signal transducer and activator of transcription 3
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The STAT3 gene is part of a family known as the STAT genes. These genes provide instructions for making proteins that are part of essential chemical signaling pathways within cells. When STAT proteins are turned on (activated) by certain chemical signals, they move into the cell's nucleus and attach (bind) to particular areas of DNA. The STAT proteins bind to regulatory regions near genes, which allows the proteins to control whether these genes are turned on or off. STAT proteins are called transcription factors on the basis of this action.
Normal function
The STAT3 gene is part of a family known as the STAT genes. These genes provide instructions for making proteins that are part of essential chemical signaling pathways within cells. When STAT proteins are turned on (activated) by certain chemical signals, they move into the cell's nucleus and attach (bind) to particular areas of DNA. The STAT proteins bind to regulatory regions near genes, which allows the proteins to control whether these genes are turned on or off. STAT proteins are called transcription factors on the basis of this action.
Through its regulation of gene activity, the STAT3 protein is involved in many cellular functions. It helps control cell growth and division (proliferation), cell movement (migration), and the self-destruction of cells (apoptosis).
The STAT3 protein is active in tissues throughout the body. It plays an important role in the development and function of several body systems and is essential for life. In the immune system, the STAT3 protein transmits signals for the maturation of immune system cells, especially T cells and B cells. These cells help control the body's response to foreign invaders such as bacteria and fungi.
In addition, the protein is involved in the regulation of inflammation, which is one way the immune system responds to infection or injury, and it plays a role in cellular processes that promote allergic reactions.
In the skeletal system, the STAT3 protein is involved in the formation of specialized cells that build and break down bone tissue. These cells are necessary for the normal development and maintenance of bones.
Conditions referring to this gene or chromosome
Altri nomi
acute-phase response factor
APRF
APRF Transcription Factor
DNA-binding protein APRF
FLJ20882
hypothetical protein MGC16063
IL6-Response Factor
LIF(leukemia inhibitory factor)-Response Factor
LIF-Response Factor
signal transducer and activator of transcription 3 (acute-phase response factor)
STAT3_HUMAN
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Ulteriori letture e riferimenti
- signal transducer and activator of transcription 3; MedlinePlus, National Library of Medicine.
- Frank DA. STAT3 as a central mediator of neoplastic cellular transformation. Cancer Lett. 2007 Jun 28;251(2):199-210. doi: 10.1016/j.canlet.2006.10.017. Epub 2006 Nov 28.
- Gao H, Ward PA. STAT3 and suppressor of cytokine signaling 3: potential targets in lung inflammatory responses. Expert Opin Ther Targets. 2007 Jul;11(7):869-80. doi: 10.1517/14728222.11.7.869.
- Haapaniemi EM, Kaustio M, Rajala HL, van Adrichem AJ, Kainulainen L, Glumoff V, Doffinger R, Kuusanmaki H, Heiskanen-Kosma T, Trotta L, Chiang S, Kulmala P, Eldfors S, Katainen R, Siitonen S, Karjalainen-Lindsberg ML, Kovanen PE, Otonkoski T, Porkka K, Heiskanen K, Hanninen A, Bryceson YT, Uusitalo-Seppala R, Saarela J, Seppanen M, Mustjoki S, Kere J. Autoimmunity, hypogammaglobulinemia, lymphoproliferation, and mycobacterial disease in patients with activating mutations in STAT3. Blood. 2015 Jan 22;125(4):639-48. doi: 10.1182/blood-2014-04-570101. Epub 2014 Oct 27.
- Hodge DR, Hurt EM, Farrar WL. The role of IL-6 and STAT3 in inflammation and cancer. Eur J Cancer. 2005 Nov;41(16):2502-12. doi: 10.1016/j.ejca.2005.08.016. Epub 2005 Sep 30.
- Holland SM, DeLeo FR, Elloumi HZ, Hsu AP, Uzel G, Brodsky N, Freeman AF, Demidowich A, Davis J, Turner ML, Anderson VL, Darnell DN, Welch PA, Kuhns DB, Frucht DM, Malech HL, Gallin JI, Kobayashi SD, Whitney AR, Voyich JM, Musser JM, Woellner C, Schaffer AA, Puck JM, Grimbacher B. STAT3 mutations in the hyper-IgE syndrome. N Engl J Med. 2007 Oct 18;357(16):1608-19. doi: 10.1056/NEJMoa073687. Epub 2007 Sep 19.
- Hox V, O'Connell MP, Lyons JJ, Sackstein P, Dimaggio T, Jones N, Nelson C, Boehm M, Holland SM, Freeman AF, Tweardy DJ, Olivera A, Metcalfe DD, Milner JD. Diminution of signal transducer and activator of transcription 3 signaling inhibits vascular permeability and anaphylaxis. J Allergy Clin Immunol. 2016 Jul;138(1):187-199. doi: 10.1016/j.jaci.2015.11.024. Epub 2016 Mar 2.
- Jerez A, Clemente MJ, Makishima H, Koskela H, Leblanc F, Peng Ng K, Olson T, Przychodzen B, Afable M, Gomez-Segui I, Guinta K, Durkin L, Hsi ED, McGraw K, Zhang D, Wlodarski MW, Porkka K, Sekeres MA, List A, Mustjoki S, Loughran TP, Maciejewski JP. STAT3 mutations unify the pathogenesis of chronic lymphoproliferative disorders of NK cells and T-cell large granular lymphocyte leukemia. Blood. 2012 Oct 11;120(15):3048-57. doi: 10.1182/blood-2012-06-435297. Epub 2012 Aug 2.
- Kane A, Deenick EK, Ma CS, Cook MC, Uzel G, Tangye SG. STAT3 is a central regulator of lymphocyte differentiation and function. Curr Opin Immunol. 2014 Jun;28:49-57. doi: 10.1016/j.coi.2014.01.015. Epub 2014 Mar 6.
- Levy DE, Loomis CA. STAT3 signaling and the hyper-IgE syndrome. N Engl J Med. 2007 Oct 18;357(16):1655-8. doi: 10.1056/NEJMe078197. Epub 2007 Sep 19. No abstract available.
- Milner JD, Vogel TP, Forbes L, Ma CA, Stray-Pedersen A, Niemela JE, Lyons JJ, Engelhardt KR, Zhang Y, Topcagic N, Roberson ED, Matthews H, Verbsky JW, Dasu T, Vargas-Hernandez A, Varghese N, McClain KL, Karam LB, Nahmod K, Makedonas G, Mace EM, Sorte HS, Perminow G, Rao VK, O'Connell MP, Price S, Su HC, Butrick M, McElwee J, Hughes JD, Willet J, Swan D, Xu Y, Santibanez-Koref M, Slowik V, Dinwiddie DL, Ciaccio CE, Saunders CJ, Septer S, Kingsmore SF, White AJ, Cant AJ, Hambleton S, Cooper MA. Early-onset lymphoproliferation and autoimmunity caused by germline STAT3 gain-of-function mutations. Blood. 2015 Jan 22;125(4):591-9. doi: 10.1182/blood-2014-09-602763. Epub 2014 Oct 30.
- Minegishi Y, Saito M, Tsuchiya S, Tsuge I, Takada H, Hara T, Kawamura N, Ariga T, Pasic S, Stojkovic O, Metin A, Karasuyama H. Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome. Nature. 2007 Aug 30;448(7157):1058-62. doi: 10.1038/nature06096. Epub 2007 Aug 5.
- Siegel AM, Stone KD, Cruse G, Lawrence MG, Olivera A, Jung MY, Barber JS, Freeman AF, Holland SM, O'Brien M, Jones N, Nelson CG, Wisch LB, Kong HH, Desai A, Farber O, Gilfillan AM, Rivera J, Milner JD. Diminished allergic disease in patients with STAT3 mutations reveals a role for STAT3 signaling in mast cell degranulation. J Allergy Clin Immunol. 2013 Dec;132(6):1388-96. doi: 10.1016/j.jaci.2013.08.045. Epub 2013 Nov 1.
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