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https://www.readbyqxmd.com/read/28702029/inflammation-related-gene-polymorphisms-associated-with-primary-immune-thrombocytopenia
#1
Ju Li, Sai Ma, Linlin Shao, Chunhong Ma, Chengjiang Gao, Xiao-Hui Zhang, Ming Hou, Jun Peng
Primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by a reduced platelet count and an increased risk of bleeding. Although immense research has improved our understanding of ITP, the pathogenesis remains unclear. Here, we investigated the involvement of 25 single-nucleotide polymorphisms (SNPs) of the inflammation-related genes, including CD24, CD226, FCRL3, IL2, IRF5, ITGAM, NLRP3, CARD8, PTPN22, SH2B2, STAT4, TNFAIP3, and TRAF1, in the pathogenesis and treatment response of ITP...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28698407/ccctc-binding-factor-inhibits-breast-cancer-cell-proliferation-and-metastasis-via-inactivation-of-the-nuclear-factor-kappab-pathway
#2
Jie Wu, Peng-Chang Li, Jun-Yi Pang, Guo-You Liu, Xue-Min Xie, Jia-Yao Li, Yi-Cong Yin, Jian-Hua Han, Xiu-Zhi Guo, Ling Qiu
CCCTC-binding factor (CTCF) is an important epigenetic regulator implicated in multiple cellular processes, including growth, proliferation, differentiation, and apoptosis. Although CTCF deletion or mutation has been associated with human breast cancer, the role of CTCF in breast cancer is questionable. We investigated the biological functions of CTCF in breast cancer and the underlying mechanism. The results showed that CTCF expression in human breast cancer cells and tissues was significantly lower than that in normal breast cells and tissues...
July 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28682481/significant-association-between-tnfaip3-inactivation-and-biased-ighv4-34-usage-in-malt-lymphoma
#3
Sarah Moody, Leire Escudero-Ibarz, Ming Wang, Alexandra Clipson, Eguzkine Ochoa Ruiz, Deborah Dunn-Walters, Xuemin Xue, Naiyan Zeng, Alistair Robson, Shih-Sung Chuang, Sergio Cogliatti, Hongxiang Liu, John Goodlad, Margaret Ashton-Key, Markus Raderer, Yingwen Bi, Ming-Qing Du
Both antigenic drive and genetic change play a critical role in the development of mucosa-associated lymphoid tissue (MALT) lymphoma [EdQ please check change], but neither alone is sufficient for malignant transformation, and lymphoma development critically depends on their cooperation. However, which of these different events concur and how they cooperate in MALT lymphomagenesis is totally unknown. To explore this, we investigated somatic mutations of 17 genes and immunoglobulin heavy chain variable region (IGHV) [EdQ please check change]usage in 179 MALT lymphomas from various sites...
July 6, 2017: Journal of Pathology
https://www.readbyqxmd.com/read/28673093/di-2-ethylhexyl-phthalate-suppresses-il-12p40-production-by-gm-csf-dependent-macrophages-via-the-ppar%C3%AE-tnfaip3-traf6-axis-after-lipopolysaccharide-stimulation
#4
R Yamaguchi, A Sakamoto, T Yamamoto, S Narahara, H Sugiuchi, A Hisada, T Katoh, Y Yamaguchi
Activation of peroxisome proliferator-activated receptor α (PPARα) by di-(2-ethylhexyl) phthalate (DEHP) has an anti-inflammatory effect. This study investigated the potential combined influence of PPARα, tumor necrosis factor α-induced protein 3 (TNFAIP3/A20), and tumor necrosis factor receptor-associated factor 6 (TRAF6) on interleukin (IL)-12p40 production by macrophages exposed to DEHP and stimulated with lipopolysaccharide (LPS). LPS upregulated IL-12p40 expression by granulocyte-macrophage colony-stimulating factor-dependent macrophages (on day 9 of culture), whereas adding DEHP to cultures significantly attenuated the response of IL-12p40 to LPS stimulation...
January 1, 2017: Human & Experimental Toxicology
https://www.readbyqxmd.com/read/28658319/hypomorphic-a20-expression-confers-susceptibility-to-psoriasis
#5
Anri Aki, Miyuki Nagasaki, Barbara Ann Malynn, Averil Ma, Takashi Kagari
Psoriasis is a common inflammatory skin disease that affects approximately 1% of the population worldwide. Tumor necrosis factor-alpha-induced protein 3 (TNFAIP3) gene polymorphisms have been strongly associated with psoriasis susceptibility. In this study, we investigate how TNFAIP3, also known as A20, may regulate psoriasis susceptibility. We found that haplo-insufficient A20+/- mice develop severe toll-like receptor (TLR)-induced skin inflammation compared to wild type mice owing to amplified production of interleukin (IL)-17 and IL-23...
2017: PloS One
https://www.readbyqxmd.com/read/28639493/pathway-analysis-to-identify-genetic-variants-associated-with-efficacy-of-adalimumab-in-rheumatoid-arthritis
#6
Frank Eektimmerman, Jesse J Swen, Stefan Böhringer, Tom Wj Huizinga, Wouter M Kooloos, Cornelia F Allaart, Henk-Jan Guchelaar
AIM: About 30% of rheumatoid arthritis patients have no clinical benefit from TNF inhibitors. Genome-wide association (GWA) and candidate gene studies tested several putative genetic variants for TNF inhibitor efficacy with inconclusive results. Therefore, this study applied a systematic pathway analysis. PATIENTS & METHODS: A total of 325 rheumatoid arthritis patients treated with adalimumab were genotyped for 223 SNPs. We tested the association between SNPs and European League Against Rheumatism response and remission at 14 weeks under the additive genetic model using logistic regression...
July 2017: Pharmacogenomics
https://www.readbyqxmd.com/read/28630090/t-cell-transcriptomes-from-paroxysmal-nocturnal-hemoglobinuria-patients-reveal-novel-signaling-pathways
#7
Kohei Hosokawa, Sachiko Kajigaya, Keyvan Keyvanfar, Wangmin Qiao, Yanling Xie, Danielle M Townsley, Xingmin Feng, Neal S Young
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disorder originating from hematopoietic stem cells and is a life-threating disease characterized by intravascular hemolysis, bone marrow (BM) failure, and venous thrombosis. The etiology of PNH is a somatic mutation in the phosphatidylinositol glycan class A gene (PIG-A) on the X chromosome, which blocks synthesis of the glycolipid moiety and causes deficiency in GPI-anchored proteins. PNH is closely related to aplastic anemia, in which T cells mediate destruction of BM...
June 19, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28574503/pathogen-induced-ubiquitin-editing-enzyme-a20-bifunctionally-shuts-off-nf-%C3%AE%C2%BAb-and-caspase-8-dependent-apoptotic-cell-death
#8
Michelle C C Lim, Gunter Maubach, Olga Sokolova, Michael H Feige, Rolf Diezko, Jörn Buchbinder, Steffen Backert, Dirk Schlüter, Inna N Lavrik, Michael Naumann
The human pathogen Helicobacter pylori infects more than half of the world's population and is a paradigm for persistent yet asymptomatic infection but increases the risk for chronic gastritis and gastric adenocarcinoma. For successful colonization, H. pylori needs to subvert the host cell death response, which serves to confine pathogen infection by killing infected cells and preventing malignant transformation. Infection of gastric epithelial cells by H. pylori provokes direct and fast activation of the proinflammatory and survival factor NF-κB, which regulates target genes, such as CXCL8, BIRC3 and TNFAIP3...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28526340/unfolding-the-pathogenesis-of-scleroderma-through-genomics-and-epigenomics
#9
REVIEW
Pei-Suen Tsou, Amr H Sawalha
With unknown etiology, scleroderma (SSc) is a multifaceted disease characterized by immune activation, vascular complications, and excessive fibrosis in internal organs. Genetic studies, including candidate gene association studies, genome-wide association studies, and whole-exome sequencing have supported the notion that while genetic susceptibility to SSc appears to be modest, SSc patients are genetically predisposed to this disease. The strongest genetic association for SSc lies within the MHC region, with loci in HLA-DRB1, HLA-DQB1, HLA-DPB1, and HLA-DOA1 being the most replicated...
May 16, 2017: Journal of Autoimmunity
https://www.readbyqxmd.com/read/28514294/tnfaip3-gene-rs7749323-polymorphism-is-associated-with-late-onset-myasthenia-gravis
#10
Hong-Wei Yang, Yanchen Xie, Yuan Zhao, Liang Sun, Xiaoquan Zhu, Shuhui Wang, Yong-Qiang Zhang, Ping Lei, Yunxiao Meng
In this study, we intended to genotype 2 single nucleotide polymorphisms (SNPs) of tumor necrosis factor α-induced protein 3 (TNFAIP3) genes and explore an association of TNFAIP3 genetic polymorphism with the patients of myasthenia gravis (MG) at clinical level. In brief, 215 of adult MG patients were divided into subgroups according to their clinical features, age of onset, thymic pathology, and autoantibodies. Two hundred thirty-five of healthy controls were also divided into subgroups with gender- and age-matched...
May 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28481875/identification-of-a-tlr2-regulated-gene-signature-associated-with-tumor-cell-growth-in-gastric-cancer
#11
A C West, K Tang, H Tye, L Yu, N Deng, M Najdovska, S J Lin, J J Balic, E Okochi-Takada, P McGuirk, B Keogh, W McCormack, P S Bhathal, M Reilly, M Oshima, T Ushijima, P Tan, B J Jenkins
Toll-like receptors (TLRs) are key regulators of innate immune responses, and their dysregulation is observed in numerous inflammation-associated malignancies, including gastric cancer (GC). However, the identity of specific TLRs and their molecular targets which promote the pathogenesis of human GC is ill-defined. Here, we sought to determine the clinical utility of TLR2 in human GC. TLR2 mRNA and protein expression levels were elevated in >50% of GC patient tumors across multiple ethnicities. TLR2 was also widely expressed among human GC cell lines, and DNA microarray-based expression profiling demonstrated that the TLR2-induced growth responsiveness of human GC cells corresponded with the up-regulation of six anti-apoptotic (BCL2A1, BCL2, BIRC3, CFLAR, IER3, TNFAIP3) and down-regulation of two tumor suppressor (PDCD4, TP53INP1) genes...
May 8, 2017: Oncogene
https://www.readbyqxmd.com/read/28479318/identification-of-somatic-mutations-in-primary-cutaneous-diffuse-large-b-cell-lymphoma-leg-type-by-massive-parallel-sequencing
#12
Sylvain Mareschal, Anne Pham-Ledard, Pierre Julien Viailly, Sydney Dubois, Philippe Bertrand, Catherine Maingonnat, Maxime Fontanilles, Elodie Bohers, Philippe Ruminy, Isabelle Tournier, Philippe Courville, Bernard Lenormand, Anne Bénédicte Duval, Emilie Andrieu, Laurence Verneuil, Beatrice Vergier, Hervé Tilly, Pascal Joly, Thierry Frebourg, Marie Beylot-Barry, Jean-Philippe Merlio, Fabrice Jardin
To determine whether the mutational profile of primary cutaneous diffuse large B-cell lymphoma leg-type (PCLBCL-LT) is unique by comparison with other diffuse large B-cell lymphoma (DLBCL) subtypes, we analyzed a total cohort of 28 PCLBCL-LT cases by next generation sequencing with a Lymphopanel designed for DLBCL. We also analyzed 12 pairs of tumor and control DNA samples by whole exome sequencing which led us to perform resequencing of three selected genes not included in the Lymphopanel: TBL1XR1, KLHL6 and IKZF3...
May 4, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28469620/nf-%C3%AE%C2%BAb-pathway-in-autoinflammatory-diseases-dysregulation-of-protein-modifications-by-ubiquitin-defines-a-new-category-of-autoinflammatory-diseases
#13
REVIEW
Ivona Aksentijevich, Qing Zhou
Autoinflammatory diseases are caused by defects in genes that regulate the innate immunity. Recently, the scope of autoinflammation has been broadened to include diseases that result from dysregulations in protein modifications by the highly conserved ubiquitin (Ub) peptides. Thus far these diseases consist of linear ubiquitin chain assembly complex (LUBAC) and OTULIN deficiencies, and haploinsufficiency of A20. The LUBAC is critical for linear ubiquitination of key signaling molecules in immune response pathways, while deubiquitinase enzymes, OTULIN and TNFAIP3/A20, reverse the effects of ubiquitination by hydrolyzing linear (Met1) and Lys63 (K63) Ub moieties, respectively, from conjugated proteins...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28465464/inflammatory-signals-from-photoreceptor-modulate-pathological-retinal-angiogenesis-via-c-fos
#14
Ye Sun, Zhiqiang Lin, Chi-Hsiu Liu, Yan Gong, Raffael Liegl, Thomas W Fredrick, Steven S Meng, Samuel B Burnim, Zhongxiao Wang, James D Akula, William T Pu, Jing Chen, Lois E H Smith
Pathological neovessels growing into the normally avascular photoreceptors cause vision loss in many eye diseases, such as age-related macular degeneration and macular telangiectasia. Ocular neovascularization is strongly associated with inflammation, but the source of inflammatory signals and the mechanisms by which these signals regulate the disruption of avascular privilege in photoreceptors are unknown. In this study, we found that c-Fos, a master inflammatory regulator, was increased in photoreceptors in a model of pathological blood vessels invading photoreceptors: the very low-density lipoprotein receptor-deficient (Vldlr(-/-) ) mouse...
June 5, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28461114/mir-17-92-promotes-leukemogenesis-in-chronic-myeloid-leukemia-via-targeting-a20-and-activation-of-nf-%C3%AE%C2%BAb-signaling
#15
Qinghua Jia, Huiyan Sun, Fengjun Xiao, Yan Sai, Qingfang Li, Xiaoyan Zhang, Shuang Yang, Hengxiang Wang, Hua Wang, Yuefeng Yang, Chu-Tse Wu, Lisheng Wang
miR-17-92 cluster are overexpressed in hematological malignancies including chronic myeloid leukemia (CML). However, their roles and mechanisms that regulate BCR-ABL induced leukemogenesis remain unclear. In this study, we demonstrated that genomic depletion of miR-17-92 inhibited the BCR-ABL induced leukemogenesis by using a mouse model of transplantation of BCR-ABL transduced hematopoietic stem cells. Furthermore, we identified that miR-19b targeted A20 (TNFAIP3). A20 overexpression results in inactivation of NF-κB activity including decrease of phosphorylation of P65 and IκBα, leads to induce apoptosis and inhibit proliferation and cycle in CML CD34 (+) cells...
June 10, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28454086/association-between-genetic-variants-and-esophageal-cancer-risk
#16
Chenli Yue, Miao Li, Chenxing Da, Hongtao Meng, Shaomin Lv, Xinhan Zhao
We investigated whether single nucleotide polymorphisms (SNPs) in the nuclear assembly factor 1 (NAF1) and TNFAIP3-interacting protein 1 (TNIP1) gene were associated with susceptibility to esophageal cancer in a Chinese Han population. Five SNPs were genotyped and their relationship with esophageal cancer risk was analyzed in a sample of 386 esophageal cancer patients and 495 unrelated healthy controls recruited from the First Affiliated Hospital of Xi'an Jiaotong University. Patients with the AG genotype of rs2320615 were at lower risk of developing esophageal cancer than those with the GG genotype (adjusted odds ratio [OR] = 0...
April 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28448618/rs10499194-polymorphism-in-the-tumor-necrosis-factor-%C3%AE-inducible-protein-3-tnfaip3-gene-is-associated-with-type-1-autoimmune-hepatitis-risk-in-chinese-han-population
#17
Enbin Xu, Hailian Cao, Liming Lin, Honglong Liu
Previous studies have found that the polymorphisms of tumor necrosis factor-α induced protein 3 (TNFAIP3) were associated with several autoimmune diseases. However, the role of TNFAIP3 polymorphisms in type-1 autoimmune hepatitis (AIH-1) remained unclear. The present study aimed to clarify the association of TNFAIP3 polymorphisms with AIH-1 risk in a Chinese Han population. The TaqMan SNP genotyping assay was used to determine the distribution of TNFAIP3 polymorphisms in 432 AIH-1 patients and 500 healthy controls...
2017: PloS One
https://www.readbyqxmd.com/read/28434122/the-status-of-pulmonary-fibrosis-in-systemic-sclerosis-is-associated-with-irf5-stat4-irak1-and-ctgf-polymorphisms
#18
Wenjie Zhao, Xiaoyang Yue, Kuai Liu, Junfeng Zheng, Runda Huang, Jun Zou, Gabriela Riemekasten, Frank Petersen, Xinhua Yu
Pulmonary fibrosis (PF) is one of the leading causes of death in systemic sclerosis (SSc) patients. Although all SSc patients are characterized by autoimmunity, only part of them suffer from PF, suggesting that beside autoimmunity, some additional factors are involved in the initiation of PF in SSc. In this study, we aimed to identify genetic polymorphisms associated with the status of PF in SSc. We performed that an exhaustive search of the PubMed database was performed to identify eligible studies. Then, a comprehensive meta-analysis was performed by comparing PF(+)-SSc and PF(-)-SSc patients to identify genetic polymorphisms associated with the status of PF in SSc...
April 22, 2017: Rheumatology International
https://www.readbyqxmd.com/read/28389907/targeted-next-generation-sequencing-identified-novel-mutations-in-triple-negative-myeloproliferative-neoplasms
#19
Yu-Cheng Chang, Huan-Chau Lin, Yi-Hao Chiang, Caleb Gon-Shen Chen, Ling Huang, Wei-Ting Wang, Chun-Chia Cheng, Johnson Lin, Yi-Fang Chang, Ming-Chih Chang, Ruey-Kuen Hsieh, Shu-Jen Chen, Ken-Hong Lim, Yuan-Yeh Kuo
Mutations in JAK2, MPL and CALR genes have been identified in the majority of myeloproliferative neoplasm (MPN) patients, and patients negative for these three mutations are the so-called triple-negative (TN) MPN. In this study, we examined the mutational profiles of 16 triple-negative MPN patients including 7 essential thrombocythemia (ET), 1 primary myelofibrosis and 8 polycythemia vera (PV). Targeted next-generation sequencing was performed using the ACTOnco Comprehensive Cancer Panel (Ion AmpliSeq Comprehensive Cancer Panel, Life Technologies) to target all coding exons of 409 cancer-related genes...
May 2017: Medical Oncology
https://www.readbyqxmd.com/read/28355611/the-effects-of-mir-136-5p-mediated-regulation-of-a20-in-astrocytes-from-cultured-spinal-cord-cultured-cells-in-vitro
#20
Xiaoming Peng, Xiongzhi Shi, Jinmin Zhao, Jichen He, Keke Li, Zhongxi Cen, Yunle Wu, Shaohui Zong, Gaofeng Zeng
BACKGROUND/AIMS: This study focused on investigating the regulatory mechanism of miR-136-5p in mouse astrocytes stimulated with interleukin-17(IL-17). METHODS: C57BL/6 mouse astrocytes were stimulated with IL-17 (100ng/ml) for various periods of time (0-48 hours) and at various doses (0-200 ng), and the expression levels of inflammatory cytokine and chemokine genes (IL-6, TNF-α, MCP-1, MCP-5 and MIP-2) were then detected by real-time PCR. The expression of the A20 gene was measured with real-time PCR in cells that were stimulated with IL-17 (50 ng/ml) for various periods of time (0-48 hours)...
2017: Cellular Physiology and Biochemistry
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