Unión de extremos mediada por microhomoloxía: Diferenzas entre revisións

Contido eliminado Contido engadido
Miguelferig (conversa | contribucións)
Sen resumo de edición
Miguelferig (conversa | contribucións)
Liña 9:
 
== Xenes necesarios para a MMEJ ==
<!--
A biochemical assay system shows that at least 6 genes are required for microhomology-mediated end joining: [[FEN1]], [[LIG3|Ligase III]], [[MRE11A|MRE11]], [[Nibrin|NBS1]], [[PARP1]] and [[XRCC1]].<ref name="pmid25789972">{{cite journal |vauthors=Sharma S, Javadekar SM, Pandey M, Srivastava M, Kumari R, Raghavan SC |title=Homology and enzymatic requirements of microhomology-dependent alternative end joining |journal=Cell Death Dis |volume=6 |issue= |pages=e1697 |year=2015 |pmid=25789972 |doi=10.1038/cddis.2015.58 |url= |pmc=4385936}}</ref> All six of these genes are up-regulated in one or more cancers.
 
AUn biochemicalsistema assayde systemensaio showsbioquímico thatatopou atque leastpolo menos son necesarios 6 genesxenes arepara requireda forunión microhomology-mediatedde endextremos joiningmediada por microhomoloxía, que son: [[FEN1]], [[LIG3|Ligase III]], [[MRE11A|MRE11]], [[NibrinNibrina|NBS1]], [[PARP1]] ande [[XRCC1]].<ref name="pmid25789972">{{cite journal |vauthors=Sharma S, Javadekar SM, Pandey M, Srivastava M, Kumari R, Raghavan SC |title=Homology and enzymatic requirements of microhomology-dependent alternative end joining |journal=Cell Death Dis |volume=6 |issue= |pages=e1697 |year=2015 |pmid=25789972 |doi=10.1038/cddis.2015.58 |url= |pmc=4385936}}</ref> Todos Alleles sixestán ofregulados theseá genesnun areou up-regulatedmáis intipos onede or more cancers[[cancro]]s.
== MMEJ no cancro ==
 
== A MMEJ no cancro ==
<!--
[[FEN1]] is over-expressed in the majority of cancers of the breast,<ref name=Singh>{{cite journal |vauthors=Singh P, Yang M, Dai H, Yu D, Huang Q, Tan W, Kernstine KH, Lin D, Shen B |title=Overexpression and hypomethylation of flap endonuclease 1 gene in breast and other cancers |journal=Mol. Cancer Res. |volume=6 |issue=11 |pages=1710–7 |year=2008 |pmid=19010819 |pmc=2948671 |doi=10.1158/1541-7786.MCR-08-0269 |url=}}</ref> prostate,<ref name="pmid16879693">{{cite journal |vauthors=Lam JS, Seligson DB, Yu H, Li A, Eeva M, Pantuck AJ, Zeng G, Horvath S, Belldegrun AS |title=Flap endonuclease 1 is overexpressed in prostate cancer and is associated with a high Gleason score |journal=BJU Int. |volume=98 |issue=2 |pages=445–51 |year=2006 |pmid=16879693 |doi=10.1111/j.1464-410X.2006.06224.x |url=}}</ref> stomach,<ref name="pmid15701830">{{cite journal |vauthors=Kim JM, Sohn HY, Yoon SY, Oh JH, Yang JO, Kim JH, Song KS, Rho SM, Yoo HS, Yoo HS, Kim YS, Kim JG, Kim NS |title=Identification of gastric cancer-related genes using a cDNA microarray containing novel expressed sequence tags expressed in gastric cancer cells |journal=Clin. Cancer Res. |volume=11 |issue=2 Pt 1 |pages=473–82 |year=2005 |pmid=15701830 |doi= |url=}}</ref><ref name="pmid24590400">{{cite journal |vauthors=Wang K, Xie C, Chen D |title=Flap endonuclease 1 is a promising candidate biomarker in gastric cancer and is involved in cell proliferation and apoptosis |journal=Int. J. Mol. Med. |volume=33 |issue=5 |pages=1268–74 |year=2014 |pmid=24590400 |doi=10.3892/ijmm.2014.1682 |url=}}</ref> neuroblastomas,<ref name="pmid15922863">{{cite journal |vauthors=Krause A, Combaret V, Iacono I, Lacroix B, Compagnon C, Bergeron C, Valsesia-Wittmann S, Leissner P, Mougin B, Puisieux A |title=Genome-wide analysis of gene expression in neuroblastomas detected by mass screening |journal=Cancer Lett. |volume=225 |issue=1 |pages=111–20 |year=2005 |pmid=15922863 |doi=10.1016/j.canlet.2004.10.035 |url=}}</ref> pancreatic,<ref name="pmid12651607">{{cite journal |vauthors=Iacobuzio-Donahue CA, Maitra A, Olsen M, Lowe AW, van Heek NT, Rosty C, Walter K, Sato N, Parker A, Ashfaq R, Jaffee E, Ryu B, Jones J, Eshleman JR, Yeo CJ, Cameron JL, Kern SE, Hruban RH, Brown PO, Goggins M |title=Exploration of global gene expression patterns in pancreatic adenocarcinoma using cDNA microarrays |journal=Am. J. Pathol. |volume=162 |issue=4 |pages=1151–62 |year=2003 |pmid=12651607 |pmc=1851213 |doi=10.1016/S0002-9440(10)63911-9 |url=}}</ref> and lung.<ref name="pmid19596913">{{cite journal |vauthors=Nikolova T, Christmann M, Kaina B |title=FEN1 is overexpressed in testis, lung and brain tumors |journal=Anticancer Res. |volume=29 |issue=7 |pages=2453–9 |year=2009 |pmid=19596913 |doi= |url=}}</ref>
 
Liña 29 ⟶ 30:
Cancers are very often deficient in expression of one or more DNA repair genes, but over-expression of a DNA repair gene is less usual in cancer. For instance, at least 36 DNA repair enzymes, when mutationally defective in germ line cells, cause increased risk of cancer (hereditary [[cancer syndrome]]s).<ref name=Bernstein>Bernstein C, Prasad AR, Nfonsam V, Bernstein H. (2013). DNA Damage, DNA Repair and Cancer, New Research Directions in DNA Repair, Prof. Clark Chen (Ed.), ISBN 978-953-51-1114-6, InTech, http://www.intechopen.com/books/new-research-directions-in-dna-repair/dna-damage-dna-repair-and-cancer</ref> (Also see [[DNA repair-deficiency disorder]].) Similarly, at least 12 DNA repair genes have frequently been found to be epigenetically repressed in one or more cancers.<ref name=Bernstein /> (See also [[DNA repair#Frequencies of epimutations in DNA repair genes|Epigenetically reduced DNA repair and cancer]].) Ordinarily, deficient expression of a DNA repair enzyme results in increased un-repaired DNA damages which, through replication errors ([[DNA repair#Translesion synthesis|translesion synthesis]]), lead to mutations and cancer. However, FEN1, Ligase III, MRE1, PARP1, NBS1 and XRCC1 mediated MMEJ repair is highly inaccurate, so in these cases, over-expression, rather than under-expression, leads to cancer. This is supported by the observation that reduction of mutagenic XRCC1 mediated MMEJ repair leads to reduced progression of cancer.<ref name=Pettan-Brewer />
-->
 
== Notas ==
{{Listaref}}