http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Goniotrichopsis reniformis (Kajimura) Kikuchi comb. nov. (Stylonematales, Rhodophyta) from Japan
신종암,Kikuchi, Norio,West, John A.,Kajimura, Mitsuo,Shin, Jong-Ahm 한국조류학회(藻類) 2006 ALGAE Vol.21 No.2
The morphology and life history of Stylonema reniforme Kajimura (Stylonematales, Rhodophyta) from Japan were investigated and its taxonomic placement was discussed. This species has 6-30 discoid chloroplasts devoid of a pyrenoid in each cell. This is a typical feature of the genus Goniotrichopsis. The species reproduced only by monospores, which were formed by the direct transformation of the vegetative cells similar to the type species Goniotrichopsis sublittoralis Smith. Goniotrichopsis reniformis (Kajimura) Kikuchi comb. nov. was proposed. The asexual life history of the present species was completed in 3-10 weeks at 15-20°C in culture.
Choi, Sung E.,Kwon, Sanghoon,Seok, Sunmi,Xiao, Zhen,Lee, Kwan-Woo,Kang, Yup,Li, Xiaoling,Shinoda, Kosaku,Kajimura, Shingo,Kemper, Byron,Kemper, Jongsook Kim American Society for Microbiology 2017 Molecular and cellular biology Vol.37 No.15
<P>Sirtuin1 (SIRT1) deacetylase delays and improves many obesity-related diseases, including nonalcoholic fatty liver disease (NAFLD) and diabetes, and has received great attention as a drug target. SIRT1 function is aberrantly low in obesity, so understanding the underlying mechanisms is important for drug development. Here, we show that obesity-linked phosphorylation of SIRT1 inhibits its function and promotes pathological symptoms of NAFLD. In proteomic analysis, Ser-164 was identified as a major serine phosphorylation site in SIRT1 in obese, but not lean, mice, and this phosphorylation was catalyzed by casein kinase 2 (CK2), the levels of which were dramatically elevated in obesity. Mechanistically, phosphorylation of SIRT1 at Ser-164 substantially inhibited its nuclear localization and modestly affected its deacetylase activity. Adenovirus-mediated liver-specific expression of SIRT1 or a phosphor-defective S164A-SIRT1 mutant promoted fatty acid oxidation and ameliorated liver steatosis and glucose intolerance in diet-induced obese mice, but these beneficial effects were not observed in mice expressing a phosphor-mimic S164D-SIRT1 mutant. Remarkably, phosphorylated S164-SIRT1 and CK2 levels were also highly elevated in liver samples of NAFLD patients and correlated with disease severity. Thus, inhibition of phosphorylation of SIRT1 by CK2 may serve as a new therapeutic approach for treatment of NAFLD and other obesity-related diseases.</P>