Molecular basis for impaired muscle differentiation in myotonic dystrophy - Test2 - elhamkhani - TriplyDB

Molecular basis for impaired muscle differentiation in myotonic dystrophy

Molecular basis for impaired muscle differentiation in myotonic dystrophy

http://www.wikidata.org/entity/Q24548314

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Competition of CUGBP1 and calreticulin for the regulation of p21 translation determines cell fate.CELF6, a member of the CELF family of RNA-binding proteins, regulates muscle-specific splicing enhancer-dependent alternative splicing Calreticulin interacts with C/EBPalpha and C/EBPbeta mRNAs and represses translation of C/EBP proteins Identification of CUG-BP1/EDEN-BP target mRNAs in Xenopus tropicalis Elevation of RNA-binding protein CUGBP1 is an early event in an inducible heart-specific mouse model of myotonic dystrophy CUG-BP1/CELF1 requires UGU-rich sequences for high-affinity binding HnRNP H inhibits nuclear export of mRNA containing expanded CUG repeats and a distal branch point sequence.Muscle wasting in myotonic dystrophies: a model of premature aging The importance of CELF control: molecular and biological roles of the CUG-BP, Elav-like family of RNA-binding proteins Structural Insights into RNA Recognition by the Alternate-Splicing Regulator CUG-Binding Protein 1 The p53 circuit board Inactivation of CUG-BP1/CELF1 causes growth, viability, and spermatogenesis defects in mice Endogenous DUX4 expression in FSHD myotubes is sufficient to cause cell death and disrupts RNA splicing and cell migration pathways The RNA-binding protein Staufen1 is increased in DM1 skeletal muscle and promotes alternative pre-mRNA splicing RNA toxicity in myotonic muscular dystrophy induces NKX2-5 expression.Woodchuck post-transcriptional element induces nuclear export of myotonic dystrophy 3' untranslated region transcripts.Functional KCa1.1 channels are crucial for regulating the proliferation, migration and differentiation of human primary skeletal myoblasts Myotonic dystrophies 1 and 2: complex diseases with complex mechanisms.Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy.Expression of a dominant negative CELF protein in vivo leads to altered muscle organization, fiber size, and subtype.p21(WAF1/CIP1) upregulation through the stress granule-associated protein CUGBP1 confers resistance to bortezomib-mediated apoptosis.Myoblasts from affected and non-affected FSHD muscles exhibit morphological differentiation defects Mouse models of the fragile X premutation and fragile X-associated tremor/ataxia syndrome Congenital fiber type disproportion--30 years on.An analysis of the sequence requirements of EDEN-BP for specific RNA binding.Differences in aberrant expression and splicing of sarcomeric proteins in the myotonic dystrophies DM1 and DM2.Expansion of CUG RNA repeats causes stress and inhibition of translation in myotonic dystrophy 1 (DM1) cells Smaug/SAMD4A restores translational activity of CUGBP1 and suppresses CUG-induced myopathy.High-content screening identifies small molecules that remove nuclear foci, affect MBNL distribution and CELF1 protein levels via a PKC-independent pathway in myotonic dystrophy cell lines.FHL1 reduces dystrophy in transgenic mice overexpressing FSHD muscular dystrophy region gene 1 (FRG1).The Drosophila Bruno paralogue Bru-3 specifically binds the EDEN translational repression element.RNA Foci, CUGBP1, and ZNF9 are the primary targets of the mutant CUG and CCUG repeats expanded in myotonic dystrophies type 1 and type 2 Identification of Targets of CUG-BP, Elav-Like Family Member 1 (CELF1) Regulation in Embryonic Heart Muscle.Mutant DMPK 3'-UTR transcripts disrupt C2C12 myogenic differentiation by compromising MyoD.GSK3β mediates muscle pathology in myotonic dystrophy Pentamidine rescues contractility and rhythmicity in a Drosophila model of myotonic dystrophy heart dysfunction.Misregulation of alternative splicing causes pathogenesis in myotonic dystrophy.miR-30-5p Regulates Muscle Differentiation and Alternative Splicing of Muscle-Related Genes by Targeting MBNL.Reduction of the rate of protein translation in patients with myotonic dystrophy 2 CELFish ways to modulate mRNA decay.

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Molecular basis for impaired muscle differentiation in myotonic dystrophy

http://www.wikidata.org/entity/Q24548314

description

2001 nî lūn-bûn

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2001 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2001 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2001年の論文

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2001年論文

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2001年論文

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2001年論文

@zh-hk

2001年論文

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2001年論文

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2001年论文

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name

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@ast

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@en

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@nl

type

label

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@ast

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@en

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@nl

prefLabel

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@ast

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@en

Molecular basis for impaired muscle differentiation in myotonic dystrophy

@nl

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MCB.21.20.6927-6938.2001

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Molecular and Cellular Biology

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Molecular basis for impaired muscle differentiation in myotonic dystrophy

@en

P2093

J R Smith

http://www.w3.org/2001/XMLSchema#string

L T Timchenko

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N A Timchenko

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P Iakova

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Z J Cai

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P2860

Cardiac elav-type RNA-binding protein (ETR-3) binds to RNA CUG repeats expanded in myotonic dystrophy

A family of human RNA-binding proteins related to the Drosophila Bruno translational regulator

Recruitment of human muscleblind proteins to (CUG)(n) expansions associated with myotonic dystrophy

Identification of a (CUG)n triplet repeat RNA-binding protein and its expression in myotonic dystrophy

CUG repeat binding protein (CUGBP1) interacts with the 5' region of C/EBPbeta mRNA and regulates translation of C/EBPbeta isoforms

HuR regulates p21 mRNA stabilization by UV light

Altered phosphorylation and intracellular distribution of a (CUG)n triplet repeat RNA-binding protein in patients with myotonic dystrophy and in myotonin protein kinase knockout mice

RNA CUG repeats sequester CUGBP1 and alter protein levels and activity of CUGBP1

Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4

The regulation of E2F by pRB-family proteins

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10.1128/MCB.21.20.6927-6938.2001

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11564876

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