CYREN (protein): Difference between revisions
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''' | '''Cell cycle regulator of non-homologous end joining''' is a [[protein]] that in humans is encoded by the '''CYREN''' [[gene]]. | ||
==References== | It prevents classical [[non-homologous end joining]], a method of repair of double-stranded DNA breaks.<ref>{{cite journal | vauthors = Arnoult N, Correia A, Ma J, Merlo A, Garcia-Gomez S, Maric M, Tognetti M, Benner CW, Boulton SJ, Saghatelian A, Karlseder J | title = Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN | journal = Nature | volume = 549 | issue = 7673 | pages = 548–552 | date = September 2017 | pmid = 28959974 | doi = 10.1038/nature24023 }}</ref> This protein is therefore important in regulating [[DNA repair]]. | ||
When alternatively spliced, is predicted to produce three different [[micropeptides]].<ref name="Slavoff_2014">{{cite journal | vauthors = Slavoff SA, Heo J, Budnik BA, Hanakahi LA, Saghatelian A | title = A human short open reading frame (sORF)-encoded polypeptide that stimulates DNA end joining | journal = The Journal of Biological Chemistry | volume = 289 | issue = 16 | pages = 10950–7 | date = April 2014 | pmid = 24610814 | doi = 10.1074/jbc.c113.533968 }}</ref> | |||
* MRI-1 was previously found to be a modulator of retrovirus infection.<ref name="Slavoff_2014" /> | |||
* MRI-2 may be important in [[non-homologous end joining]] (NHEJ) of DNA double strand breaks. In Co-Immunoprecipitation experiments, MRI-2 bound to [[Ku70]] and [[Ku80]], two subunits of [[Ku (protein)|Ku]], which play a major role in the NHEJ pathway.<ref name="Slavoff_2014" /> | |||
*MRI-3 | |||
== References == | |||
{{reflist}} | {{reflist}} | ||
[[Category:DNA repair]] | [[Category:DNA repair]] | ||
{{Protein-stub}} | {{Protein-stub}} | ||
Latest revision as of 05:16, 18 January 2019
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Cell cycle regulator of non-homologous end joining is a protein that in humans is encoded by the CYREN gene.
It prevents classical non-homologous end joining, a method of repair of double-stranded DNA breaks.[1] This protein is therefore important in regulating DNA repair.
When alternatively spliced, is predicted to produce three different micropeptides.[2]
- MRI-1 was previously found to be a modulator of retrovirus infection.[2]
- MRI-2 may be important in non-homologous end joining (NHEJ) of DNA double strand breaks. In Co-Immunoprecipitation experiments, MRI-2 bound to Ku70 and Ku80, two subunits of Ku, which play a major role in the NHEJ pathway.[2]
- MRI-3
References
- ↑ Arnoult N, Correia A, Ma J, Merlo A, Garcia-Gomez S, Maric M, Tognetti M, Benner CW, Boulton SJ, Saghatelian A, Karlseder J (September 2017). "Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN". Nature. 549 (7673): 548–552. doi:10.1038/nature24023. PMID 28959974.
- ↑ 2.0 2.1 2.2 Slavoff SA, Heo J, Budnik BA, Hanakahi LA, Saghatelian A (April 2014). "A human short open reading frame (sORF)-encoded polypeptide that stimulates DNA end joining". The Journal of Biological Chemistry. 289 (16): 10950–7. doi:10.1074/jbc.c113.533968. PMID 24610814.
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