Down-regulation of CD81 tetraspanin in human cells producing retroviral-based particles: Tailoring vector composition

2011 ◽  
Vol 108 (11) ◽  
pp. 2623-2633 ◽  
Author(s):  
A.F. Rodrigues ◽  
M.R. Guerreiro ◽  
V.M. Santiago ◽  
C. Dalba ◽  
D. Klatzmann ◽  
...  
Keyword(s):  
Human Cells ◽  
Down Regulation ◽  
Cd81 Tetraspanin

scholarly journals N6-Methyladenine DNA Modification in Human Genome

2017 ◽  
Author(s):  
Chuan-Le Xiao ◽  
Song Zhu ◽  
Minghui He ◽  
De Chen ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Human Genome ◽  
Genomic Dna ◽  
Human Cells ◽  
Human Diseases ◽  
Dna Modification ◽  
Down Regulation ◽  
Coding Regions

SummaryDNA N6-methyladenine (6mA) modification is the most prevalent DNA modification in prokaryotes, but whether it exists in human cells and whether it plays a role in human diseases remain enigmatic. Here, we showed that 6mA is extensively present in human genome, and we cataloged 881,240 6mA sites accounting for ∼0.051% of the total adenines. [G/C]AGG[C/T] was the most significantly associated motif with 6mA modification. 6mA sites were enriched in the coding regions and mark actively transcribed genes in human cells. We further found that DNA N6-methyladenine and N6-demethyladenine modification in human genome were mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The abundance of 6mA was significantly lower in cancers, accompaning with decreased N6AMT1 and increased ALKBH1 levels, and down-regulation of 6mA modification levels promoted tumorigenesis. Collectively, our results demonstrate that DNA 6mA modification is extensively present in human cells and the decrease of genomic DNA 6mA promotes human tumorigenesis.

XRCC1 down-regulation in human cells leads to DNA-damaging agent hypersensitivity, elevated sister chromatid exchange, and reduced survival ofBRCA2mutant cells

2007 ◽  
Vol 48 (6) ◽  
pp. 491-500 ◽  
Author(s):  
Jinshui Fan ◽  
Paul F. Wilson ◽  
Heng-Kuan Wong ◽  
Salustra S. Urbin ◽  
Larry H. Thompson ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Cells ◽  
Down Regulation

Accumulation of multiple forms of lamin A with down-regulation of FACE-1 suppresses growth in senescent human cells

2007 ◽  
Vol 12 (3) ◽  
pp. 397-406 ◽  
Author(s):  
Ryo Ukekawa ◽  
Kensuke Miki ◽  
Michihiko Fujii ◽  
Hisashi Hirano ◽  
Dai Ayusawa
Keyword(s):  
Human Cells ◽  
Lamin A ◽  
Multiple Forms ◽  
Down Regulation

scholarly journals Down-regulation of CD81 in human cells producing HCV-E1/E2 retroVLPs

2011 ◽  
Vol 5 (Suppl 8) ◽  
pp. P72 ◽  
Author(s):  
Ana F Rodrigues ◽  
Miguel R Guerreiro ◽  
Rute Castro ◽  
Hélio A Tomás ◽  
Charlotte Dalba ◽  
...  
Keyword(s):  
Human Cells ◽  
Down Regulation

scholarly journals The COP9 Signalosome Regulates Skp2 Levels and Proliferation of Human Cells

2006 ◽  
Vol 281 (43) ◽  
pp. 32188-32196 ◽  
Author(s):  
Simona Denti ◽  
Maria Elena Fernandez-Sanchez ◽  
Lars Rogge ◽  
Elisabetta Bianchi
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Kinase Inhibitor ◽  
Human Cells ◽  
Cop9 Signalosome ◽  
Mammalian Development ◽  
Down Regulation ◽  
Protein Levels

The COP9 signalosome (CSN) is a conserved, multisubunit complex first identified as a developmental regulator in plants. Gene inactivation of single CSN subunits results in early embryonic lethality in mice, indicating that the CSN is essential for mammalian development. The pleiotropic function of the CSN may be related to its ability to remove the ubiquitin-like peptide Nedd8 from cullin-RING ubiquitin ligases, such as the SCF complex, and therefore regulate their activity. However, the mechanism of CSN regulatory action on cullins has been debated, since, paradoxically, the CSN has an inhibitory role in vitro, while genetic evidence supports a positive regulatory role in vivo. We have targeted expression of CSN subunits 4 and 5 in human cells by lentivirus-mediated small hairpin RNA delivery. Down-regulation of either subunit resulted in disruption of the CSN complex and in Cullin1 hyperneddylation. Functional consequences of CSN down-regulation were decreased protein levels of Skp2, the substrate recognition subunit of SCFSkp2, and stabilization of a Skp2 target, the cyclin-dependent kinase inhibitor p27Kip1. CSN down-regulation caused an impairment in cell proliferation, which could be partially reversed by suppression of p27Kip1. Moreover, restoring Skp2 levels in CSN-deficient cells recovered cell cycle progression, indicating that loss of Skp2 in these cells plays an important role in their proliferation defect. Our data indicate that the CSN is necessary to ensure the assembly of a functional SCFSkp2 complex and therefore contributes to cell cycle regulation of human cells.

scholarly journals Down-regulation of the expression of alcohol dehydrogenase 4 and CYP2E1 by the combination of α-endosulfan and dioxin in HepaRG human cells

2017 ◽  
Vol 45 ◽  
pp. 309-317 ◽  
Author(s):  
Eléonore A. Attignon ◽  
Emilie Distel ◽  
Béatrice Le-Grand ◽  
Alix F. Leblanc ◽  
Robert Barouki ◽  
...  
Keyword(s):  
Alcohol Dehydrogenase ◽  
Human Cells ◽  
Down Regulation
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