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Rüdiger Göke

Researcher at University of Marburg

Publications -  96
Citations -  7289

Rüdiger Göke is an academic researcher from University of Marburg. The author has contributed to research in topics: Receptor & Insulin. The author has an hindex of 39, co-authored 95 publications receiving 7056 citations. Previous affiliations of Rüdiger Göke include University of Göttingen & University of Michigan.

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Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma.

TL;DR: The molecular cloning of a cDNA for the GIP‐receptor from a human insulinoma λgt11 cDNA library showed high homology to the human glucagon‐like peptide 1 (GLP‐1) receptor which will aid in the understanding of incretin hormone's failure to exert its biological action at the pancreatic B‐cell in type II diabetes mellitus.
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DUG is a novel homologue of translation initiation factor 4G that binds eIF4A.

TL;DR: DUG is a novel homologous to eukaryotic translation initiation factor (eIF) 4G and binds to eIF4A presumably through MA3 domains and inhibits both intrinsic and extrinsic pathways of apoptosis.
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Glucose-dependency of the insulin stimulatory effect of glucagon-like peptide-1 (7-36) amide on the rat pancreas.

TL;DR: A slight but not dose-dependent stimulation of insulin secretion by supramaximal GLP-1 loads under basal glucose levels was found, but the necessary GLp-1 concentrations to achieve this in vitro effect are beyond physiological or postprandial levels.
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Pdcd4 inhibits growth of tumor cells by suppression of carbonic anhydrase type II

TL;DR: The translation inhibitor pdcd4 represses endocrine tumor cell growth by suppression of carbonic anhydase II, and might represent promising tools for anti-endocrine tumor treatment.
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Molecular cloning of a cDNA encoding for the GLP-1 receptor expressed in rat lung.

TL;DR: It is concluded that tissue-specificity for GLP-1 receptors is based upon posttranslational modifications of the receptor protein (for example glycosilation) or alternative splicing of primary transcripts and not on variations within the coding sequence of the receptors gene.