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2024 | 1 |
PubMed (GeneRIF) for id: 75828
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The N-terminal modification of HORMAD2 causes its ectopic persistence on synapsed chromosomes without meiotic blockade.
Reproduction. 2024 Mar 13;167(4):e230330. doi: 10.1530/REP-23-0330. Print 2024 Apr 1.
Reproduction. 2024.
PMID: 38401263
HORMAD2 is essential for synapsis surveillance during meiotic prophase via the recruitment of ATR activity.
Kogo H, Tsutsumi M, Inagaki H, Ohye T, Kiyonari H, Kurahashi H.
Kogo H, et al.
Genes Cells. 2012 Nov;17(11):897-912. doi: 10.1111/gtc.12005. Epub 2012 Oct 8.
Genes Cells. 2012.
PMID: 23039116
Free article.
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Meiotic DNA double-strand breaks and chromosome asynapsis in mice are monitored by distinct HORMAD2-independent and -dependent mechanisms.
Wojtasz L, Cloutier JM, Baumann M, Daniel K, Varga J, Fu J, Anastassiadis K, Stewart AF, Reményi A, Turner JM, Tóth A.
Wojtasz L, et al.
Genes Dev. 2012 May 1;26(9):958-73. doi: 10.1101/gad.187559.112.
Genes Dev. 2012.
PMID: 22549958
Free PMC article.
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Mouse HORMAD1 and HORMAD2, two conserved meiotic chromosomal proteins, are depleted from synapsed chromosome axes with the help of TRIP13 AAA-ATPase.
Wojtasz L, Daniel K, Roig I, Bolcun-Filas E, Xu H, Boonsanay V, Eckmann CR, Cooke HJ, Jasin M, Keeney S, McKay MJ, Toth A.
Wojtasz L, et al.
PLoS Genet. 2009 Oct;5(10):e1000702. doi: 10.1371/journal.pgen.1000702. Epub 2009 Oct 23.
PLoS Genet. 2009.
PMID: 19851446
Free PMC article.
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