scholarly journals A multi-shRNA vector enhances the silencing efficiency of exogenous and endogenous genes in human cells

2017 ◽  
Vol 13 (3) ◽  
pp. 1553-1562
Author(s):  
Yanjie Weng ◽  
Ying Shi ◽  
Xi Xia ◽  
Wenjuan Zhou ◽  
Hongyan Wang ◽  
...  
Keyword(s):  
Human Cells ◽  
Shrna Vector ◽  
Endogenous Genes

scholarly journals Plasmodium falciparum translational machinery condones polyadenosine repeats

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Slavica Pavlovic Djuranovic ◽  
Jessey Erath ◽  
Ryan J Andrews ◽  
Peter O Bayguinov ◽  
Joyce J Chung ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Protein Synthesis ◽  
Causative Agent ◽  
Human Cells ◽  
Translational Machinery ◽  
Human Malaria ◽  
Ribosome Stalling ◽  
Mrna Surveillance ◽  
Endogenous Genes ◽  
Stark Contrast

Plasmodium falciparum is a causative agent of human malaria. Sixty percent of mRNAs from its extremely AT-rich (81%) genome harbor long polyadenosine (polyA) runs within their ORFs, distinguishing the parasite from its hosts and other sequenced organisms. Recent studies indicate polyA runs cause ribosome stalling and frameshifting, triggering mRNA surveillance pathways and attenuating protein synthesis. Here, we show that P. falciparum is an exception to this rule. We demonstrate that both endogenous genes and reporter sequences containing long polyA runs are efficiently and accurately translated in P. falciparum cells. We show that polyA runs do not elicit any response from No Go Decay (NGD) or result in the production of frameshifted proteins. This is in stark contrast to what we observe in human cells or T. thermophila, an organism with similar AT-content. Finally, using stalling reporters we show that Plasmodium cells evolved not to have a fully functional NGD pathway.

Alpha-Tocopherol Protects Cultured Human Cells from the Acute Lethal Cytotoxicity of Dioxin

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Smooth Endoplasmic Reticulum ◽  
Dehydroascorbic Acid ◽  
Human Cells ◽  
Alpha Tocopherol ◽  
Cervical Cancer Cells ◽  
Cultured Human Cells ◽  
Nuclear Damage ◽  
Conjunctival Epithelial Cells

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

Chromium oxidation state mapping in human cells

2003 ◽  
Vol 104 ◽  
pp. 289-292 ◽  
Author(s):  
R. Ortega ◽  
B. Fayard ◽  
M. Salomé ◽  
G. Devès ◽  
J. Susini
Keyword(s):  
Oxidation State ◽  
Human Cells ◽  
Chromium Oxidation

Transport of clozapine and its major metabolites into human cells of glial and neuronal origin

2004 ◽  
Vol 36 (05) ◽  
Author(s):  
U Henning ◽  
K Krieger ◽  
S Loeffler ◽  
A Klimke
Keyword(s):  
Human Cells

Lineage conversion of human cells to an adrenocortical phenotype: a new technology to study the adrenal gland

2015 ◽  
Author(s):  
Gerard Ruiz Babot ◽  
Irene Hadjidemetriou ◽  
Sharon Jane Ajodha ◽  
David Taylor ◽  
Norman Taylor ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
New Technology ◽  
Human Cells
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