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Interleukin-1 and tumor necrosis factor-α trigger restriction of hepatitis B virus infection via a cytidine deaminase activation-induced cytidine deaminase (AID).
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Virus infection is restricted by intracellular immune responses in host cells, and this is typically modulated by stimulation of cytokines. The cytokines and host factors that determine the host cell restriction against hepatitis B virus (HBV) infection are not well understood. We screened 36
TP53 mutations coincide with the ectopic expression of activation-induced cytidine deaminase in the fibroblast-like synoviocytes derived from a fraction of patients with rheumatoid arthritis.
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Main features of rheumatoid arthritis (RA), hyperplasia of fibroblast-like synoviocytes (FLS) and joint destruction are caused by inflammatory cytokines produced in chronic autoimmune inflammation. Cell-intrinsic acquisition of tumour-like phenotypes of RA-FLS could also be responsible for the
Activation-induced cytidine deaminase mRNA expression in oral squamous cell carcinoma-derived cell lines is upregulated by inflammatory cytokines.
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Activation-induced cytidine deaminase (AID) induces cytosine deamination to generate somatic hypermutation and class switch recombnation in immunoglobulin genes. AID expression is upregulated by inflammatory cytokines such as interferon-γ and tumor necrosis factor (TNF)-α, which in turn induce p53
Transcriptional regulation of APOBEC3G, a cytidine deaminase that hypermutates human immunodeficiency virus.
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Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G) is an antiretroviral deoxycytidine deaminase that lethally hypermutates human immunodeficiency virus type 1 (HIV-1) but is itself neutralized by the HIV-1-encoded viral infectivity factor. Accordingly, APOBEC3G occurs
Amino acid-mediated stimulation of renal phospholipid biosynthesis after acute tubular necrosis.
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The mechanism by which amino acid infusion stimulates membrane physpholipid biosynthesis during renal regeneration after mercuric-chloride-induced acute tubular necrosis was studied in the rat. Amino acids can act directly on regenerating renal tissue to enhance net phospholipid synthesis because
Phospholipid metabolism during renal regeneration after acute tubular necrosis.
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Renal function, structure, and membrane metabolism were studied during regeneration of proximal tubular cells in rats. A reversible syndrome of nonoliguric acute renal failure was induced by the intravenous administration of a low dose of mercuric chloride (1.0 mg Hg/kg). At day 1 there was a marked
Cytidine-5'-Diphosphocholine Protects the Liver From Ischemia/Reperfusion Injury Preserving Mitochondrial Function and Reducing Oxidative Stress.
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Cytidine-5'-diphosphocholine (CDP-choline) participates as an intermediary in the synthesis of phosphatidylcholine, an essential component of cellular membranes. Citicoline treatment has shown beneficial effects in cerebral ischemia, but its potential to diminish reperfusion damage in liver has not
DNA methylation profiles in the human genes for tumor necrosis factors alpha and beta in subpopulations of leukocytes and in leukemias.
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The genomic sequencing technique has been applied to assess the state of methylation in the DNA from human leukocyte subpopulations from healthy individuals and in the DNA from several individuals with myeloid or lymphatic leukemias or non-Hodgkin lymphomas. Leukocyte populations were purified by
The etiology of steroid-induced avascular necrosis of bone. A laboratory and clinical study.
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An attempt was made to reproduce in the experimental animal the clinical condition of steroid induced avascular necrosis of bone. There was a decrease in the ability of subchondral osteocytes to metabolize H3 cytidine and an increased amount of cell death as indicated by the number of empty
Expression of activation-induced cytidine deaminase splicing variants in patients with ankylosing spondylitis.
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To investigate the expression patterns of activation-induced cytidine deaminase (AID) variants in peripheral blood mononuclear cells (PBMCs) of patients with ankylosing spondylitis (AS) and examine their clinical implications, we isolated PBMCs from healthy controls (HC, n = 33) and patients with AS
Inhibitory effects of EICAR on infectious pancreatic necrosis virus replication.
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Recently, the antiviral 5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide (EICAR) was shown to inhibit the replication of the infectious pancreatic necrosis virus (IPNV). In order to obtain more information about the mechanism of the antiviral action of EICAR we studied its effect on viral
Cytidine deaminase enables Toll-like receptor 8 activation by cytidine or its analogs.
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Toll-like receptor 8 (TLR8), a sensor for pathogen-derived single-stranded RNA (ssRNA), binds to uridine (Uri) and ssRNA to induce defense responses. We here show that cytidine (Cyd) with ssRNA also activated TLR8 in peripheral blood leukocytes (PBLs) and a myeloid cell line U937, but not in an
Decreased vascular endothelial growth factor expression associated with tumor regression induced by (E)-2'-deoxy-2'-(fluoromethylene)cytidine (MDL 101,731).
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The effect of the antitumor drug MDL 101,731 [(E)-2'-deoxy-2'-(fluoromethylene)cytidine] on tumor growth and on steady-state vascular endothelial growth factor (VEGF) mRNA levels in MDA-MB-231, PC-3, MCF-7, and HT-29 human tumor xenografts grown in nude mice was examined, using quantitative in situ
Activation-induced cytidine deaminase links between inflammation and the development of colitis-associated colorectal cancers.
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OBJECTIVE
Activation-induced cytidine deaminase (AID) was originally identified as an inducer of somatic hypermutations in the immunoglobulin gene. We recently revealed that ectopic AID expression serves as a link between the cellular editing machinery and high mutation frequencies, leading to human
Targeting activation-induced cytidine deaminase prevents colon cancer development despite persistent colonic inflammation.
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Inflammatory bowel disease (IBD) is an important etiologic factor in the development of colorectal cancer. However, the mechanism underlying carcinogenesis through chronic inflammation is still unknown. Activation-induced cytidine deaminase (AID) is induced by the inflammation and involved in
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