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Alain Laederach

Researcher at University of North Carolina at Chapel Hill

Publications -  95
Citations -  4724

Alain Laederach is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: RNA & Gene. The author has an hindex of 34, co-authored 88 publications receiving 4078 citations. Previous affiliations of Alain Laederach include New York State Department of Health & University of Neuchâtel.

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Modeling protein recognition of carbohydrates.

TL;DR: An atomic‐level view of carbohydrate recognition through structures of carbohydrate‐active enzymes complexed with transition‐state inhibitors reveals some of the distinctive molecular features unique to protein–carbohydrate complexes.
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Evaluating our ability to predict the structural disruption of RNA by SNPs

TL;DR: A large-scale meta-analysis of Selective 2'-Hydroxyl Acylation analyzed by Primer Extension data, which probes the structure of RNA found that several single point mutations exist that significantly disrupt RNA secondary structure in the five transcripts the authors analyzed.
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Specific empirical free energy function for automated docking of carbohydrates to proteins

TL;DR: The electrostatic empirical coefficient is larger than in a previously obtained model using a training set comprised of various types of protein–ligand complexes, indicating that electrostatic interactions play a more important role in determining the affinity between a carbohydrate and a protein.
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An RNA structure-mediated, posttranscriptional model of human α-1-antitrypsin expression

TL;DR: A series of structural and functional experiments are presented to derive a quantitative, structure-dependent model of translation that accurately predicts translation efficiency in reporter assays and primary human tissue for a complex and medically important protein, α-1-antitrypsin.
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Structural effects of linkage disequilibrium on the transcriptome

TL;DR: The data confirm that the FTL 5' UTR is a "RiboSNitch," an RNA that changes structure if a particular disease-associated SNP is present, and suggest that specific pairs of SNPs in high linkage disequilibrium (LD) will form RNA structure-stabilizing haplotypes (SSHs).