Genes to Cells
© The Molecular Biology Society of Japan/John Wiley & Sons Australia, Ltd
Edited By: Mitsuhiro Yanagida
Impact Factor: 2.481
ISI Journal Citation Reports © Ranking: 2015: 85/166 (Genetics & Heredity); 123/187 (Cell Biology)
Online ISSN: 1365-2443
See and read about our journal covers, each available as free pdf downloads from cover gallery on the MBSJ homepage.
Genes to Cells is online only from 2015. To receive electronic Table of Content alerts each time a new issue is published online, please see here.
Recently Published Articles
- Octopamine enhances oxidative stress resistance through the fasting-responsive transcription factor DAF-16/FOXO in C. elegans
Haruka Hoshikawa, Masaharu Uno, Sakiko Honjoh and Eisuke Nishida
Version of Record online: 20 JAN 2017 | DOI: 10.1111/gtc.12469
In this study, we found that OA administration enhanced organismal resistance to oxidative stress. This enhanced resistance was suppressed by a mutation of the OA receptors, SER-3 and SER-6. Moreover, we found that OA administration promoted the nuclear translocation of DAF-16, the key transcription factor in fasting responses, and that the OA-induced enhancement of stress resistance required DAF-16. Altogether, our results suggest that OA signaling, which is triggered by the absence of food, shifts the organismal state to a more protective one to prepare for environmental stresses.
- PKN2 is essential for mouse embryonic development and proliferation of mouse fibroblasts
Sally Danno, Koji Kubouchi, Mona Mehruba, Manabu Abe, Rie Natsume, Kenji Sakimura, Satoshi Eguchi, Masahiro Oka, Masanori Hirashima, Hiroki Yasuda and Hideyuki Mukai
Version of Record online: 19 JAN 2017 | DOI: 10.1111/gtc.12470
Constitutive disruption of the mouse PKN2 gene resulted in growth retardation and lethality before embryonic day 10.5. PKN2 knockout fibroblasts showed impaired cell proliferation.
- Immature Core protein of hepatitis C virus induces an unfolded protein response through inhibition of ERAD-L in a yeast model system
Shota Takahashi, Naoko Sato, Junichi Kikuchi, Hideaki Kakinuma, Jun Okawa, Yukiko Masuyama, Singo Iwasa, Hayato Irokawa, Gi-Wook Hwang, Akira Naganuma, Michinori Kohara and Shusuke Kuge
Version of Record online: 18 JAN 2017 | DOI: 10.1111/gtc.12464
Structural protein Core of hepatitis C virus (HCV), a cytosolic protein, induces endoplasmic reticulum (ER) stress and unfolded protein response (UPR) in hepatocytes, and is responsible for the pathogenesis of persistent HCV infection. Utilizing yeast as a model system, we found that the immature Core inhibits ERAD-L, a degradation system responsible for misfolded/unfolded proteins in the ER lumen, and induces UPR. Requirement of an unfolded protein sensor in the ER lumen suggested that inhibition of ERAD-L is probably responsible for Core-dependent UPR activation.
- In situ electrical monitoring of cancer cells invading vascular endothelial cells with semiconductor-based biosensor
Toshiya Sakata and Yusuke Matsuse
Version of Record online: 18 JAN 2017 | DOI: 10.1111/gtc.12473
Cellular dynamics is very closely related to ionic behaviors, most of which have been hardly monitored in real time, whereas semiconductor-based biosensors have the unique advantage of direct detection of ionic charges in a real-time and noninvasive manner. In this study, we monitored the invasion process of cancer cells into the vascular endothelial layer in real time by a label-free method using a field-effect transistor (FET) biosensor.
- Activin A in combination with ERK1/2 MAPK pathway inhibition sustains propagation of mouse embryonic stem cells
Yuhei Ashida, May Nakajima-Koyama, Akira Hirota, Takuya Yamamoto and Eisuke Nishida
Version of Record online: 18 JAN 2017 | DOI: 10.1111/gtc.12467
Activin A has an ability to efficiently propagate ESCs when combined with a MEK inhibitor PD0325901. ESCs cultured in Activin+PD show naive pluripotency features, including the gene expression profile, the preferential usage of the Oct4 distal enhancer, and the self-renewal response to Wnt signaling pathway activation.