Fuentes NL, Fuller GM | title = STAT3 acts as a co-activator of glucocorticoid receptor signaling | url = https://archive.org/details/sim_journal-of-biological-chemistry_1997-12-05_272_49/page/30606 | journal = J. Biol. Chem. | volume = 272 | issue = 49 | pages = 30607–10 | year = 1997 | pmid = 9388192 | doi = 10.1074/jbc.272.49.30607}}</ref>
* [[Nuclear receptor coactivator 1|NCOA1]]<ref name = pmid11773079>{{cite journal | author = Giraud S, Bienvenu F, Avril S, Gascan H, Heery DM, Coqueret O | title = Functional interaction of STAT3 transcription factor with the coactivator NcoA/SRC1a | url = https://archive.org/details/sim_journal-of-biological-chemistry_2002-03-08_277_10/page/8004 | journal = J. Biol. Chem. | volume = 277 | issue = 10 | pages = 8004–11 | year = 2002 | pmid = 11773079 | doi = 10.1074/jbc.M111486200 }}</ref>
* [[早幼粒细胞白血病蛋白|PML]]<ref name = pmid12506013>{{cite journal | author = Kawasaki A, Matsumura I, Kataoka Y, Takigawa E, Nakajima K, Kanakura Y | title = Opposing effects of PML and PML/RAR alpha on STAT3 activity | url = https://archive.org/details/sim_blood_2003-05-01_101_9/page/3668 | journal = Blood | volume = 101 | issue = 9 | pages = 3668–73 | year = 2003 | pmid = 12506013 | doi = 10.1182/blood-2002-08-2474 }}</ref>
* [[RAC1]]<ref name = pmid11021801>{{cite journal | author = Simon AR, Vikis HG, Stewart S, Fanburg BL, Cochran BH, Guan KL | title = Regulation of STAT3 by direct binding to the Rac1 GTPase | url = https://archive.org/details/sim_science_2000-10-06_290_5489/page/144 | journal = Science | volume = 290 | issue = 5489 | pages = 144–7 | year = 2000 | pmid = 11021801 | doi = 10.1126/science.290.5489.144}}</ref>
* [[RELA]]<ref name = pmid12057007>{{cite journal | author = Yu Z, Zhang W, Kone BC | title = Signal transducers and activators of transcription 3 (STAT3) inhibits transcription of the inducible nitric oxide synthase gene by interacting with nuclear factor kappaB | journal = Biochem. J. | volume = 367 | issue = Pt 1 | pages = 97–105 | year = 2002 | pmid = 12057007 | pmc = 1222853 | doi = 10.1042/BJ20020588 }}</ref>
* [[RET proto-oncogene|RET]]<ref name = pmid15485908>{{cite journal | author = Yuan ZL, Guan YJ, Wang L, Wei W, Kane AB, Chin YE | title = Central role of the threonine residue within the p+1 loop of receptor tyrosine kinase in STAT3 constitutive phosphorylation in metastatic cancer cells | url = https://archive.org/details/sim_molecular-and-cellular-biology_2004-11_24_21/page/9390 | journal = Mol. Cell. Biol. | volume = 24 | issue = 21 | pages = 9390–400 | year = 2004 | pmid = 15485908 | pmc = 522220 | doi = 10.1128/MCB.24.21.9390-9400.2004 }}</ref><ref name = pmid12637586>{{cite journal | author = Hwang JH, Kim DW, Suh JM, Kim H, Song JH, Hwang ES, Park KC, Chung HK, Kim JM, Lee TH, Yu DY, Shong M | title = Activation of signal transducer and activator of transcription 3 by oncogenic RET/PTC (rearranged in transformation/papillary thyroid carcinoma) tyrosine kinase: roles in specific gene regulation and cellular transformation | journal = Mol. Endocrinol. | volume = 17 | issue = 6 | pages = 1155–66 | year = 2003 | pmid = 12637586 | doi = 10.1210/me.2002-0401 }}</ref><ref name = pmid11536047>{{cite journal | author = Schuringa JJ, Wojtachnio K, Hagens W, Vellenga E, Buys CH, Hofstra R, Kruijer W | title = MEN2A-RET-induced cellular transformation by activation of STAT3 | journal = Oncogene | volume = 20 | issue = 38 | pages = 5350–8 | year = 2001 | pmid = 11536047 | doi = 10.1038/sj.onc.1204715 }}</ref>
* [[RPA2]]<ref name = pmid10875894>{{cite journal | author = Kim J, Kim D, Chung J | title = Replication protein a 32 kDa subunit (RPA p32) binds the SH2 domain of STAT3 and regulates its transcriptional activity | journal = Cell Biol. Int. | volume = 24 | issue = 7 | pages = 467–73 | year = 2000 | pmid = 10875894 | doi = 10.1006/cbir.2000.0525 }}</ref>
* [[STAT1]]<ref name = pmid11722592/><ref name = pmid11594781>{{cite journal | author = Gunaje JJ, Bhat GJ | title = Involvement of tyrosine phosphatase PTP1D in the inhibition of interleukin-6-induced Stat3 signaling by alpha-thrombin | journal = Biochem. Biophys. Res. Commun. | volume = 288 | issue = 1 | pages = 252–7 | year = 2001 | pmid = 11594781 | doi = 10.1006/bbrc.2001.5759 }}</ref><ref name = pmid12070153>{{cite journal | author = Xia L, Wang L, Chung AS, Ivanov SS, Ling MY, Dragoi AM, Platt A, Gilmer TM, Fu XY, Chin YE | title = Identification of both positive and negative domains within the epidermal growth factor receptor COOH-terminal region for signal transducer and activator of transcription (STAT) activation | url = https://archive.org/details/sim_journal-of-biological-chemistry_2002-08-23_277_34/page/30716 | journal = J. Biol. Chem. | volume = 277 | issue = 34 | pages = 30716–23 | year = 2002 | pmid = 12070153 | doi = 10.1074/jbc.M202823200 }}</ref>
* [[Src (gene)|Src]]<ref name = pmid8657134>{{cite journal | author = Cao X, Tay A, Guy GR, Tan YH | title = Activation and association of Stat3 with Src in v-Src-transformed cell lines | url = https://archive.org/details/sim_molecular-and-cellular-biology_1996-04_16_4/page/1595 | journal = Mol. Cell. Biol. | volume = 16 | issue = 4 | pages = 1595–603 | year = 1996 | pmid = 8657134 | pmc = 231145 | doi = }}</ref>
* [[TRIP10]]<ref name = pmid15163742>{{cite journal | author = Chung YH, Cho NH, Garcia MI, Lee SH, Feng P, Jung JU | title = Activation of Stat3 transcription factor by Herpesvirus saimiri STP-A oncoprotein | url = https://archive.org/details/sim_journal-of-virology_2004-06_78_12/page/6489 | journal = J. Virol. | volume = 78 | issue = 12 | pages = 6489–97 | year = 2004 | pmid = 15163742 | pmc = 416526 | doi = 10.1128/JVI.78.12.6489-6497.2004 }}</ref>
{{Div col end}}

==参考文献==
{{Reflist|2}}

==延伸阅读==
{{refbegin | 2}}
*{{cite journal | author=Hoey T, Grusby MJ |title=STATs as mediators of cytokine-induced responses |journal=Adv. Immunol. |volume=71 |issue= |pages= 145–162 |year= 1999 |pmid= 9917912 |doi=10.1016/S0065-2776(08)60401-0 | series=Advances in Immunology | isbn=978-0-12-022471-5 }}
*{{cite journal | author=Kisseleva T, Bhattacharya S, Braunstein J, Schindler CW |title=Signaling through the JAK/STAT pathway, recent advances and future challenges |journal=Gene |volume=285 |issue= 1–2 |pages= 1–24 |year= 2002 |pmid= 12039028 |doi=10.1016/S0378-1119(02)00398-0 }}
*{{cite journal | author=Joseph AM, Kumar M, Mitra D |title=Nef: "necessary and enforcing factor" in HIV infection |journal=Curr. HIV Res. |volume=3 |issue= 1 |pages= 87–94 |year= 2005 |pmid= 15638726 |doi=10.2174/1570162052773013 }}
*{{cite journal | author=Inghirami G |title=New and old functions of STAT3: a pivotal target for individualized treatment of cancer |journal=Cell Cycle |volume=4 |issue= 9 |pages= 1131–3 |year= 2006 |pmid= 16082218 |doi= | author2=Chiarle R | author3=Simmons WJ | display-authors=3 | last4=Piva | first4=R | last5=Schlessinger | first5=K | last6=Levy | first6=DE }}
*{{cite journal | author=Leeman RJ, Lui VW, Grandis JR |title=STAT3 as a therapeutic target in head and neck cancer |journal=Expert opinion on biological therapy |volume=6 |issue= 3 |pages= 231–241 |year= 2006 |pmid= 16503733 |doi= 10.1517/14712598.6.3.231 }}
*{{cite journal | author=Aggarwal BB |title=Targeting signal-transducer-and-activator-of-transcription-3 for prevention and therapy of cancer: modern target but ancient solution |journal=Ann. N. Y. Acad. Sci. |volume=1091 |issue= |pages= 151–169 |year= 2007 |pmid= 17341611 |doi= 10.1196/annals.1378.063 | author2=Sethi G | author3=Ahn KS | display-authors=3 | last4=Sandur | first4=Santosh K. | last5=Pandey | first5=Manoj K. | last6=Kunnumakkara | first6=Ajaikumar B. | last7=Sung | first7=Bokyung | last8=Ichikawa | first8=Haruyo }}
{{refend}}

==外部链接==
* {{FactorBook|STAT3}}
{{PDB Gallery|geneid=6774}}
{{Transcription factors|g4}}
{{JAK-STAT信号通路}}

[[Category:转录因子]]
[[Category:信号转导]]
[[Category:兼职蛋白质]]

STAT3 - 版本历史

imported>InternetArchiveBot：​Add 14 books for verifiability (20251017sim)) #IABot (v2.0.9.5) (GreenC bot

imported>InternetArchiveBot：Add 14 books for verifiability (20251017sim)) #IABot (v2.0.9.5) (GreenC bot