Genes to Cells

Cover image for Vol. 21 Issue 10

Edited By: Mitsuhiro Yanagida

Impact Factor: 2.481

ISI Journal Citation Reports © Ranking: 2015: 85/165 (Genetics & Heredity); 123/187 (Cell Biology)

Online ISSN: 1365-2443

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Recently Published Articles

  1. SFP1-mediated prion-dependent lethality is caused by increased Sup35 aggregation and alleviated by Sis1

    Andrew G. Matveenko, Polina B. Drozdova, Mikhail V. Belousov, Svetlana E. Moskalenko, Stanislav A. Bondarev, Yury A. Barbitoff, Anton A. Nizhnikov and Galina A. Zhouravleva

    Version of Record online: 12 OCT 2016 | DOI: 10.1111/gtc.12444

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    Sfp1 is a transcriptional regulator that, when overproduced, causes [PSI+] prion-dependent lethality via up-regulating yeast release factor Sup35 (eRF3). Increased levels of Hsp40 chaperone Sis1 alleviate the prion toxicity caused by either SFP1 or SUP35 over-expression and revert the distribution of Sup35 between monomers and aggregate fractions back to normal. Finally, Sfp1 forms detergent-resistant aggregates and may partially colocalize with Sup35 aggregates, suggesting an additional mechanism of Sfp1-derived [PSI+] prion toxicity.

  2. Small Maf deficiency recapitulates the liver phenotypes of Nrf1- and Nrf2-deficient mice

    Fumiki Katsuoka, Hiromi Yamazaki and Masayuki Yamamoto

    Version of Record online: 10 OCT 2016 | DOI: 10.1111/gtc.12445

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    Small Maf (sMaf) liver-specific conditional knockout (LCKO) mice show hepatic steatosis. sMaf LCKO livers share common gene expression profiles with Nrf1 LCKO and Nrf2 KO livers. This study provides genetic evidence that sMaf proteins are indispensable for liver functions as heterodimeric partners for Nrf1 and Nrf2.

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    RNA decay systems enhance reciprocal switching of sense and antisense transcripts in response to glucose starvation

    Atsuko Miki, Josephine Galipon, Satoshi Sawai, Toshifumi Inada and Kunihiro Ohta

    Version of Record online: 10 OCT 2016 | DOI: 10.1111/gtc.12443

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    fbp1-as antisense noncoding RNA carries a 5′-cap and poly(A)-tail like mRNAs, associates with polyribosomes despite being annotated as ‘noncoding’ and is degraded cotranslationally by the nonsense-mediated decay (NMD) pathway. This mechanism is not exclusive to fbp1-as, as antisense RNAs transcribed from other stress-responsive loci are also regulated by a similar mechanism. We propose a model by which NMD constantly degrades antisense RNA transcribed from stress-responsive loci, to quicken their disappearance when their transcriptional activity is shut off upon stress.

  4. TAK1 maintains the survival of immunoglobulin λ-chain-positive B cells

    Hisaaki Shinohara, Takeshi Nagashima, Marilia I. Cascalho and Tomohiro Kurosaki

    Version of Record online: 3 OCT 2016 | DOI: 10.1111/gtc.12442

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    TAK1 regulates the development of λ-chain-positive B cells by maintaining Bcl-2 expression through NF-κB signaling.

  5. Ubiquitin-proteasome-dependent degradation of TBP-like protein is prevented by direct binding of TFIIA

    Momoko Isogai, Hidefumi Suzuki, Ryo Maeda and Taka-aki Tamura

    Version of Record online: 3 OCT 2016 | DOI: 10.1111/gtc.12441

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    TBP-family protein TLP is degraded by ubiquitin-proteasome pathway. We showed that the degradation of TLP is prevented by TFIIA. Our data suggest that the TFIIA-induced TLP stabilization is required for transcription regulation.