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cytidine/inflamación
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Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis.
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In recent years, the notion that ovarian carcinoma results from ovulation-induced inflammation of the fallopian tube epithelial cells (FTECs) has gained evidence. However, the mechanistic pathway for this process has not been revealed yet. In the current study, we propose the mutator protein
The antihyperalgesic effect of cytidine-5'-diphosphate-choline in neuropathic and inflammatory pain models.
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This study was designed to test the effects of intracerebroventricularly (i.c.v.) administered CDP-choline (cytidine-5'-diphosphate-choline; citicoline) and its metabolites in rat models of inflammatory and neuropathic pain. The i.c.v. administration of CDP-choline (0.5, 1.0 and 2.0 µmol) produced a
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
Cytidine-phosphate-guanosine oligodeoxynucleotides in combination with CD40 ligand decrease periodontal inflammation and alveolar bone loss in a TLR9-independent manner.
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Local administration of toll-like receptor 9 (TLR9), agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG ODNs), and CD40 ligand (CD40L) can decrease ligature-induced periodontal inflammation and bone loss in wild type (WT) mouse.
OBJECTIVE
This study aimed to explore whether such effect
Acquisition of Genetic Aberrations by Activation-Induced Cytidine Deaminase (AID) during Inflammation-Associated Carcinogenesis.
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Genetic abnormalities such as nucleotide alterations and chromosomal disorders that accumulate in various tumor-related genes have an important role in cancer development. The precise mechanism of the acquisition of genetic aberrations, however, remains unclear. Activation-induced cytidine deaminase
A novel mechanism for inflammation-associated carcinogenesis; an important role of activation-induced cytidine deaminase (AID) in mutation induction.
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Inflammation is a risk for cancer development; however, its mechanism is unknown. Recent studies have revealed that activation-induced cytidine deaminase (AID), which plays essential roles in both class-switch recombination and somatic hypermutation of immunoglobulin gene in B lymphocytes, is
Cytidine deaminase activity as a measure of acute inflammation in rheumatoid arthritis.
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Cytidine deaminase (CD), a cytoplasmic enzyme, is thought to leak out of damaged cells and can be measured in fluids by a simple biochemical assay. This study has shown that serum CD activity is raised in rheumatoid arthritis (RA) compared with osteoarthritis (OA). Synovial fluid (SF) CD activity
Activation-induced cytidine deaminase (AID)-associated multigene signature to assess impact of AID in etiology of diseases with inflammatory component.
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Activation-induced cytidine deaminase (AID) is expressed in B cells within germinal centers and is critically involved in class switch recombination and somatic hypermutation of immunoglobulin loci. Functionally active AID can additionally be detected within ectopic follicular structures developed
Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer.
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Activation-induced cytidine deaminase (AID) is critically involved in class switch recombination and somatic hypermutation of Ig loci resulting in diversification of antibodies repertoire and production of high-affinity antibodies and as such represents a physiological tool to introduce DNA
Serum cytidine deaminase levels after withdrawal of non-steroidal anti-inflammatory treatment in rheumatoid arthritis.
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Increases in joint inflammation in nine patients with rheumatoid arthritis were provoked by withdrawal of their non-steroidal anti-inflammatory drugs. Pain score, duration of morning stiffness, Ritchie articular index score, and the number of analgesic tablets consumed reached peaks after five,
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
Human cytidine deaminases facilitate hepatitis B virus evolution and link inflammation and hepatocellular carcinoma.
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During hepatitis B virus (HBV)-induced hepatocarcinogenesis, chronic inflammation facilitates the evolution of hepatocellular carcinoma (HCC)-promoting HBV mutants. Cytidine deaminases, whose expression is stimulated by inflammatory cytokines and/or chemokines, play an important role in bridging
Activation-induced cytidine deaminase links bile duct inflammation to human cholangiocarcinoma.
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Chronic inflammation plays a critical role in oncogenesis in various human organs. Epidemiological studies have demonstrated that patients with primary sclerosing cholangitis have a predisposition to develop cholangiocarcinoma (CC). However, the molecular mechanisms that account for the development
Inflammation-mediated genomic instability: roles of activation-induced cytidine deaminase in carcinogenesis.
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Chronic inflammation is a strong risk factor for the development of cancer. Many previous studies have demonstrated that a transcriptional factor, nuclear factor (NF)-κB, plays an important role in the association between inflammation and cancer development, particularly tumor promotion and tumor
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