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Hans-Michael Jantzen

Researcher at Millennium Pharmaceuticals

Publications -  17
Citations -  3011

Hans-Michael Jantzen is an academic researcher from Millennium Pharmaceuticals. The author has contributed to research in topics: Receptor & P2Y receptor. The author has an hindex of 11, co-authored 17 publications receiving 2921 citations. Previous affiliations of Hans-Michael Jantzen include University of California, Berkeley.

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Identification of the platelet ADP receptor targeted by antithrombotic drugs.

TL;DR: The cloning of this receptor, designated P2Y12, is described and evidence that a patient with a bleeding disorder has a defect in this gene is provided, which should facilitate the development of better antiplatelet agents to treat cardiovascular diseases.
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Nucleolar transcription factor hUBF contains a DNA-binding motif with homology to HMG proteins

TL;DR: The eukaryotic upstream binding factor (DBF) recognizes the ribosomal RNA gene promoter and activates transcription mediated by RNA polymerase I through cooperative interactions with the species-specific factor, SL1 as mentioned in this paper.
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Functional cooperativity between transcription factors UBF1 and SL1 mediates human ribosomal RNA synthesis

TL;DR: In vitro transcription experiments indicate that formation of the U BF1-SL1 complex is vital for transcriptional activation by UBF1, and protein-protein interactions between UBF2 and SL1 are required for targeting of SL1 to cis-control sequences of the promoter.
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Evidence for two distinct G-protein-coupled ADP receptors mediating platelet activation.

TL;DR: Results support the existence of two G protein-coupled ADP receptors mediating platelet aggregation, one of which is coupled to Gi proteins and blocked by 2MeSAMP, whereas the second receptor is similar or identical to P2Y1 and coupled to Gq.
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Cisplatin-DNA adducts are molecular decoys for the ribosomal RNA transcription factor hUBF (human upstream binding factor).

TL;DR: The results suggest that a cisplatin-mediated transcription-factor-hijacking mechanisms could disrupt rRNA synthesis, which is stimulated in proliferating cells, and the hUBF-promoter interaction is highly sensitive to the antagonistic effects of cisPlatin-DNA adducts.