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Exonic splicing silencer
An Exonic Splicing Silencer Is Involved in the Regulated Splicing of Glucose 6-Phosphate Dehydrogenase Mrna Wioletta Szeszel-Fedorowicz
In Silico Tools for Splicing Defect Prediction: a Survey from the Viewpoint of End Users
Position-Dependent Splicing Activation and Repression by SR and Hnrnp Proteins Rely on Common Mechanisms
Determinants of Exon 7 Splicing in the Spinal Muscular Atrophy Genes, SMN1 and SMN2 Luca Cartegni,*,† Michelle L
HIV-1: to Splice Or Not to Splice, That Is the Question
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Systematic Identification and Analysis of Exonic Splicing Silencers
Progress in Therapeutic Antisense Applications for Neuromuscular Disorders
Using Positional Distribution to Identify Splicing Elements and Predict Pre-Mrna Processing Defects in Human Genes
Alternative Splicing
Perspective in Alternative Splicing Coupled to Nonsense-Mediated Mrna Decay
Finding Signals That Regulate Alternative Splicing in the Post- Comment Genomic Era Andrea N Ladd and Thomas a Cooper
Snapshot: Formation of Mrnps Megan Bergkessel, Gwendolyn M
Downloaded from Classification Method Theucscgenomebrowser[45]
Position-Dependent Splicing Activation and Repression by SR and Hnrnp Proteins Rely on Common Mechanisms
Mechanism of Splicing Regulation of Spinal Muscular Atrophy Genes
Splicing of Designer Exons Reveals Unexpected Complexity in Pre-Mrna Splicing
Splice Sites and the Problems of Too Many Choices
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Evidence for the Function of an Exonic Splicing Enhancer After the First Catalytic Step of Pre-Mrna Splicing
Alternative Splicing and Its Regulation Under Normal and Abnormal Conditions
Alternative Splicing Role in New Therapies of Spinal Muscular Atrophy
Splicing of Designer Exons Informs a Biophysical Model for Exon Definition
A Simple Answer for a Splicing Conundrum
GGGG Motifs Intron 3 Splicing by DQB1 Promotion of Position
An Intronic Element Contributes to Splicing Repression in Spinal Muscular Atrophy
SMN2 Exon 7 Splicing Is Inhibited by Binding of Hnrnp A1 to a Common
RNA-Binding Proteins in Neurodegeneration: Mechanisms in Aggregate
Exon Identity Crisis: Disease-Causing Mutations That Disrupt the Splicing Code Timothy Sterne-Weiler1 and Jeremy R Sanford2*
Rahman MA, Nasrin F, Masuda A, Et Al. Decoding Abnormal Splicing Code in Human Diseases
An Intronic Element Contributes to Splicing Repression in Spinal Muscular Atrophy
An Alu-Derived Intronic Splicing Enhancer Facilitates Intronic
TALKING POINT Exonic Splicing Enhancers