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Rudolf Grosschedl

Researcher at Max Planck Society

Publications -  149
Citations -  27284

Rudolf Grosschedl is an academic researcher from Max Planck Society. The author has contributed to research in topics: Transcription factor & Enhancer. The author has an hindex of 79, co-authored 139 publications receiving 26062 citations. Previous affiliations of Rudolf Grosschedl include Massachusetts Institute of Technology & University of California, San Francisco.

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Journal ArticleDOI

Functional interaction of beta-catenin with the transcription factor LEF-1.

TL;DR: β-catenin regulates gene expression by direct interaction with transcription factors such as LEF-1, providing a molecular mechanism for the transmission of signals from cell-adhesion components or wnt protein to the nucleus.
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Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

TL;DR: The pattern of defects suggest an essential role for LEF-1 in the formation of several organs and structures that require inductive tissue interactions in mice carrying a homozygous germ-line mutation in the LEf-1 gene.
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HMG domain proteins: architectural elements in the assembly of nucleoprotein structures

TL;DR: DNA bending induced by the H MG domain can facilitate the formation of higher-order nucleoprotein complexes, suggesting that HMG domain proteins may have an architectural role in assembling such complexes.
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Expression of the int-1 gene in transgenic mice is associated with mammary gland hyperplasia and adenocarcinomas in male and female mice.

TL;DR: Mammary and salivary adenocarcinomas occur in these animals at rates indicating that transcriptional activation of int-1 and associated hyperplasia are initiating events in multistep carcinogenesis.
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Failure of B-cell differentiation in mice lacking the transcription factor EBF

TL;DR: It is shown that EBF is necessary for the generation of immunoglobulin-expressing B cells in EBF-deficient mice, and that various non-lymphoid tissues that express EBF are apparently normal in homozygous mutant mice, including olfactory neurons in which EBF was identified as Olf-1.