The NTP pyrophosphatase DCTPP1 contributes to the homoeostasis and cleansing of the dNTP pool in human cells

2014 ◽  
Vol 459 (1) ◽  
pp. 171-180 ◽  
Author(s):  
Cristina E. Requena ◽  
Guiomar Pérez-Moreno ◽  
Luis M. Ruiz-Pérez ◽  
Antonio E. Vidal ◽  
Dolores González-Pacanowska

Human DCTPP1 is an all-α nucleotidohydrolase which hydrolyses intracellular dCTP and genotoxic nucleotide analogues, thus preventing their incorporation into DNA. DCTPP1 localizes in the nucleus, cytosol and mitochondria where it contributes to the homoeostasis and cleansing of dNTP pools.

2021 ◽  
Vol 8 (5) ◽  
pp. 201979
Author(s):  
Jana Wiedermannová ◽  
Christina Julius ◽  
Yulia Yuzenkova

Recent years witnessed the discovery of ubiquitous and diverse 5′-end RNA cap-like modifications in prokaryotes as well as in eukaryotes. These non-canonical caps include metabolic cofactors, such as NAD + /NADH, FAD, cell wall precursors UDP-GlcNAc, alarmones, e.g. dinucleotides polyphosphates, ADP-ribose and potentially other nucleoside derivatives. They are installed at the 5′ position of RNA via template-dependent incorporation of nucleotide analogues as an initiation substrate by RNA polymerases. However, the discovery of NAD-capped processed RNAs in human cells suggests the existence of alternative post-transcriptional NC capping pathways. In this review, we compiled growing evidence for a number of these other mechanisms which produce various non-canonically capped RNAs and a growing repertoire of capping small molecules. Enzymes shown to be involved are ADP-ribose polymerases, glycohydrolases and tRNA synthetases, and may potentially include RNA 3′-phosphate cyclases, tRNA guanylyl transferases, RNA ligases and ribozymes. An emerging rich variety of capping molecules and enzymes suggests an unrecognized level of complexity of RNA metabolism.


2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  

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.


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

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

2015 ◽  
Author(s):  
Gerard Ruiz Babot ◽  
Irene Hadjidemetriou ◽  
Sharon Jane Ajodha ◽  
David Taylor ◽  
Norman Taylor ◽  
...  

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