2019
DOI: 10.20944/preprints201911.0292.v1
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Generation of a Mouse Model Lacking the Non-Homologous End-Joining Factor Mri/Cyren

Abstract: Classical non-homologous end joining (NHEJ) is a molecular pathway that detects, processes and ligates DNA double-strand breaks (DSBs) throughout the cell cycle. Mutations in several NHEJ genes result in neurological abnormalities and immunodeficiency both in humans and mice. The NHEJ pathway is required for the V(D)J recombination in developing B and T lymphocytes, and for class switch recombination in mature B cells. Ku heterodimer formed by Ku70 and Ku80 recognizes DSBs and facilitates the recruitment of ac… Show more

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Cited by 16 publications
(29 citation statements)
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“…Recent findings by our and other research groups suggest that MRI forms heterogeneous complexes involving PAXX or XLF, which function during DNA DSB repair by NHEJ [5]. Furthermore, genetic inactivation of Xlf [11], Paxx [4,[14][15][16], or Mri [5,18] in mice leads to development of modest or no detectable phenotype. However, combined inactivation of Xlf and Mri [5] or Xlf and Paxx [4,14,15] Previously, we showed that mice lacking XLF, PAXX and p53 were live-born and had nearly no B and T cells, reduced size of spleen and hardly detectable thymus [20] ( Figure 5).…”
Section: Discussionmentioning
confidence: 78%
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“…Recent findings by our and other research groups suggest that MRI forms heterogeneous complexes involving PAXX or XLF, which function during DNA DSB repair by NHEJ [5]. Furthermore, genetic inactivation of Xlf [11], Paxx [4,[14][15][16], or Mri [5,18] in mice leads to development of modest or no detectable phenotype. However, combined inactivation of Xlf and Mri [5] or Xlf and Paxx [4,14,15] Previously, we showed that mice lacking XLF, PAXX and p53 were live-born and had nearly no B and T cells, reduced size of spleen and hardly detectable thymus [20] ( Figure 5).…”
Section: Discussionmentioning
confidence: 78%
“…Combined inactivation of Xlf and Mri has previously been shown to result in synthetic lethality in mice [5]. To generate XLF/MRI deficient mice with altered expression of Trp53, we intercrossed an Mri -/strain [18] with an Xlf -/-Trp53 +/- [20] strain. Next, we selected and intercrossed triple heterozygous (Xlf +/-Mri +/-Trp53 +/-), and later, Xlf -/-Mri +/-Trp53 +/mice.…”
Section: Inactivation Of Trp53 Gene Rescued Embryonic Lethality In MImentioning
confidence: 99%
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