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https://www.readbyqxmd.com/read/29772429/long-non-coding-rna-nron-is-downregulated-in-hcc-and-suppresses-tumour-cell-proliferation-and-metastasis
#1
Zhicheng Yao, Zhiyong Xiong, Ruixi Li, Hao Liang, Changchang Jia, Meihai Deng
Dysregulation of long non-coding RNAs is a newly identified mechanism for tumour progression. Previous studies have suggested that the nuclear factor of activated T cells (NFAT) gene plays a very important role in cancer growth and metastasis. However, lncNRON is a newly identified repressor of NFAT, and its function is largely unknown, especially in hepatocellular carcinoma (HCC). Therefore, the expression levels of lncNRON in 215 pairs of HCC tissue were evaluated by qRT-PCR, and its relationship to clinicopathological parameters, recurrence, and survival was analysed...
May 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29770600/how-does-glucagon-like-peptide-1-stimulate-human-%C3%AE-cell-proliferation-a-lesson-from-islet-graft-experiments
#2
Yoshio Fujitani
The incidence of type 2 diabetes increases with age. The age-dependent decline in functional β-cell mass contributes to the increased risk of onset of diabetes, reflecting the central role of pancreatic β cells in glucose homeostasis. Indeed, the replication rate of human and rodent β cells is known to decline sharply with age, and such a characteristic of β cells may explain the increased onset of type 2 diabetes in the older population. The molecular mechanism involved in the age-dependent decline of β-cell proliferation has been extensively studied, mainly using rodents and in vitro culture systems, but its molecular basis is still largely unknown...
May 16, 2018: Journal of Diabetes Investigation
https://www.readbyqxmd.com/read/29760186/hypertrophic-cardiomyopathy-mutations-increase-myofilament-ca-2-buffering-alter-intracellular-ca-2-handling-and-stimulate-ca-2-dependent-signalling
#3
Paul Robinson, Xing Liu, Alexander Sparrow, Suketu Patel, Yin Hua Zhang, Barbara Casadei, Hugh Watkins, Charles S Redwood
Mutations in thin filament regulatory proteins that cause hypertrophic cardiomyopathy (HCM) increase myofilament Ca2+ -sensitivity. Mouse models exhibit increased Ca2+ buffering and arrhythmias, and we hypothesized that these changes are primary effects of the mutations (independent of compensatory changes) and that increased Ca2+ - buffering and altered Ca2+ -handling contribute to HCM pathogenesis via activation of Ca2+ -dependent signalling. Here, we determined the primary effects of HCM mutations on intracellular Ca2+ -handling and Ca2+ -dependent signalling in a model system possessing Ca2+ -handling mechanisms and contractile protein isoforms close to human in the absence of potentially confounding remodeling...
May 14, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29758183/increasing-cardiomyocyte-atrogin-1-reduces-aging-associated-fibrosis-and-regulates-remodeling-in-vivo
#4
Roberto Mota, Traci L Parry, Cecelia Yates, Zhaoyan Qiang, Samuel C Eaton, Jean Marie Mwiza, Deepthi Tulasi, Jonathan C Schisler, Cam Patterson, Tania Zaglia, Marco Sandri, Monte S Willis
The muscle-specific ubiquitin ligase atrogin-1 (MAFbx) has been identified as a critical regulator of pathologic and physiologic cardiac hypertrophy; it regulates these processes by ubiquitinating transcription factors (NFAT and FOXO1/3). However, the role of Atrogin-1 in regulating transcription factors in aging has not previously been described. Atrogin-1 cardiomyocyte-specific transgenic (Tg+) adult mice (αMHC promoter driven) have normal cardiac function and size. Here we demonstrate that 18-month-old Atrogin-1 Tg+ hearts exhibit significantly increased anterior wall thickness without functional impairment vs wild-type mice...
May 11, 2018: American Journal of Pathology
https://www.readbyqxmd.com/read/29751971/cardiac-hypertrophy-elevates-serum-levels-of-fibroblast-growth-factor-23
#5
Isao Matsui, Tatsufumi Oka, Yasuo Kusunoki, Daisuke Mori, Nobuhiro Hashimoto, Ayumi Matsumoto, Karin Shimada, Satoshi Yamaguchi, Keiichi Kubota, Sayoko Yonemoto, Tomoaki Higo, Yusuke Sakaguchi, Yoshitsugu Takabatake, Takayuki Hamano, Yoshitaka Isaka
Several experimental studies have shown that fibroblast growth factor 23 (FGF23) induces left ventricular hypertrophy (LVH). However, the opposite directional relationship, namely a potential effect of LVH on FGF23, remains uncertain. Here we evaluated the effects of LVH on FGF23 using cardiomyocyte-specific calcineurin A transgenic mice. At six weeks, these mice showed severe LVH, with elevated levels of serum intact FGF23. FGF23 levels were elevated in cardiomyocytes, but not osteocytes, of the transgenic animals...
May 8, 2018: Kidney International
https://www.readbyqxmd.com/read/29748308/fibroblast-growth-factor-23-and-klotho-contribute-to-airway-inflammation
#6
Stefanie Krick, Alexander Grabner, Nathalie Baumlin, Christopher Yanucil, Scott Helton, Astrid Grosche, Juliette Sailland, Patrick Geraghty, Liliana Viera, Derek W Russell, J Michael Wells, Xin Xu, Amit Gaggar, Jarrod Barnes, Gwendalyn D King, Michael Campos, Christian Faul, Matthias Salathe
Circulating levels of fibroblast growth factor (FGF) 23 are associated with systemic inflammation and increased mortality in chronic kidney disease. α-klotho, a co-receptor for FGF23, is downregulated in chronic obstructive pulmonary disease (COPD). However, whether FGF23 and klotho-mediated FGFR activation delineates a pathophysiologic mechanism in COPD remains unclear. We hypothesized that FGF23 can potentiate airway inflammation via klotho independent FGFR4 activation. FGF23 and its effect were studied using plasma and transbronchial biopsies from COPD and control patients and primary human bronchial epithelial cells isolated from COPD patients as well as a murine COPD model...
May 10, 2018: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/29742440/dyrk1a-kinase-positively-regulates-angiogenic-responses-in-endothelial-cells
#7
Esteban J Rozen, Julia Roewenstrunk, María José Barallobre, Chiara Di Vona, Carole Jung, Ana F Figueiredo, Jeroni Luna, Cristina Fillat, Maria L Arbonés, Mariona Graupera, Miguel A Valverde, Susana de la Luna
Angiogenesis is a highly regulated process essential for organ development and maintenance, and its deregulation contributes to inflammation, cardiac disorders, and cancer. The Ca2+ /nuclear factor of activated T cells (NFAT) signaling pathway is central to endothelial cell angiogenic responses, and it is activated by stimuli like vascular endothelial growth factor (VEGF) A. NFAT phosphorylation by dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs) is thought to be an inactivating event. Contrary to expectations, we show that the DYRK family member DYRK1A positively regulates VEGF-dependent NFAT transcriptional responses in primary endothelial cells...
May 8, 2018: Cell Reports
https://www.readbyqxmd.com/read/29736023/mc4r-agonism-promotes-durable-weight-loss-in-patients-with-leptin-receptor-deficiency
#8
Karine Clément, Heike Biebermann, I Sadaf Farooqi, Lex Van der Ploeg, Barbara Wolters, Christine Poitou, Lia Puder, Fred Fiedorek, Keith Gottesdiener, Gunnar Kleinau, Nicolas Heyder, Patrick Scheerer, Ulrike Blume-Peytavi, Irina Jahnke, Shubh Sharma, Jacek Mokrosinski, Susanna Wiegand, Anne Müller, Katja Weiß, Knut Mai, Joachim Spranger, Annette Grüters, Oliver Blankenstein, Heiko Krude, Peter Kühnen
Genetic defects underlying the melanocortin-4 receptor (MC4R) signaling pathway lead to severe obesity. Three severely obese LEPR-deficient individuals were administered the MC4R agonist setmelanotide, resulting in substantial and durable reductions in hyperphagia and body weight over an observation period of 45-61 weeks. Compared to formerly developed and tested MC4R agonists, setmelanotide has the unique capability of activating nuclear factor of activated T cell (NFAT) signaling and restoring function of this signaling pathway for selected MC4R variants...
May 7, 2018: Nature Medicine
https://www.readbyqxmd.com/read/29735309/the-elevation-of-circulating-fibroblast-growth-factor-23-without-kidney-disease-does-not-increase-cardiovascular-disease-risk
#9
Eva-Maria Pastor-Arroyo, Nicole Gehring, Christiane Krudewig, Sarah Costantino, Carla Bettoni, Thomas Knöpfel, Sibylle Sabrautzki, Bettina Lorenz-Depiereux, Johanne Pastor, Tim M Strom, Martin Hrabě de Angelis, Giovanni G Camici, Francesco Paneni, Carsten A Wagner, Isabel Rubio-Aliaga
High circulating fibroblast growth factor 23 (FGF23) levels are probably a major risk factor for cardiovascular disease in chronic kidney disease. FGF23 interacts with the receptor FGFR4 in cardiomyocytes inducing left ventricular hypertrophy. Moreover, in the liver FGF23 via FGFR4 increases the risk of inflammation which is also found in chronic kidney disease. In contrast, X-linked hypophosphatemia is characterized by high FGF23 circulating levels due to loss of function mutations of the phosphate-regulating gene with homologies to an endopeptidase on the X chromosome (PHEX), but is not characterized by high cardiovascular morbidity...
May 5, 2018: Kidney International
https://www.readbyqxmd.com/read/29725603/stimulation-of-dectin-1-and-dectin-2-during-parenteral-immunization-but-not-mincle-induces-secretory-iga-in-intestinal-mucosa
#10
Alina S Dzharullaeva, Amir I Tukhvatulin, Alina S Erokhova, Alina S Bandelyuk, Nikita B Polyakov, Andrey I Solovyev, Natalia A Nikitenko, Dmitry V Shcheblyakov, Boris S Naroditsky, Denis Y Logunov, Alexander L Gintsburg
Induction of a robust and long-lived mucosal immune response during vaccination is critical to achieve protection against numerous pathogens. However, traditional injected vaccines are generally poor inducers of mucosal immunity. One of the effective strategies to improve vaccine efficacy is incorporation of adjuvant molecules that enhance and polarize adaptive immune reactions. Effects of Syk-coupled lectin receptor agonists as adjuvants to induce mucosal immune reactions during parenteral immunization are not fully studied...
2018: Journal of Immunology Research
https://www.readbyqxmd.com/read/29719087/regulation-of-inward-rectifier-potassium-current-ionic-channel-remodeling-by-at-1-calcineurin-nfat-signaling-pathway-in-stretch-induced-hypertrophic-atrial-myocytes
#11
Jionghong He, Yanan Xu, Long Yang, Guiling Xia, Na Deng, Yongyao Yang, Ye Tian, Zenan Fu, Yongqi Huang
Previous studies have shown that the activation of angiotensin II receptor type I (AT1 ) is attributed to cardiac remodeling stimulated by increased heart load, and that it is followed by the activation of the calcineurin-nuclear factor of activated T-cells (NFAT) signaling pathway. Additionally, AT1 has been found to be a regulator of cardiocyte ionic channel remodeling, and calcineurin-NFAT signals participate in the regulation of cardiocyte ionic channel expression. A hypothesis therefore follows that stretch stimulation may regulate cardiocyte ionic channel remodeling by activating the AT1 -calcineurin-NFAT pathway...
May 2, 2018: Cell Biology International
https://www.readbyqxmd.com/read/29707134/a-jurkat-76-based-triple-parameter-reporter-system-to-evaluate-tcr-functions-and-adoptive-t-cell-strategies
#12
Sandra Rosskopf, Judith Leitner, Wolfgang Paster, Laura T Morton, Renate S Hagedoorn, Peter Steinberger, Mirjam H M Heemskerk
Adoptive T cell therapy using TCR transgenic autologous T cells has shown great potential for the treatment of tumor patients. Thorough characterization of genetically reprogrammed T cells is necessary to optimize treatment success. Here, we describe the generation of triple parameter reporter T cells based on the Jurkat 76 T cell line for the evaluation of TCR and chimeric antigen receptor functions as well as adoptive T cell strategies. This Jurkat subline is devoid of endogenous TCR alpha and TCR beta chains, thereby circumventing the problem of TCR miss-pairing and unexpected specificities...
April 3, 2018: Oncotarget
https://www.readbyqxmd.com/read/29705696/microrna-139-5p-suppresses-myosin-heavy-chain-i-and-iia-expression-via-inhibition-of-the-calcineurin-nfat-signaling-pathway
#13
Meng Xu, Xiaoling Chen, Zhiqing Huang, Daiwen Chen, Bing Yu, Hong Chen, Jun He, Ping Zheng, Junqiu Luo, Jie Yu, Yuheng Luo
MicroRNAs (miRNAs) are a class of small non-coding RNAs that are widely involved in a variety of biological processes. Different skeletal muscle fiber type composition exhibits characteristic differences in functional properties and energy metabolism of skeletal muscle. However, the molecular mechanism by which miRNAs control the different type of muscle fiber formation is still not fully understood. In the present study, we characterized the role of microRNA-139-5p (miR-139-5p) in the regulation of myosin heavy chain (MyHC) isoform expression and its underlying mechanisms...
April 26, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29692354/acetyl-coa-directed-gene-transcription-in-cancer-cells
#14
REVIEW
Inmaculada Martínez-Reyes, Navdeep S Chandel
Fluctuations in acetyl-coenzyme A (acetyl-CoA) levels have been previously associated with changes in global histone acetylation and gene expression. The study by Lee and colleagues (pp. 497-511) in this issue of Genes & Development demonstrates that acetyl-CoA can promote the up-regulation of cell migration- and adhesion-related genes in glioblastoma by controlling Ca2+ -NFAT (nuclear factor of activated T cells) signaling.
April 1, 2018: Genes & Development
https://www.readbyqxmd.com/read/29691251/nfatc1-promotes-anti-tumoral-effector-functions-and-memory-cd8-t-cell-differentiation-during-non-small-cell-lung-cancer-development
#15
Lisanne Heim, Juliane Friedrich, Marina Engelhardt, Denis I Trufa, Carol I Geppert, Ralf Joachim Rieker, Horia Sirbu, Susetta Finotto
Nuclear factor of activated T cells 1 (NFATc1) is a transcription factor activated by T cell receptor (TCR) and Ca2+-signaling that affects T cell activation and effector function. Upon tumor antigen challenge, TCR and calcium-release-activated channels are induced, promoting NFAT dephosphorylation and translocation into the nucleus. In this study, we report a progressive decrease of NFATc1 in lung tumor tissue and in tumor-infiltrating lymphocytes (TIL) of patients suffering from advanced stage non-small cell lung cancer (NSCLC)...
April 24, 2018: Cancer Research
https://www.readbyqxmd.com/read/29686316/publisher-correction-nfat-calcineurin-signaling-promotes-oligodendrocyte-differentiation-and-myelination-by-transcription-factor-network-tuning
#16
Matthias Weider, Laura Julia Starost, Katharina Groll, Melanie Küspert, Elisabeth Sock, Miriam Wedel, Franziska Fröb, Christian Schmitt, Tina Baroti, Anna C Hartwig, Simone Hillgärtner, Sandra Piefke, Tanja Fadler, Marc Ehrlich, Corinna Ehlert, Martin Stehling, Stefanie Albrecht, Ammar Jabali, Hans R Schöler, Jürgen Winkler, Tanja Kuhlmann, Michael Wegner
The originally published version of this Article omitted Tanja Kuhlmann and Michael Wegner as jointly supervising authors. This has now been corrected in both the PDF and HTML versions of the Article.
April 23, 2018: Nature Communications
https://www.readbyqxmd.com/read/29685981/angiotensin-1-7-reduces-cardiac-effects-of-thyroid-hormone-by-gsk3%C3%AE-nfatc3-signaling-pathway
#17
Nathalia Senger, Marcos Barrouin Melo, Gabriela Placoná Diniz, Maria José Campagnole-Santos, Robson Augusto Souza Dos Santos, Maria Luiza M Barreto-Chaves
Patients with hyperthyroidism exhibit increased risk of development and progression of cardiac diseases. The activation of the Renin Angiotensin System (RAS) has been indirectly implicated in these cardiac effects observed in hyperthyroidism. Angiotensin-(1-7) (Ang-(1-7)) has previously been shown to counterbalance pathological effects of Angiotensin II (Ang II). The aim of this study was to investigate the effects of elevated circulating Ang-(1-7) levels on cardiac effects promoted by hyperthyroidism in a transgenic rat (TG) model that constitutively overexpress an Ang-(1-7)-producing fusion protein [TGR(A1-7)3292]...
April 23, 2018: Clinical Science (1979-)
https://www.readbyqxmd.com/read/29674394/acetyl-coa-promotes-glioblastoma-cell-adhesion-and-migration-through-ca-2-nfat-signaling
#18
Joyce V Lee, Corbett T Berry, Karla Kim, Payel Sen, Taehyong Kim, Alessandro Carrer, Sophie Trefely, Steven Zhao, Sully Fernandez, Lauren E Barney, Alyssa D Schwartz, Shelly R Peyton, Nathaniel W Snyder, Shelley L Berger, Bruce D Freedman, Kathryn E Wellen
The metabolite acetyl-coenzyme A (acetyl-CoA) is the required acetyl donor for lysine acetylation and thereby links metabolism, signaling, and epigenetics. Nutrient availability alters acetyl-CoA levels in cancer cells, correlating with changes in global histone acetylation and gene expression. However, the specific molecular mechanisms through which acetyl-CoA production impacts gene expression and its functional roles in promoting malignant phenotypes are poorly understood. Here, using histone H3 Lys27 acetylation (H3K27ac) ChIP-seq (chromatin immunoprecipitation [ChIP] coupled with next-generation sequencing) with normalization to an exogenous reference genome (ChIP-Rx), we found that changes in acetyl-CoA abundance trigger site-specific regulation of H3K27ac, correlating with gene expression as opposed to uniformly modulating this mark at all genes...
April 19, 2018: Genes & Development
https://www.readbyqxmd.com/read/29662170/c-maf-controls-immune-responses-by-regulating-disease-specific-gene-networks-and-repressing-il-2-in-cd4-t-cells
#19
Leona Gabryšová, Marisol Alvarez-Martinez, Raphaëlle Luisier, Luke S Cox, Jan Sodenkamp, Caroline Hosking, Damián Pérez-Mazliah, Charlotte Whicher, Yashaswini Kannan, Krzysztof Potempa, Xuemei Wu, Leena Bhaw, Hagen Wende, Michael H Sieweke, Greg Elgar, Mark Wilson, James Briscoe, Vicki Metzis, Jean Langhorne, Nicholas M Luscombe, Anne O'Garra
The transcription factor c-Maf induces the anti-inflammatory cytokine IL-10 in CD4+ T cells in vitro. However, the global effects of c-Maf on diverse immune responses in vivo are unknown. Here we found that c-Maf regulated IL-10 production in CD4+ T cells in disease models involving the TH 1 subset of helper T cells (malaria), TH 2 cells (allergy) and TH 17 cells (autoimmunity) in vivo. Although mice with c-Maf deficiency targeted to T cells showed greater pathology in TH 1 and TH 2 responses, TH 17 cell-mediated pathology was reduced in this context, with an accompanying decrease in TH 17 cells and increase in Foxp3+ regulatory T cells...
April 16, 2018: Nature Immunology
https://www.readbyqxmd.com/read/29651892/the-intracerebral-hemorrhage-blood-transcriptome-in-humans-differs-from-the-ischemic-stroke-and-vascular-risk-factor-control-blood-transcriptomes
#20
Boryana Stamova, Bradley P Ander, Glen Jickling, Farah Hamade, Marc Durocher, Xinhua Zhan, Da Zhi Liu, Xiyuan Cheng, Heather Hull, Alan Yee, Kwan Ng, Natasha Shroff, Frank R Sharp
Understanding how the blood transcriptome of human intracerebral hemorrhage (ICH) differs from ischemic stroke (IS) and matched controls (CTRL) will improve understanding of immune and coagulation pathways in both disorders. This study examined RNA from 99 human whole-blood samples using GeneChip® HTA 2.0 arrays to assess differentially expressed transcripts of alternatively spliced genes between ICH, IS and CTRL. We used a mixed regression model with FDR-corrected p(Dx) < 0.2 and p < 0.005 and |FC| > 1...
January 1, 2018: Journal of Cerebral Blood Flow and Metabolism
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