Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA. - Wikidata - awgldk - TriplyDB

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

http://www.wikidata.org/entity/Q41960596

about

Neuronal Elav-like (Hu) proteins regulate RNA splicing and abundance to control glutamate levels and neuronal excitability.Alternative splicing of the neurofibromatosis type I pre-mRNA Regulation of alternative splicing by local histone modifications: potential roles for RNA-guided mechanisms RNA protein interaction in neurons T-cell intracellular antigens in health and disease Binding of hnRNP H and U2AF65 to respective G-codes and a poly-uridine tract collaborate in the N50-5'ss selection of the REST N exon in H69 cells Mechanisms of alternative splicing regulation: insights from molecular and genomics approaches Regulation of protein stability by GSK3 mediated phosphorylation.Intracellular localization and interaction of mRNA binding proteins as detected by FRET.A computational screen for site selective A-to-I editing detects novel sites in neuron specific Hu proteins.The neurofibromatosis type I pre-mRNA is a novel target of CELF protein-mediated splicing regulation.iCLIP predicts the dual splicing effects of TIA-RNA interactions.Neurofibromatosis type 1 alternative splicing is a key regulator of Ras signaling in neurons Promiscuity in post-transcriptional control of gene expression: Drosophila sex-lethal and its regulatory partnerships Promotion of exon 6 inclusion in HuD pre-mRNA by Hu protein family members Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related/like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R.Alternative splicing of the neurofibromatosis type 1 pre-mRNA is regulated by the muscleblind-like proteins and the CUG-BP and ELAV-like factors A biophysical model for identifying splicing regulatory elements and their interactions.Post-transcriptional regulation of programmed cell death 4 (PDCD4) mRNA by the RNA-binding proteins human antigen R (HuR) and T-cell intracellular antigen 1 (TIA1)Hu proteins regulate alternative splicing by inducing localized histone hyperacetylation in an RNA-dependent manner.ELAV-mediated 3'-end processing of ewg transcripts is evolutionarily conserved despite sequence degeneration of the ELAV-binding site.T-cell intracellular antigens function as tumor suppressor genes.Characterization of conserved tandem donor sites and intronic motifs required for alternative splicing in corticosteroid receptor genes Three RNA recognition motifs participate in RNA recognition and structural organization by the pro-apoptotic factor TIA-1.Concentration and Localization of Coexpressed ELAV/Hu Proteins Control Specificity of mRNA Processing.All three RNA recognition motifs and the hinge region of HuC play distinct roles in the regulation of alternative splicing.Diverse molecular functions of Hu proteins.HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA.Neuronal ELAVL proteins utilize AUF-1 as a co-partner to induce neuron-specific alternative splicing of APP Trans-acting factors governing acetylcholinesterase mRNA metabolism in neurons.Emerging complexity of the HuD/ELAVl4 gene; implications for neuronal development, function, and dysfunction RNA-binding proteins in neurological diseases.Effect of histone modifications on hMLH1 alternative splicing in gastric cancer.Protein methylation and stress granules: posttranslational remodeler or innocent bystander?HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress.Neurofibromin 1 is a miRNA target in neurons.Post-transcriptional control of CCAAT/enhancer-binding protein beta (C/EBPbeta) expression: formation of a nuclear HuR-C/EBPbeta mRNA complex determines the amount of message reaching the cytosol.T-Cell Intracellular Antigens and Hu Antigen R Antagonistically Modulate Mitochondrial Activity and Dynamics by Regulating Optic Atrophy 1 Gene Expression.Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition.Neuron-specific alternative splicing of transcriptional machineries: Implications for neurodevelopmental disorders.

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P2860

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

http://www.wikidata.org/entity/Q41960596

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

@en

type

label

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

@en

prefLabel

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

@en

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Molecular and Cellular Biology

P1476

Regulation of neuron-specific alternative splicing of neurofibromatosis type 1 pre-mRNA.

@en

P2093

Hua Lou

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

Hui Zhu

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

Melissa N Hinman

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Priyesh Mehta

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Robert A Hasman

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P2860

The apoptosis-promoting factor TIA-1 is a regulator of alternative pre-mRNA splicing

Function of quaking in myelination: regulation of alternative splicing.

Homologues of the Caenorhabditis elegans Fox-1 protein are neuronal splicing regulators in mammals

Cooperative assembly of an hnRNP complex induced by a tissue-specific homolog of polypyrimidine tract binding protein

Nova regulates GABA(A) receptor gamma2 alternative splicing via a distal downstream UCAU-rich intronic splicing enhancer

U1 snRNP-dependent function of TIAR in the regulation of alternative RNA processing of the human calcitonin/CGRP pre-mRNA

A combinatorial code for splicing silencing: UAGG and GGGG motifs

CLIP identifies Nova-regulated RNA networks in the brain

NF1 tumor suppressor gene function: narrowing the GAP

TIA-1 and TIAR activate splicing of alternative exons with weak 5' splice sites followed by a U-rich stretch on their own pre-mRNAs

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1240-1251

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scholarly article

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10.1128/MCB.01509-07

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4

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28

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18086893

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2258745

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