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1.
Single Cell Transcriptome Amplification with MALBAC 总被引:1,自引:0,他引:1
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Abstract Clostridium perfringens alpha-toxin was produced in a protein-hyperproducing strain, Bacillus brevis 47, by cloning the gene into the constructed expression-secretion vector which has the multiple promoters and the signal peptide coding region of an outer cell wall protein gene. The amount of alpha-toxin produced by the B. brevis 47 transformant carrying the gene was approximately 10 times greater than that produced by a B. subtilis transformant carrying the toxin gene. Biological activities and the N-terminal amino acid sequence of the toxin secreted by the B. brevis 47 transformant were identical to those of wild-type alpha-toxin. 相似文献
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Pasupathi Sundaramoorthy Jae Jun Sim Yeong-Su Jang Siddhartha Kumar Mishra Keun-Yeong Jeong Poonam Mander Oh Byung Chul Won-Sik Shim Seung Hyun Oh Ky-Youb Nam Hwan Mook Kim 《PloS one》2015,10(1)
Cancer cell motility is a key phenomenon regulating invasion and metastasis. Focal adhesion kinase (FAK) plays a major role in cellular adhesion and metastasis of various cancers. The relationship between dietary supplementation of calcium and colon cancer has been extensively investigated. However, the effect of calcium (Ca2+) supplementation on calpain-FAK-motility is not clearly understood. We sought to identify the mechanism of FAK cleavage through Ca2+ bound lactate (CaLa), its downstream signaling and role in the motility of human colon cancer cells. We found that treating HCT116 and HT-29 cells with CaLa immediately increased the intracellular Ca2+ (iCa2+) levels for a prolonged period of time. Ca2+ influx induced cleavage of FAK into an N-terminal FAK (FERM domain) in a dose-dependent manner. Phosphorylated FAK (p-FAK) was also cleaved in to its p-N-terminal FAK. CaLa increased colon cancer cells motility. Calpeptin, a calpain inhibitor, reversed the effects of CaLa on FAK and pFAK cleavage in both cancer cell lines. The cleaved FAK translocates into the nucleus and modulates p53 stability through MDM2-associated ubiquitination. CaLa-induced Ca2+ influx increased the motility of colon cancer cells was mediated by calpain activity through FAK and pFAK protein destabilization. In conclusion, these results suggest that careful consideration may be given in deciding dietary Ca2+ supplementation to patient undergoing treatment for metastatic cancer. 相似文献
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Janne Alahuhta Sarian Kosten Munemitsu Akasaka Dominique Auderset Mattia M. Azzella Rossano Bolpagni Claudia P. Bove Patricia A. Chambers Eglantine Chappuis John Clayton Mary de Winton Frauke Ecke Esperança Gacia Gana Gecheva Patrick Grillas Jennifer Hauxwell Seppo Hellsten Jan Hjort Mark V. Hoyer Christiane Ilg Agnieszka Kolada Minna Kuoppala Torben Lauridsen En Hua Li Balázs A. Lukács Marit Mjelde Alison Mikulyuk Roger P. Mormul Jun Nishihiro Beat Oertli Laila Rhazi Mouhssine Rhazi Laura Sass Christine Schranz Martin Søndergaard Takashi Yamanouchi Qing Yu Haijun Wang Nigel Willby Xiao Ke Zhang Jani Heino 《Journal of Biogeography》2017,44(8):1758-1769
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Two protein bands with laccase activity were found after PAGE of culture liquid or mycelium extract of Pleurotus eryngii, grown on glucose–ammonium tartrate–yeast extract medium with and without inducers. A major and a minor laccase band were
observed in the basal medium. The intensity of the major band (laccase I) did not change after the addition of inducers. However,
the minor band (laccase II), characterized by higher electrophoretic mobility, was strongly induced by wheat–straw alkalilignin
and vanillic and veratric acids. Laccase activity in the basal medium had an optimum pH of 4.5 and was stable from pH 3 to
10 during 24 h at room temperature. This enzyme had wide substrate specificity on hydroquinones, methoxy-substituted monophenols,
and aromatic amines. In general, laccase activity was found only with compounds having a redox potential lower than 0.5 mV.
The highest activity was obtained with methoxy- and methyl-substituted p-hydroquinones and aromatic diamines. Some activity also occurred with the aliphatic compound 3,5-cyclohexadiene-1,2-diol.
Received: 22 April 1996 / Accepted: 29 June 1996 相似文献