Literature DB >> 32416578

iPSC reprogramming of fibroblasts from a patient with a Rothmund-Thomson syndrome RTS.

Vincent Gatinois1, Romain Desprat2, Lydiane Pichard3, Fabienne Becker2, Alice Goldenberg4, Xavier Balguerie5, Franck Pellestor6, Jean-Marc Lemaitre7.   

Abstract

Rothmund-Thomson Syndrome (RTS) is a rare autosomal recessive disease that manifests several clinical features of accelerated aging. These findings include atrophic skin and pigment changes, alopecia, osteopenia, cataracts, and an increased incidence of cancer for patients. Mutations in RECQL4 gene are responsible for cases of RTS. RECQL4 belongs to the RECQ DNA helicase family which has been shown to participate in many aspects of DNA metabolism. To be able to study the cellular defects related to the pathology, we derived an induced pluripotent cell line from RTS patient fibroblasts, with the ability to re-differentiate into the three embryonic germ layers.
Copyright © 2020. Published by Elsevier B.V.

Entities:  

Mesh:

Year:  2020        PMID: 32416578     DOI: 10.1016/j.scr.2020.101807

Source DB:  PubMed          Journal:  Stem Cell Res        ISSN: 1873-5061            Impact factor:   2.020


  2 in total

Review 1.  Molecular Mechanisms of the RECQ4 Pathogenic Mutations.

Authors:  Xiaohua Xu; Chou-Wei Chang; Min Li; Chao Liu; Yilun Liu
Journal:  Front Mol Biosci       Date:  2021-11-18

2.  Case Report: Diverse phenotypes of congenital poikiloderma associated with FAM111B mutations in codon 628: A case report and literature review.

Authors:  Yuhao Wu; Long Wen; Peiru Wang; Xiuli Wang; Guolong Zhang
Journal:  Front Genet       Date:  2022-08-25       Impact factor: 4.772

  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.