المؤلفون: Higashi, Haruka, Kato, Yoshinobu, Fujita, Tomoya, Iwasaki, Shintaro, Nakamura, Masayuki, Nishimura, Yoshiki, Takenaka, Mizuki, Shikanai, Toshiharu

المصدر: Plant & Cell Physiology; Jul2021, Vol. 62 Issue 7, p1146-1155, 10p

مصطلحات موضوعية: TRANSLATING & interpreting, RNA-binding proteins, GENETIC translation, NON-coding RNA, RIBOSOMES, PROTEINS, RNA sequencing

مستخلص: PGR3 is a P-class pentatricopeptide repeat (PPR) protein required for the stabilization of petL operon RNA and the translation of the petL gene in plastids. Irrespective of its important roles in plastids, key questions have remained unanswered, including how PGR3 protein promotes translation and which plastid mRNA PGR3 activates the translation. Here, we show that PGR3 facilitates the translation from ndhG, in addition to petL, through binding to their 5′ untranslated regions (UTRs). Ribosome profiling and RNA sequencing in pgr3 mutants revealed that translation from petL and ndhG was specifically suppressed. Harnessing small RNA fragments protected by PPR proteins in vivo, we probed the PGR3 recruitment to the 5′ UTRs of petL and ndhG. The putative PGR3-bound RNA segments per se repress the translation possibly with a strong secondary structure and thereby block ribosomes' access. However, the PGR3 binding antagonizes the effects and facilitates the protein synthesis from petL and ndhG in vitro. The prediction of the 3-dimensional structure of PGR3 suggests that the 26th PPR motif plays important roles in target RNA binding. Our data show the specificity of a plastidic RNA-binding protein and provide a mechanistic insight into translational control. [ABSTRACT FROM AUTHOR]

: Copyright of Plant & Cell Physiology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Masuda, Ken, Tokito, Takaaki, Azuma, Koichi, Yanagida, Eriko, Nakamura, Masayuki, Naito, Yoshiko, Matsuo, Norikazu, Ishii, Hidenobu, Yamada, Kazuhiko, Akiba, Jun, Hoshino, Tomoaki

المصدر: Thoracic Cancer; Jun2018, Vol. 9 Issue 6, p754-757, 4p

مصطلحات موضوعية: CANCER chemotherapy, CANCER genetics, PROTEIN-tyrosine kinase inhibitors, ERLOTINIB, AUTOPSY, ADENOCARCINOMA, BIOPSY, CELL receptors, CHEST tumors, EPIDERMAL growth factor, GENE expression, LUNGS, GENETIC mutation, LUNG tumors, TREATMENT effectiveness, DISEASE progression, DIAGNOSIS, GENETICS, THERAPEUTICS

مصطلحات جغرافية: JAPAN

مستخلص: Pulmonary pleomorphic carcinoma (PPC) is a very rare type of primary lung cancer with an aggressive clinical course. Few reports have documented therapeutic options for PPC with EGFR mutations. Herein, we report a case of PPC with EGFR mutation treated with EGFR‐tyrosine kinase inhibitors (TKIs). A 65‐year‐old Japanese woman was diagnosed with stage IV lung adenocarcinoma with L858R point mutation in exon 21. Despite treatment with erlotinib, the patient died after two weeks as a result of rapid disease progression. Postmortem examination indicated that the thoracic tumors consisted primarily of spindle/sarcomatous components, while expression of the mutated EGFR protein was only observed in adenocarcinoma components. We speculate that the tumor was not driven by EGFR mutation. Clinicians should bear in mind the possibility of pleomorphic carcinoma if EGFR‐TKI treatment fails to achieve a clinical response for adenocarcinoma harboring an activating EGFR mutation diagnosed on the basis of small biopsy specimens. [ABSTRACT FROM AUTHOR]

: Copyright of Thoracic Cancer is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Kurano, Yutaka¹, Nakamura, Masayuki¹, Ichiba, Mio¹, Matsuda, Mieko¹, Mizuno, Emiko¹, Kato, Maiko¹, Izumo, Shuji², Sano, Akira¹ sano@m3.kufm.kagoshima-u.ac.jp

المصدر: Biochemical & Biophysical Research Communications. Dec2006, Vol. 351 Issue 2, p438-442. 5p.

مصطلحات موضوعية: *GABA, *GENE expression, *NEURODEGENERATION, *GENETICS

مستخلص: Abstract: Chorea-acanthocytosis (ChAc) is a hereditary neurodegenerative disorder caused by loss of function mutations in the VPS13A gene encoding chorein. Recently, using a gene-targeting technique to delete exons 60–61, we produced a ChAc-model mouse that corresponds to a human disease mutation. In this study, a comparative microarray analysis of gene expression in the striatum revealed an increased level of gephyrin gene expression in the ChAc-model mice compared with wild type mice. Since gephyrin is known as a GABAA receptor-anchoring protein, we compared the protein-level expression and localization of gephyrin and the GABAA receptor α1 (GABRA1) and γ2 (GABRG2) subunits. Gephyrin and GABRG2 immunoreactivities in the striatum and hippocampus of the ChAc-model mice were significantly higher than those in the wild types. Our results suggest that chorein functional loss may lead to a compensatory upregulation of gephyrin and GABRG2 in the pathologic condition in ChAc. [Copyright &y& Elsevier]

المؤلفون: Nakamura, Masayuki¹, Iwai, Hisashi² topcrop@agri.kagoshima-u.ac.jp, Arai, Kei²

المصدر: Journal of General Plant Pathology. Oct2003, Vol. 69 Issue 5, p283-291. 9p. 2 Color Photographs, 4 Diagrams, 2 Charts, 1 Graph.

مصطلحات موضوعية: *POLYGALACTURONASE, *GEOTRICHUM candidum, *SCHIZOSACCHAROMYCES pombe, *GENE expression, *LEMON

مستخلص: Gene S31pg1, which encodes a polygalacturonase (PG), was previously isolated from citrus race S31 of Geotrichum candidum, the causal agent of citrus sour rot. We have now isolated and sequenced an additional PG gene, S31pg2, with 95% identity to S31pg1 in the mature proteins. To evaluate the contribution of the two PG genes in the development of citrus sour rot, each gene was expressed in the fission yeast Schizosaccharomyces pombe. Both genes conferred PG activity to the yeast. Crude enzyme solutions containing S31PG1 severely degraded the albedo tissue of lemon peel, but those containing S31PG2 did not. Concentrated crude S31PG1 solutions also caused soft rot on lemon fruit, indicating that not S31PG2 but S31PG1 is an important pathogenicity factor in citrus sour rot. Next, the protopectinase (PP) activity of each PG was measured. Although S31PG1 and S31PG2 are highly homologous, S31PG1 had high PP activity, whereas S31PG2 had much lower activity. PG from G. candidum noncitrus race S63 (nonpathogenic to citrus fruits) was also assayed but did not have any PP activity at all. These results suggest that the different PP activities of the PGs are a key to the pathogenicity of G. candidum to lemon fruit. [ABSTRACT FROM AUTHOR]

المؤلفون: Liang, Yideng¹, Jiang, Haibing¹, Ratovitski, Tamara¹, Jie, Chunfa², Nakamura, Masayuki¹, Hirschhorn, Ricky R.³, Wang, Xiaofang¹, Smith, Wanli W.¹, Hai, Tsonwin⁴, Poirier, Michelle A.¹, Ross, Christopher A.^1,5,6 caross@jhu.edu

المصدر: Brain Research. Aug2009, Vol. 1286, p221-229. 9p.

مصطلحات موضوعية: *MOLECULAR immunology, *TRANSCRIPTION factors, *HUNTINGTON disease, *GENE expression, *GLUTAMINE, *NEUROTOXICOLOGY, *CELL death, *PREVENTION

مستخلص: Abstract: Huntington''s disease is a progressive neurodegenerative disorder caused by a polyglutamine expansion near the N-terminus of huntingtin. The mechanisms of polyglutamine neurotoxicity, and cellular responses are not fully understood. We have studied gene expression profiles by short oligo array using an inducible PC12 cell model expressing an N-terminal huntingtin fragment with expanded polyglutamine (Htt-N63-148Q). Mutant huntingtin Htt-N63 induced cell death and increased the mRNA and protein levels of activating transcription factor 3 (ATF3). Mutant Htt-N63 also significantly enhanced ATF3 transcriptional activity by a promoter-based reporter assay. Overexpression of ATF3 protects against mutant Htt-N63 toxicity and knocking down ATF3 expression reduced Htt-N63 toxicity in a stable PC12 cell line. These results indicated that ATF3 plays a critical role in toxicity induced by mutant Htt-N63 and may lead to a useful therapeutic target. [Copyright &y& Elsevier]

المؤلفون: Nagata, Tomoshi¹, Tohda, Yukihiko¹, Yokomizo, Yuichi², Nakamura, Masayuki¹, Takehara, Kazuaki¹ takehara@vmas.kitasato-u.ac.jp

المصدر: Veterinary Immunology & Immunopathology. Nov2003, Vol. 96 Issue 1/2, p105. 6p.

مصطلحات موضوعية: *GRANULOCYTE-macrophage colony-stimulating factor, *GENE expression, *BACULOVIRUS genetics, *CELL culture

مستخلص: A bovine granulocyte-colony stimulating factor (bG-CSF) cDNA clone bearing a C-terminal poly-His-tag (bG-CSFHis) was constructed and expressed by the baculovirus expression system. The bG-CSFHis was expressed as an approximately 19 kDa protein in the culture supernatants and was purified using a nickel chelate column. The purified bG-CSFHis had bioactivity in vitro in the NFS-60 bioassay. In order to evaluate activity in vivo, purified bG-CSFHis was administered to cattle as single or multiple dosages. The bG-CSFHis increased neutrophil counts in peripheral blood and modulated the phagocytic activity of the neutrophils. The data indicates that the recombinant protein had activity in vivo. [Copyright &y& Elsevier]