Reverzna transkriptaza telomeraze (TERT, ili hTERT kod ljudi) je katalitička podjedinica enzimatelomeraza, koja, zajedno sa telomeraznom RNK komponentom (TERC), sačinjava najvažniju jedinicu telomeraznog kompleksa.[1][2]
Telomeraze su deo distinktne podgrupe RNK-zavisnih polimeraza. Telomeraze produžavaju telomere u DNK lancima, čime omogućavaju starećim ćelijama koje bi postale postmitotičke i podlegle apoptozi da premaše Hejflikov limit i postanu potencijalno besmrtne, kao što je to često slučaj sa ćelijama raka. Specifično, TERT je odgovoran za katalizu adicije nukleotida u TTAGGG sequenci na krajevima hromozomskihtelomera.[3] Ova adicija ponavljajućih DNK sekvenci spečava degradaciju krajeva hromozoma nakon višestrukih ciklusa replikacije.[4]
↑Weinrich SL, Pruzan R, Ma L, Ouellette M, Tesmer VM, Holt SE, Bodnar AG, Lichtsteiner S, Kim NW, Trager JB, Taylor RD, Carlos R, Andrews WH, Wright WE, Shay JW, Harley CB, Morin GB (December 1997). „Reconstitution of human telomerase with the template RNA component hTR and the catalytic protein subunit hTRT”. Nat. Genet.17 (4): 498–502. DOI:10.1038/ng1297-498. PMID9398860.
↑Kirkpatrick KL, Mokbel K (2001). „The significance of human telomerase reverse transcriptase (hTERT) in cancer”. Eur J Surg Oncol27 (8): 754–60. DOI:10.1053/ejso.2001.1151. PMID11735173.
↑Poole JC, Andrews LG, Tollefsbol TO (May 2001). „Activity, function, and gene regulation of the catalytic subunit of telomerase (hTERT)”. Gene269 (1-2): 1–12. DOI:10.1016/S0378-1119(01)00440-1. PMID11376932.
↑Haendeler J, Hoffmann J, Rahman S, Zeiher AM, Dimmeler S (February 2003). „Regulation of telomerase activity and anti-apoptotic function by protein-protein interaction and phosphorylation”. FEBS Lett.536 (1-3): 180–6. DOI:10.1016/S0014-5793(03)00058-9. PMID12586360.
↑Kawauchi K, Ihjima K, Yamada O (May 2005). „IL-2 increases human telomerase reverse transcriptase activity transcriptionally and posttranslationally through phosphatidylinositol 3'-kinase/Akt, heat shock protein 90, and mammalian target of rapamycin in transformed NK cells”. J. Immunol.174 (9): 5261–9. DOI:10.4049/jimmunol.174.9.5261. PMID15843522.
↑ 9,09,1Chai W, Ford LP, Lenertz L, Wright WE, Shay JW (December 2002). „Human Ku70/80 associates physically with telomerase through interaction with hTERT”. J. Biol. Chem.277 (49): 47242–7. DOI:10.1074/jbc.M208542200. PMID12377759.
↑Song H, Li Y, Chen G, Xing Z, Zhao J, Yokoyama KK, Li T, Zhao M (April 2004). „Human MCRS2, a cell-cycle-dependent protein, associates with LPTS/PinX1 and reduces the telomere length”. Biochem. Biophys. Res. Commun.316 (4): 1116–23. DOI:10.1016/j.bbrc.2004.02.166. PMID15044100.
↑Khurts S, Masutomi K, Delgermaa L, Arai K, Oishi N, Mizuno H, Hayashi N, Hahn WC, Murakami S (December 2004). „Nucleolin interacts with telomerase”. J. Biol. Chem.279 (49): 51508–15. DOI:10.1074/jbc.M407643200. PMID15371412.
Mattson MP, Fu W, Zhang P (2001). „Emerging roles for telomerase in regulating cell differentiation and survival: a neuroscientist's perspective”. Mech. Ageing Dev.122 (7): 659–71. DOI:10.1016/S0047-6374(01)00221-4. PMID11322991.
Castillo Ureta H, Barrera Saldaña HA, Martínez Rodríguez HG (2003). „[Telomerase: an enzyme with multiple applications in cancer research]”. Rev. Invest. Clin.54 (4): 342–8. PMID12415959.
Beliveau A, Yaswen P (2007). „Soothing the watchman: telomerase reduces the p53-dependent cellular stress response”. Cell Cycle6 (11): 1284–7. DOI:10.4161/cc.6.11.4298. PMID17534147.
Bellon M, Nicot C (2007). „Telomerase: a crucial player in HTLV-I-induced human T-cell leukemia”. Cancer genomics & proteomics4 (1): 21–5. PMID17726237.