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https://www.readbyqxmd.com/read/27915160/histone-deacetylase-9-plays-a-role-in-the-antifibrogenic-effect-of-astaxanthin-in-hepatic-stellate-cells
#1
Yue Yang, Minkyung Bae, Young-Ki Park, Yoojin Lee, Tho X Pham, Swetha Rudraiah, José Manautou, Sung I Koo, Ji-Young Lee
Activation of hepatic stellate cells (HSCs) is critical for liver fibrosis development. Previously, we showed that astaxanthin (ASTX), a xanthophyll carotenoid, has antifibrogenic effects in LX-2 cells, a human HSC cell line. We sought to determine the effect of ASTX on HSC activation, and to identify molecular mediators that are critically involved in the processes. ASTX prevented the activation of mouse primary HSCs, as evidenced by attenuated induction of procollagen type I α1. In human primary HSCs, ASTX also inhibited transforming growth factor β1 (TGFβ1)-induced fibrogenic gene expression...
November 12, 2016: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/27901321/copy-number-variants-in-a-population-based-investigation-of-klippel-trenaunay-syndrome
#2
Aggeliki Dimopoulos, Robert J Sicko, Denise M Kay, Shannon L Rigler, Ruzong Fan, Paul A Romitti, Marilyn L Browne, Charlotte M Druschel, Michele Caggana, Lawrence C Brody, James L Mills
Klippel-Trenaunay syndrome (KTS) is a rare congenital vascular disorder that is thought to occur sporadically; however, reports of familial occurrence suggest a genetic component. We examined KTS cases to identify novel, potentially causal copy number variants (CNVs). We identified 17 KTS cases from all live-births occurring in New York (1998-2010). Extracted DNA was genotyped using Illumina microarrays and CNVs were called using PennCNV software. CNVs selected for follow-up had ≥10 single nucleotide polymorphisms (SNPs) and minimal overlap with in-house controls or controls from the Database of Genomic Variants...
November 30, 2016: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/27833022/hdac9-regulates-the-alternative-lengthening-of-telomere-alt-pathway-via-the-formation-of-alt-associated-pml-bodies
#3
Mohd Raeed Jamiruddin, Taku Kaitsuka, Farzana Hakim, Atsushi Fujimura, Fan-Yan Wei, Hisato Saitoh, Kazuhito Tomizawa
Cancer cells overcome cellular senescence by activating the telomere maintenance mechanism, which can be either through telomerase or the alternative lengthening of telomeres (ALT). Being exclusive to cancer cells, targeting ALT is a more promising route for the development of drugs against cancer. The histone deacetylase (HDAC) family plays significant roles in various cellular processes. In addition to the regulation of gene expression, HDACs are also known to directly interact with many proteins. We focused on this family, and found that HDAC9 was up-regulated in ALT-positive cells...
December 2, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27827316/brm-promoter-polymorphisms-risk-and-survival-of-advanced-non-small-cell-lung-cancer-patients-in-the-princess-margaret-cohort-and-ncic-ctg-br-24-trial
#4
Geoffrey Liu, Sinead Cuffe, Shermi Liang, Abul K Azad, Lu Cheng, Yonathan Brhane, Xin Qiu, David W Cescon, Jeff P Bruce, Zhuo Chen, Dangxiao Cheng, Devalben Patel, Brandon C Tse, Scott A Laurie, Glenwood D Goss, Natasha B Leighl, Rayjean J Hung, Penelope A Bradbury, Lesley Seymour, Frances A Shepherd, Ming-Sound Tsao, Bingshu E Chen, Wei Xu, David Reisman
PURPOSE: BRM, a key catalytic subunit of the SWI/SNF chromatin remodeling complex, is a putative tumor susceptibility gene that is silenced in 15% of non-small cell lung cancer (NSCLC). Two novel BRM promoter polymorphisms (BRM-741, BRM-1321) are associated with reversible epigenetic silencing of BRM protein expression. EXPERIMENTAL DESIGN: Advanced NSCLC patients from the Princess Margaret (PM) cohort study and from the CCTG BR.24 clinical trial were genotyped for BRM promoter polymorphisms...
November 8, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/27824051/genomic-analyses-identify-recurrent-mef2d-fusions-in-acute-lymphoblastic-leukaemia
#5
Zhaohui Gu, Michelle Churchman, Kathryn Roberts, Yongjin Li, Yu Liu, Richard C Harvey, Kelly McCastlain, Shalini C Reshmi, Debbie Payne-Turner, Ilaria Iacobucci, Ying Shao, I-Ming Chen, Marcus Valentine, Deqing Pei, Karen L Mungall, Andrew J Mungall, Yussanne Ma, Richard Moore, Marco Marra, Eileen Stonerock, Julie M Gastier-Foster, Meenakshi Devidas, Yunfeng Dai, Brent Wood, Michael Borowitz, Eric E Larsen, Kelly Maloney, Leonard A Mattano, Anne Angiolillo, Wanda L Salzer, Michael J Burke, Francesca Gianni, Orietta Spinelli, Jerald P Radich, Mark D Minden, Anthony V Moorman, Bella Patel, Adele K Fielding, Jacob M Rowe, Selina M Luger, Ravi Bhatia, Ibrahim Aldoss, Stephen J Forman, Jessica Kohlschmidt, Krzysztof Mrózek, Guido Marcucci, Clara D Bloomfield, Wendy Stock, Steven Kornblau, Hagop M Kantarjian, Marina Konopleva, Elisabeth Paietta, Cheryl L Willman, Mignon L Loh, Stephen P Hunger, Charles G Mullighan
Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5...
November 8, 2016: Nature Communications
https://www.readbyqxmd.com/read/27799148/deregulated-expression-of-hdac9-in-b-cells-promotes-development-of-lymphoproliferative-disease-and-lymphoma
#6
V S Gil, G Bhagat, L Howell, J Zhang, C H Kim, S Stengel, F Vega, A Zelent, K Petrie
Histone Deacetylase 9 (HDAC9) is expressed in B-cells and its overexpression has been observed in B-lymphoproliferative disorders and B-cell non-Hodgkin lymphomas (B-NHL). We examined HDAC9 protein expression and copy number alterations in primary B-NHL samples, identifying high HDAC9 expression among various lymphoma entities and HDAC9 copy number gains in 50% of diffuse large B-cell lymphoma (DLBCL). To study the role of HDAC9 in lymphomagenesis we generated a genetically engineered mouse (GEM) model that constitutively expressed an HDAC9 transgene throughout B-cell development under the control of the immunoglobulin heavy chain (IgH) enhancer (Eμ)...
October 28, 2016: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/27796860/genetic-risk-factors-for-ischemic-and-hemorrhagic-stroke
#7
REVIEW
Ganesh Chauhan, Stéphanie Debette
Understanding the genetic risk factors for stroke is an essential step to decipher the underlying mechanisms, facilitate the identification of novel therapeutic targets, and optimize the design of prevention strategies. A very small proportion of strokes are attributable to monogenic conditions, the vast majority being multifactorial, with multiple genetic and environmental risk factors of small effect size. Genome-wide association studies and large international consortia have been instrumental in finding genetic risk factors for stroke...
December 2016: Current Cardiology Reports
https://www.readbyqxmd.com/read/27753926/os-05-01-prox1-gene-cc-genotype-as-a-major-determinant-of-early-onset-of-t2d-and-cardiovascular-complications-in-slavic-subjects-from-advance-study
#8
Pavel Hamet, Mounsif Haloui, François Harvey, François-Christophe Marois-Blanchet, Paul Simon, John Raelson, Michael Phillips, John Chalmers, Mark Woodward, Michel Marre, Stephen Harrap, Johanne Tremblay
OBJECTIVE: We have previously reported distinct genetic architectures of renal impairment in T2D patients of Slavic and Celtic origins participating in the ADVANCE trial (J Hypertens. 2015 Jun;33 Suppl 1:e3). Further analysis suggests that the major driver of the difference in the prevalence of T2D complications between Slavic and Celtic groups is due to an earlier onset of diabetes in Slavic patients. In an attempt to distinguish between environmental and genetic factors on age of onset of diabetes, we have determined the age of onset of T2D in Slavic subjects living in Celtic countries and confirmed the same earlier onset (-2 years) in these subjects, notwithstanding their living environment...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27702909/transcriptome-analysis-of-trigeminal-ganglia-following-masseter-muscle-inflammation-in-rats
#9
Man-Kyo Chung, Jennifer Park, Jamila Asgar, Jin Y Ro
BACKGROUND: Chronic pain in masticatory muscles is a major medical problem. Although mechanisms underlying persistent pain in masticatory muscles are not fully understood, sensitization of nociceptive primary afferents following muscle inflammation or injury contributes to muscle hyperalgesia. It is well known that craniofacial muscle injury or inflammation induces regulation of multiple genes in trigeminal ganglia, which is associated with muscle hyperalgesia. However, overall transcriptional profiles within trigeminal ganglia following masseter inflammation have not yet been determined...
2016: Molecular Pain
https://www.readbyqxmd.com/read/27643319/os-05-01-prox1-gene-cc-genotype-as-a-major-determinant-of-early-onset-of-t2d-and-cardiovascular-complications-in-slavic-subjects-from-advance-study
#10
Pavel Hamet, Mounsif Haloui, François Harvey, François-Christophe Marois-Blanchet, Paul Simon, John Raelson, Michael Phillips, John Chalmers, Mark Woodward, Michel Marre, Stephen Harrap, Johanne Tremblay
OBJECTIVE: We have previously reported distinct genetic architectures of renal impairment in T2D patients of Slavic and Celtic origins participating in the ADVANCE trial (J Hypertens. 2015 Jun;33 Suppl 1:e3). Further analysis suggests that the major driver of the difference in the prevalence of T2D complications between Slavic and Celtic groups is due to an earlier onset of diabetes in Slavic patients. In an attempt to distinguish between environmental and genetic factors on age of onset of diabetes, we have determined the age of onset of T2D in Slavic subjects living in Celtic countries and confirmed the same earlier onset (-2 years) in these subjects, notwithstanding their living environment...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27642596/polymorphism-of-hdac9-gene-is-associated-with-increased-risk-of-acute-coronary-syndrome-in-chinese-han-population
#11
Zhenhua Han, Xin Dong, Chaoying Zhang, Yue Wu, Zuyi Yuan, Xinhong Wang
Recent genome-wide association studies (GWAS) have indicated an association of histone deacetylase 9 (HDAC9) genetic variant with large-vessel stroke and coronary artery disease, among the European population. However, whether HDAC9 gene is associated with an increased susceptibility to acute coronary syndrome (ACS) in Chinese Han population is not known. A total of 472 patients, including patients with ACS (N = 309), and those with chest pain syndrome (controls, N = 163) were enrolled. Genotyping for HDAC9 gene was performed using the ligation detection reaction assay...
2016: BioMed Research International
https://www.readbyqxmd.com/read/27633396/silencing-of-histone-deacetylase-9-expression-in-podocytes-attenuates-kidney-injury-in-diabetic-nephropathy
#12
Feng Liu, Ming Zong, Xiaofei Wen, Xuezhu Li, Jun Wang, Yi Wang, Wei Jiang, Xiaojun Li, Zhongliang Guo, Hualin Qi
Podocyte dysfunction is important in the onset and development of diabetic nephropathy (DN). Histone deacetylases (HDACs) have been recently proved to play critical roles in the pathogenesis of DN. As one subtype of the class IIa HDACs, HDAC9 is capable to repress/de-repress their target genes in tumor, inflammation, atherosclerosis and metabolic diseases. In the present study, we investigate whether HDAC9 is involved in the pathophysiologic process of DN, especially the podocyte injury. Firstly, we explored the expression patterns and localization of HDAC9 and found that HDAC9 expression was significantly up-regulated in high glucose (HG)-treated mouse podocytes, as well as kidney tissues from diabetic db/db mice and patients with DN...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27558292/the-microrna-cluster-mir-183-96-182-contributes-to-long-term-memory-in-a-protein-phosphatase-1-dependent-manner
#13
Bisrat T Woldemichael, Ali Jawaid, Eloïse A Kremer, Niharika Gaur, Jacek Krol, Antonin Marchais, Isabelle M Mansuy
Memory formation is a complex cognitive function regulated by coordinated synaptic and nuclear processes in neurons. In mammals, it is controlled by multiple molecular activators and suppressors, including the key signalling regulator, protein phosphatase 1 (PP1). Here, we show that memory control by PP1 involves the miR-183/96/182 cluster and its selective regulation during memory formation. Inhibiting nuclear PP1 in the mouse brain, or training on an object recognition task similarly increases miR-183/96/182 expression in the hippocampus...
2016: Nature Communications
https://www.readbyqxmd.com/read/27540854/a-new-dna-methyltransferase-histone-deacetylase-kinase-axis-in-innate-immunity
#14
Gourisankar Ghosh, Malini Sen
Regulatory roles of protein and DNA modifications in gene expression during host defense have long been appreciated. In a recent article published in Nature Immunology, Li et al. (2016) provide a unique glimpse of yet another aspect of coordinated DNA methylation and protein acetylation in host response to pathogenic stimuli. They elegantly demonstrate that DNA methylation and transcriptional activation at the HDAC9 promoter by DNMT3a, along with lysine deacetylation of TBK1 by HDAC9, are essential events during host defense...
August 18, 2016: Molecular Cell
https://www.readbyqxmd.com/read/27507882/mef2d-bcl9-fusion-gene-is-associated-with-high-risk-acute-b-cell-precursor-lymphoblastic-leukemia-in-adolescents
#15
Kyogo Suzuki, Yusuke Okuno, Nozomu Kawashima, Hideki Muramatsu, Tatsuya Okuno, Xinan Wang, Shinsuke Kataoka, Yuko Sekiya, Motoharu Hamada, Norihiro Murakami, Daiei Kojima, Kotaro Narita, Atsushi Narita, Hirotoshi Sakaguchi, Kimiyoshi Sakaguchi, Nao Yoshida, Nobuhiro Nishio, Asahito Hama, Yoshiyuki Takahashi, Kazuko Kudo, Koji Kato, Seiji Kojima
PURPOSE: Acute lymphoblastic leukemia (ALL) makes up a significant proportion of all pediatric cancers, and relapsed ALL is a leading cause of cancer-associated deaths in children. Identification of risk factors and druggable molecular targets in ALL can lead to a better stratification of treatments and subsequent improvement in prognosis. PATIENTS AND METHODS: We enrolled 59 children with relapsed or primary refractory ALL who were treated in our institutions. We primarily performed RNA sequencing (RNA-seq) using patients' leukemic cells to comprehensively detect gene fusions and analyze gene expression profiles...
October 1, 2016: Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology
https://www.readbyqxmd.com/read/27494404/hdac9-variant-rs2107595-modifies-susceptibility-to-coronary-artery-disease-and-the-severity-of-coronary-atherosclerosis-in-a-chinese-han-population
#16
Xue-Bin Wang, Ya-di Han, Shrestha Sabina, Ning-Hua Cui, Shuai Zhang, Ze-Jin Liu, Cong Li, Fang Zheng
A previous genome-wide association study showed that a single nucleotide polymorphism (SNP) rs2107595 in histone deacetylase 9 (HDAC9) gene was associated with large artery stroke (LAS) in Caucasians. Based on the similar atherosclerotic pathogenesis between LAS and coronary artery disease (CAD), we aimed to evaluate the associations of SNP rs2107595 with CAD risk and the severity of coronary atherosclerosis in a Chinese Han population, and explore the potential gene-environment interactions among SNP rs2107595 and conventional CAD risk factors...
2016: PloS One
https://www.readbyqxmd.com/read/27434014/erratum-methyltransferase-dnmt3a-upregulates-hdac9-to-deacetylate-the-kinase-tbk1-for-activation-of-antiviral-innate-immunity
#17
Xia Li, Qian Zhang, Yuanyuan Ding, Yiqi Liu, Dezhi Zhao, Kai Zhao, Qicong Shen, Xingguang Liu, Xuhui Zhu, Nan Li, Zhongyi Cheng, Guoping Fan, Qingqing Wang, Xuetao Cao
No abstract text is available yet for this article.
July 19, 2016: Nature Immunology
https://www.readbyqxmd.com/read/27343431/ampk-activates-lxr%C3%AE-and-abca1-expression-in-human-macrophages
#18
Marina Kemmerer, Ilka Wittig, Florian Richter, Bernhard Brüne, Dmitry Namgaladze
ATP-binding cassette transporter A1 (ABCA1) is a key modulator of macrophage cholesterol homeostasis. We studied the impact of AMP-activated protein kinase (AMPK) on ABCA1 expression in primary human and THP-1 macrophages. Pharmacological or genetic activation of AMPK increased mRNA and protein expression of ABCA1 and its transcriptional activator liver X receptor (LXR) α, resulting in increased cholesterol efflux to apolipoprotein AI-containing medium. On the other side, an AMPK knockdown decreased ABCA1 and LXRα mRNA and protein...
September 2016: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/27333946/hdac1-hdac4-and-hdac9-bind-to-pc3-tis21-btg2-and-are-required-for-its-inhibition-of-cell-cycle-progression-and-cyclin-d1-expression
#19
Laura Micheli, Giorgio D'Andrea, Luca Leonardi, Felice Tirone
PC3/Tis21 is a transcriptional cofactor that inhibits proliferation in several cell types, including neural progenitors. Here we report that PC3/Tis21 associates with HDAC1, HDAC4 and HDAC9 in vivo, in fibroblast cells. Furthermore, when HDAC1, HDAC4 or HDAC9 are silenced in fibroblasts or in a line of cerebellar progenitor cells, the ability of PC3/Tis21 to inhibit proliferation is significantly reduced. Overexpression of HDAC1, HDAC4 or HDAC9 in fibroblasts and in cerebellar precursor cells synergizes with PC3/Tis21 in inhibiting the expression of cyclin D1, a cyclin selectively inhibited by PC3/Tis21...
June 23, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27312341/a-post-translational-modification-cascade-employing-hdac9-piasy-rnf4-axis-regulates-chondrocyte-hypertrophy-by-modulating-nkx3-2-protein-stability
#20
Hye-Jeong Choi, Seongran Kwon, Dae-Won Kim
While Nkx3.2/Bapx1 promotes chondrogenic differentiation and plays a role in maintaining chondrocyte viability and suppressing chondrocyte hypertrophy, the regulatory mechanisms of Nkx3.2 remain poorly understood. Here we show that p300- and HDAC9-induced Nkx3.2 acetylation and de-acetylation, respectively, play critical roles in controlling Nkx3.2 protein stability. In addition, we also found that HDAC9-dependent de-acetylation of Nkx3.2 triggers PIASy-mediated sumoylation and subsequent RNF4-mediated SUMO-targeted ubiquitination...
September 2016: Cellular Signalling
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