Regulatory
hTERT

Part:BBa_K1925001

Designed by: Zi Yue Wang   Group: iGEM16_Fudan   (2016-10-08)


human Telomerase reverse transcriptase Promoter

Tihis is the promoter of human Telomerase reverse transcriptase,after which genes are expressed only in pluripotent cells and cancer cells theoretically.Using restriction enzymes to cut or PCR from biobrick,then putting it on the upstream of genes of interest is available ways to use the element.

Usage and Biology

Telomerase reverse transcriptase (abbreviated to TERT, or hTERT in humans) is a catalytic subunit of the enzyme telomerase, which, together with the telomerase RNA component (TERC), comprises the most important unit of the telomerase complex.

Telomerases are part of a distinct subgroup of RNA-dependent polymerases. Telomerase lengthens telomeres in DNA strands, thereby allowing senescent cells that would otherwise become postmitotic and undergo apoptosis to exceed the Hayflick limit and become potentially immortal, as is often the case with cancerous cells. To be specific, TERT is responsible for catalyzing the addition of nucleotides in a TTAGGG sequence to the ends of a chromosome’s telomeres. This addition of repetitive DNA sequences prevents degradation of the chromosomal ends following multiple rounds of replication.

hTERT absence (usually as a result of a chromosomal mutation) is associated with the disorder Cri du chat.

Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]



References

(1)Sharma S, Javadekar SM, Pandey M, Srivastava M, Kumari R, Raghavan SC (2015). "Homology and enzymatic requirements of microhomology-dependent alternative end joining". Cell Death Dis. 6: e1697. doi:10.1038/cddis.2015.58. PMC 4385936free to read. PMID 25789972. (2)Chen J, Miller BF, Furano AV (2014). "Repair of naturally occurring mismatches can induce mutations in flanking DNA". Elife. 3: e02001. doi:10.7554/elife.02001. PMC 3999860free to read. PMID 24843013. (3)Rodgers K, McVey M (2016). "Error-Prone Repair of DNA Double-Strand Breaks". J. Cell. Physiol. 231 (1): 15–24. doi:10.1002/jcp.25053. PMID 26033759. (4)Bertram, John S. (December 2000). "The molecular biology of cancer". Molecular Aspects of Medicine. Amsterdam, the Netherlands: Elsevier. 21 (6): 167–223. doi:10.1016/S0098-2997(00)00007-8. ISSN 0098-2997. PMID 11173079. (5)Aminetzach, Yael T.; Macpherson, J. Michael; Petrov, Dmitri A. (July 29, 2005). "Pesticide Resistance via Transposition-Mediated Adaptive Gene Truncation in Drosophila". Science. Washington, D.C.: American Association for the (6)Advancement of Science. 309 (5735): 764–767. Bibcode:2005Sci...309..764A. doi:10.1126/science.1112699. ISSN 0036-8075. PMID 16051794. (7)Burrus, Vincent; Waldor, Matthew K. (June 2004). "Shaping bacterial genomes with integrative and conjugative elements". Research in Microbiology. Amsterdam, the Netherlands: Elsevier. 155 (5): 376–386. doi:10.1016/j.resmic.2004.01.012. ISSN 0923-2508. PMID 15207870. (8)Sawyer, Stanley A.; Parsch, John; Zhi Zhang; et al. (April 17, 2007). "Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila". Proc. Natl. Acad. Sci. U.S.A. Washington, D.C.: National Academy of Sciences. 104 (16): 6504–6510. Bibcode:2007PNAS..104.6504S. doi:10.1073/pnas.0701572104. ISSN 0027-8424. PMC 1871816free to read. PMID 17409186. (9)Hastings, P. J.; Lupski, James R.; Rosenberg, Susan M.; et al. (August 2009). "Mechanisms of change in gene copy number". Nature Reviews Genetics. London: Nature Publishing Group. 10 (8): 551–564. doi:10.1038/nrg2593. ISSN 1471-0056. PMC 2864001free to read. PMID 19597530.

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Categories
//promoter
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