Enhanced gene expression in insect cells and silkworm larva by modified polyhedrin promoter using repeated burst sequence and very late transcriptional factor-1

2010 ◽  
Vol 107 (6) ◽  
pp. 909-916 ◽  
Author(s):  
Suganthi Lavender Manohar ◽  
Shin Kanamasa ◽  
Takuya Nishina ◽  
Tatsuya Kato ◽  
Enoch Y. Park
Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 343
Author(s):  
Ying-Chin Lin ◽  
Tso-Hsiao Chen ◽  
Yu-Min Huang ◽  
Po-Li Wei ◽  
Jung-Chun Lin

MicroRNAs (miRNAs) function as the post-transcriptional factor that finetunes the gene expression by targeting to the specific candidate. Mis-regulated expression of miRNAs consequently disturbs gene expression profile, which serves as the pivotal mechanism involved in initiation or progression of human malignancy. Cancer-relevant miRNA is potentially considered the therapeutic target or biomarker toward the precise treatment of cancer. Nevertheless, the regulatory mechanism underlying the altered expression of miRNA in cancer is largely uncovered. Detailed knowledge regarding the influence of miRNAs on solid cancer is critical for exploring its potential of clinical application. Herein, we elucidate the regulatory mechanism regarding how miRNA expression is manipulated and its impact on the pathogenesis of distinct solid cancer.


Author(s):  
Maren Schubert ◽  
Manfred Nimtz ◽  
Federico Bertoglio ◽  
Stefan Schmelz ◽  
Peer Lukat ◽  
...  

2017 ◽  
Vol 124 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Keita Mori ◽  
Hirotsugu Hamada ◽  
Takafumi Ogawa ◽  
Yuki Ohmuro-Matsuyama ◽  
Tomohisa Katsuda ◽  
...  

2001 ◽  
Vol 21 (17) ◽  
pp. 5857-5868 ◽  
Author(s):  
Alla Danilkovitch-Miagkova ◽  
Alexei Miagkov ◽  
Alison Skeel ◽  
Noboru Nakaigawa ◽  
Berton Zbar ◽  
...  

ABSTRACT β-Catenin is an oncogenic protein involved in regulation of cell-cell adhesion and gene expression. Accumulation of cellular β-catenin occurs in many types of human cancers. Four mechanisms are known to cause increases in β-catenin: mutations of β-catenin, adenomatous polyposis coli, or axin genes and activation of Wnt signaling. We report a new cause of β-catenin accumulation involving oncogenic mutants of RON and MET receptor tyrosine kinases (RTKs). Cells transfected with oncogenic RON or MET were characterized by β-catenin tyrosine phosphorylation and accumulation; constitutive activation of a Tcf transcriptional factor; and increased levels of β-catenin/Tcf target oncogene proteins c-mycand cyclin D1. Interference with the β-catenin pathway reduced the transforming potential of mutated RON and MET. Activation of β-catenin by oncogenic RON and MET constitutes a new pathway, which might lead to cell transformation by these and other mutant growth factor RTKs.


Author(s):  
SHUICHIRO TOMITA ◽  
YUKIE KAWAI ◽  
SOO DONG WOO ◽  
MANABU KAMIMURA ◽  
KIKUO IWABUCHI ◽  
...  

1992 ◽  
Vol 10 (5) ◽  
pp. 565-569 ◽  
Author(s):  
Matti Karp ◽  
Karl Åkerman ◽  
Christer Lindqvist ◽  
Ari Kuusisto ◽  
Petri Saviranta ◽  
...  

1990 ◽  
Vol 28 (2) ◽  
pp. 215-224 ◽  
Author(s):  
Allan E. Atkinson ◽  
Matthew D. Weitzman ◽  
Louis Obosi ◽  
David J. Beadle ◽  
Linda A. King

1988 ◽  
Vol 13 (2) ◽  
pp. 65-71 ◽  
Author(s):  
J. J. M. Janssen ◽  
W. J. M. van de Ven ◽  
W. A. H. M. van Groningen-Luyben ◽  
J. Roosien ◽  
J. M. Vlak ◽  
...  

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