Intellectual disability and abnormal cortical neuron phenotypes in patients with Bloom syndrome
Author:
Funder
the Health and Labor Sciences Research Grants for Research on Measures for Intractable Diseases of the Ministry of Health, Labour and Welfare.
Publisher
Springer Science and Business Media LLC
Subject
Genetics (clinical),Genetics
Link
https://www.nature.com/articles/s10038-023-01121-9.pdf
Reference29 articles.
1. Ellis NA, Groden J, Ye TZ, Straughen J, Lennon DJ, Ciocci S, et al. The Bloom’s syndrome gene product is homologous to RecQ helicases. Cell. 1995;83:655–66.
2. Chaganti RS, Schonberg S, German J. A manyfold increase in sister chromatid exchanges in Bloom’s syndrome lymphocytes. Proc Natl Acad Sci USA. 1974;71:4508–12.
3. McDaniel LD, Schultz RA. Elevated sister chromatid exchange phenotype of Bloom syndrome cells is complemented by human chromosome 15. Proc Natl Acad Sci USA. 1992;89:7968–72.
4. Raynard S, Bussen W, Sung P. A double Holliday junction dissolvasome comprising BLM, topoisomerase IIIα, and BLAP75. J Biol Chem. 2006;281:13861–4.
5. Yin J, Sobeck A, Xu C, Meetei AR, Hoatlin M, Li L, et al. BLAP75, an essential component of Bloom’s syndrome protein complexes that maintain genome integrity. EMBO J. 2005;24:1465i1476.
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