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Nox4 as the Major Catalytic Component of an Endothelial NAD(P)H Oxidase
TLDR
Findings suggest that Nox4 may function as the major catalytic component of an endothelial NAD(P)H oxidase, a homologue of gp91phox/Nox2, which was abundantly expressed in endothelial cells.
Cancer-Related PRUNE2 Protein Is Associated with Nucleotides and Is Highly Expressed in Mature Nerve Tissues
TLDR
The present study indicates that C9orf65 and BMCC1/BNIPXL are transcribed asPRUNE2 mRNA, which is translated to a large PRUNE2 protein, which suggests that PRune2 may contribute to the maintenance of mature nervous systems.
NUDT16 is a (deoxy)inosine diphosphatase, and its deficiency induces accumulation of single-strand breaks in nuclear DNA and growth arrest
TLDR
It is concluded that NUDT16 is a (deoxy)inosine diphosphatase that may function mainly in the nucleus to protect cells from deleterious effects of (d)ITP.
NUDT16 and ITPA play a dual protective role in maintaining chromosome stability and cell growth by eliminating dIDP/IDP and dITP/ITP from nucleotide pools in mammals
TLDR
It is concluded that NUDT16 and ITPA play a dual protective role for eliminating dIDP/IDP and dITP/ITP from nucleotide pools in mammals.
Cockayne syndrome group A and B proteins converge on transcription-linked resolution of non-B DNA
TLDR
Evidence is presented that loss of CSA or CSB in a neuroblastoma cell line converges on mitochondrial dysfunction caused by defects in ribosomal DNA transcription and activation of the DNA damage sensor poly-ADP ribose polymerase 1 (PARP1).
CSB interacts with SNM1A and promotes DNA interstrand crosslink processing
TLDR
The results indicate that CSB coordinates the resolution of ICLs, possibly in a transcription-associated repair mechanism involving SNM1A, and that defects in the process could contribute to the post-mitotic degenerative pathologies associated with CS.
Deoxyinosine triphosphate induces MLH1/PMS2- and p53-dependent cell growth arrest and DNA instability in mammalian cells
TLDR
It is found that both growth suppression and accumulation of single-strand breaks in nuclear DNA of ITPA-deficient cells depended on MLH1/PMS2, and MLH 1 may also contribute to cell growth arrest by increasing the basal level of p53 activity.
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