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Jürg Bähler

Researcher at University College London

Publications -  237
Citations -  24955

Jürg Bähler is an academic researcher from University College London. The author has contributed to research in topics: Schizosaccharomyces pombe & Gene. The author has an hindex of 67, co-authored 227 publications receiving 21327 citations. Previous affiliations of Jürg Bähler include University of Debrecen & European Bioinformatics Institute.

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An essential role for dNTP homeostasis following CDK-induced replication stress

TL;DR: It is shown that cyclin-dependent kinase (CDK)-induced replication stress, resulting from Wee1 inactivation, is synthetic lethal with mutations disrupting dNTP homeostasis in fission yeast, and this findings support a ‘dNTP supply and demand’ model in which maintaining dN TPHomeostasis is essential to prevent replication catastrophe in response to CDK- induced replication stress.
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Activation of AP-1-Dependent transcription by a truncated translation initiation factor

TL;DR: It is shown for the first time that Int6CT acts to increase the transcriptional activity of Pap1, a highly conserved subunit of eukaryotic translation initiation factor 3 (eIF3) that has been reported to interact with subunits of the proteasome and the COP9 signalosome.
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Improved tools for efficient mapping of fission yeast genes: identification of microtubule nucleation modifier mod22-1 as an allele of chromatin- remodelling factor gene swr1.

TL;DR: A set of strains designed to make swi5‐based mapping more efficient and more powerful are described, and it is determined that mod22‐1, a modifier of microtubule nucleation phenotypes, encodes a truncation allele of Swr 1, a chromatin‐remodelling factor involved in nucleosomal deposition of H2A.
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Genetic interactions and functional analyses of the fission yeast gsk3 and amk2 single and double mutants defective in TORC1-dependent processes.

TL;DR: Common and specialized roles of AMPK and Gsk3 in mediating TOR-dependent processes are revealed, indicating that AM PK and GSk3 act in parallel to inhibit TOR function in fission yeast.
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Cdk9 and H2Bub1 signal to Clr6-CII/Rpd3S to suppress aberrant antisense transcription.

TL;DR: It is shown that Cdk9 inhibition or H2Bub1 loss induces intragenic antisense transcription of ∼10% of fission yeast genes, with each perturbation affecting largely distinct subsets; ablation of both pathways de-represses antisensecription of over half the genome.