Correction of Glycogen Synthase Kinase 3β in Myotonic Dystrophy 1 Reduces the Mutant RNA and Improves Postnatal Survival of DMSXL Mice | Zendy

Mei Wang | Zendy; WenChin Weng | Zendy; Lauren Stock | Zendy; Diana M. Lindquist | Zendy; Ana Martı́nez | Zendy; Geneviève Gourdon | Zendy; Nikolai A. Timchenko | Zendy; Mike Snape | Zendy; Lubov Timchenko | Zendy

Open Access

Correction of Glycogen Synthase Kinase 3β in Myotonic Dystrophy 1 Reduces the Mutant RNA and Improves Postnatal Survival of DMSXL Mice

Author(s) -

Mei Wang,

WenChin Weng,

Lauren Stock,

Diana M. Lindquist,

Ana Martı́nez,

Geneviève Gourdon,

Nikolai A. Timchenko,

Mike Snape,

Lubov Timchenko

Publication year - 2019

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.00155-19

Subject(s) - myotonic dystrophy , biology , gsk 3 , gsk3b , rna , glycogen synthase , endocrinology , kinase , mutation , messenger rna , medicine , microbiology and biotechnology , cancer research , glycogen , gene , genetics

Myotonic dystrophy type 1 (DM1) is a multisystem neuromuscular disease without cure. One of the possible therapeutic approaches for DM1 is correction of the RNA-binding proteins CUGBP1 and MBNL1, misregulated in DM1. CUGBP1 activity is controlled by glycogen synthase kinase 3β (GSK3β), which is elevated in skeletal muscle of patients with DM1, and inhibitors of GSK3 were suggested as therapeutic molecules to correct CUGBP1 activity in DM1.

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