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https://www.readbyqxmd.com/read/28340264/identification-of-19-loci-for-reproductive-traits-in-a-local-chinese-chicken-by-genome-wide-study
#1
Q C Fan, P F Wu, G J Dai, G X Zhang, T Zhang, Q Xue, H Q Shi, J Y Wang
Reproductive traits have long been studied and have an important influence on chicken breeding. To identify quantitative trait loci affecting reproductive traits, a genome-wide analysis of a Chinese chicken breed was performed to analyze age at first egg body weight at first egg, first egg weight, egg weight at the age of 300 days, egg weight at the age of 462 days, egg number at the age of 300 days, egg number between the ages of 300 and 462 days and egg number at the age of 462 days. Nineteen SNPs related to reproductive traits were presented (P < 1...
March 22, 2017: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/28339401/is-huntingtin-dispensable-in-the-adult-brain
#2
Jeh-Ping Liu, Scott O Zeitlin
Huntingtin (HTT) is an essential protein during early embryogenesis and the development of the central nervous system (CNS). Conditional knock-out of mouse Huntingtin (Htt) expression in the CNS beginning during neural development, as well as reducing Htt expression only during embryonic and early postnatal stages, results in neurodegeneration in the adult brain. These findings suggest that HTT is important for the development and/or maintenance of the CNS, but they do not address the question of whether HTT is required specifically in the adult CNS for its normal functions and/or homeostasis...
March 21, 2017: Journal of Huntington's Disease
https://www.readbyqxmd.com/read/28339398/n-terminal-fragments-of-huntingtin-longer-than-residue-170-form-visible-aggregates-independently-to-polyglutamine-expansion
#3
Moore Z Chen, Sue-Ann Mok, Angelique R Ormsby, Paul J Muchowski, Danny M Hatters
BACKGROUND: A hallmark of Huntington's disease is the progressive aggregation of full length and N-terminal fragments of polyglutamine (polyQ)-expanded Huntingtin (Htt) into intracellular inclusions. The production of N-terminal fragments appears important for enabling pathology and aggregation; and hence the direct expression of a variety of N-terminal fragments are commonly used to model HD in animal and cellular models. OBJECTIVE: It remains unclear how the length of the N-terminal fragments relates to polyQ - mediated aggregation...
March 22, 2017: Journal of Huntington's Disease
https://www.readbyqxmd.com/read/28334820/high-resolution-time-course-mapping-of-early-transcriptomic-molecular-and-cellular-phenotypes-in-huntington-s-disease-cag-knock-in-mice-across-multiple-genetic-backgrounds
#4
Seth A Ament, Jocelynn R Pearl, Andrea Grindeland, Jason St Claire, John C Earls, Marina Kovalenko, Tammy Gillis, Jayalakshmi Mysore, James F Gusella, Jong-Min Lee, Seung Kwak, David Howland, Min Young Lee, David Baxter, Kelsey Scherler, Kai Wang, Donald Geman, Jeffrey B Carroll, Marcy E MacDonald, George Carlson, Vanessa C Wheeler, Nathan D Price, Leroy E Hood
Huntington's disease is a dominantly inherited neurodegenerative disease caused by the expansion of a CAG repeat in the HTT gene. In addition to the length of the CAG expansion, factors such as genetic background have been shown to contribute to the age at onset of neurological symptoms. A central challenge in understanding the disease progression that leads from the HD mutation to massive cell death in the striatum is the ability to characterize the subtle and early functional consequences of the CAG expansion longitudinally...
February 27, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28334749/ctg-repeat-targeting-oligonucleotides-for-down-regulating-huntingtin-expression
#5
Eman M Zaghloul, Olof Gissberg, Pedro M D Moreno, Lee Siggens, Mattias Hällbrink, Anna S Jørgensen, Karl Ekwall, Rula Zain, Jesper Wengel, Karin E Lundin, C I Edvard Smith
Huntington's disease (HD) is a fatal, neurodegenerative disorder in which patients suffer from mobility, psychological and cognitive impairments. Existing therapeutics are only symptomatic and do not significantly alter the disease progression or increase life expectancy. HD is caused by expansion of the CAG trinucleotide repeat region in exon 1 of the Huntingtin gene (HTT), leading to the formation of mutant HTT transcripts (muHTT). The toxic gain-of-function of muHTT protein is a major cause of the disease...
February 17, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28325208/a-systematic-review-of-team-training-in-health-care-ten-questions
#6
Shannon L Marlow, Ashley M Hughes, Shirley C Sonesh, Megan E Gregory, Christina N Lacerenza, Lauren E Benishek, Amanda L Woods, Claudia Hernandez, Eduardo Salas
BACKGROUND: As a result of the recent proliferation of health care team training (HTT), there was a need to update previous systematic reviews examining the underlying structure driving team training initiatives. METHODS: This investigation was guided by 10 research questions. A literature search identified 197 empirical samples detailing the evaluation of team training programs within the health care context; 1,764 measures of HTT effectiveness were identified within these samples...
April 2017: Joint Commission Journal on Quality and Patient Safety
https://www.readbyqxmd.com/read/28322270/huntington-s-disease-blood-and-brain-show-a-common-gene-expression-pattern-and-share-an-immune-signature-with-alzheimer-s-disease
#7
Davina J Hensman Moss, Michael D Flower, Kitty K Lo, James R C Miller, Gert-Jan B van Ommen, Peter A C 't Hoen, Timothy C Stone, Amelia Guinee, Douglas R Langbehn, Lesley Jones, Vincent Plagnol, Willeke M C van Roon-Mom, Peter Holmans, Sarah J Tabrizi
There is widespread transcriptional dysregulation in Huntington's disease (HD) brain, but analysis is inevitably limited by advanced disease and postmortem changes. However, mutant HTT is ubiquitously expressed and acts systemically, meaning blood, which is readily available and contains cells that are dysfunctional in HD, could act as a surrogate for brain tissue. We conducted an RNA-Seq transcriptomic analysis using whole blood from two HD cohorts, and performed gene set enrichment analysis using public databases and weighted correlation network analysis modules from HD and control brain datasets...
March 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28314127/suicide-attempt-in-mental-disorders-medi-association-with-5-htt-il-10-and-tnf-alpha-polymorphisms
#8
Verônica de Medeiros Alves, Aline Cristine Pereira E Silva, Elaine Virgínia Martins de Souza, Leilane Camila Ferreira de Lima Francisco, Edilson Leite de Moura, Valfrido Leão de-Melo-Neto, Antonio E Nardi
BACKGROUND: Mental disorders (MeDi) and suicide attempts (SA) are influenced by environmental and genetic factors. Genetic polymorphism studies have identified some candidate genes for suicidal behaviour in people with MeDi. OBJECTIVE: To evaluate MeDi and SA in relation to the presence of rs2020933 (5-HTT), rs1800871 (IL-10) and rs1800629 (TNF-α) polymorphisms. METHODS: A questionnaire for identification and general data, a brief quality of life assessment (WHOQOL-brief), the scale of suicide ideation by Beck and the MINI International Neuropsychiatric Interview were used in this study...
February 27, 2017: Journal of Psychiatric Research
https://www.readbyqxmd.com/read/28303108/transcriptional-signature-of-an-altered-purine-metabolism-in-the-skeletal-muscle-of-a-huntington-s-disease-mouse-model
#9
Michal Mielcarek, Ryszard T Smolenski, Mark Isalan
Huntington's disease (HD) is a fatal neurodegenerative disorder, caused by a polyglutamine expansion in the huntingtin protein (HTT). HD has a peripheral component to its pathology: skeletal muscles are severely affected, leading to atrophy, and malfunction in both pre-clinical and clinical settings. We previously used two symptomatic HD mouse models to demonstrate the impairment of the contractile characteristics of the hind limb muscles, which was accompanied by a significant loss of function of motor units...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28300621/acute-exposure-to-chlorpyrifos-caused-nadph-oxidase-mediated-oxidative-stress-and-neurotoxicity-in-a-striatal-cell-model-of-huntington-s-disease
#10
Gifty A Dominah, Rachael A McMinimy, Sallay Kallon, Gunnar F Kwakye
We hypothesized that expression of mutant Huntingtin (HTT) would modulate the neurotoxicity of the commonly used organophosphate insecticide, chlorpyrifos (CPF), revealing cellular mechanisms underlying neurodegeneration. Using a mouse striatal cell model of HD, we report that mutant HD cells are more susceptible to CPF-induced cytotoxicity as compared to wild-type. This CPF-induced cytotoxicity caused increased production of reactive oxygen species, reduced glutathione levels, decreased superoxide dismutase activity, and increased malondialdehyde levels in mutant HD cells relative to wild-type...
March 11, 2017: Neurotoxicology
https://www.readbyqxmd.com/read/28291238/polymorphisms-of-5-htt-lpr-and-gn%C3%AE-3-825c-t-and-response-to-antidepressant-treatment-in-functional-dyspepsia-a-study-from-the-functional-dyspepsia-treatment-trial
#11
Yuri A Saito, G Richard Locke, Ann E Almazar, Ernest P Bouras, Colin W Howden, Brian E Lacy, John K DiBaise, Charlene M Prather, Bincy P Abraham, Hashem B El-Serag, Paul Moayyedi, Linda M Herrick, Lawrence A Szarka, Michael Camilleri, Frank A Hamilton, Cathy D Schleck, Katherine E Tilkes, Alan R Zinsmeister, Nicholas J Talley
OBJECTIVES: The Functional Dyspepsia Treatment Trial reported that amitriptyline (AMI) was associated with adequate relief of functional dyspepsia (FD) symptoms, but the pharmacogenetics of antidepressant response in FD are not known. GNβ3 825C>T CC genotype has been previously linked to FD and TT genotype to antidepressant response in depression. The ss genotype of the 5-HTT LPR variant of the serotonin transporter gene (SLC6A4) has been linked to selective serotonin reuptake inhibitor (SSRI) response...
March 14, 2017: American Journal of Gastroenterology
https://www.readbyqxmd.com/read/28288000/age-associated-chromatin-relaxation-is-enhanced-in-huntington-s-disease-mice
#12
Myungsun Park, Byungkuk Min, Kyuheum Jeon, Sunwha Cho, Jung Sun Park, Jisun Kim, Jeha Jeon, Jinhoi Song, Seokho Kim, Sangkyun Jeong, Hyemyung Seo, Yong-Kook Kang
Expansion of polyglutamine stretch in the huntingtin (HTT) protein is a major cause of Huntington's disease (HD). The polyglutamine part in HTT interacts with various proteins implicated in epigenetic regulation of genes, suggesting that mutant HTT may disturb the integrity of the epigenetic system. Here, we used a PCRseq-based method to examine expression profile of 395 exonic segments from 260 "epi-driver" genes in splenic T lymphocytes from aged HD mice. We identified 67 exonic segments differentially expressed between young and aged HD mice, most of them upregulated in the aged...
March 12, 2017: Aging
https://www.readbyqxmd.com/read/28286283/prior-fear-conditioning-does-not-impede-enhanced-active-avoidance-in-serotonin-transporter-knockout-rats
#13
Pieter Schipper, Marloes J A G Henckens, Bart Borghans, Marlies Hiemstra, Tamas Kozicz, Judith R Homberg
Stressors can be actively or passively coped with, and adequate adaption of the coping response to environmental conditions can reduce their potential deleterious effects. One major factor influencing stress coping behaviour is serotonin transporter (5-HTT) availability. Abolishment of 5-HTT is known to impair fear extinction but facilitates acquisition of signalled active avoidance (AA), a behavioural task in which an animal learns to avoid an aversive stimulus that is predicted by a cue. Flexibility in adapting coping behaviour to the nature of the stressor shapes resilience to stress-related disorders...
March 7, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28282438/a-new-caenorhabditis-elegans-model-of-human-huntingtin-513-aggregation-and-toxicity-in-body-wall-muscles
#14
Amy L Lee, Hailey M Ung, L Paul Sands, Elise A Kikis
Expanded polyglutamine repeats in different proteins are the known determinants of at least nine progressive neurodegenerative disorders whose symptoms include cognitive and motor impairment that worsen as patients age. One such disorder is Huntington's Disease (HD) that is caused by a polyglutamine expansion in the human huntingtin protein (htt). The polyglutamine expansion destabilizes htt leading to protein misfolding, which in turn triggers neurodegeneration and the disruption of energy metabolism in muscle cells...
2017: PloS One
https://www.readbyqxmd.com/read/28282362/gene-to-gene-interactions-regulate-endogenous-pain-modulation-in-fibromyalgia-patients-and-healthy-controls-antagonistic-effects-between-opioid-and-serotonin-related-genes
#15
Tour Jeanette, Löfgren Monika, Mannerkorpi Kaisa, Gerdle Björn, Larsson Anette, Palstam Annie, Bileviciute-Ljungar Indre, Bjersing Jan, Ingvar Martin, Ernberg Malin, Schalling Martin, Kosek Eva
Chronic pain is associated with dysfunctional endogenous pain modulation, involving both central opioid and serotonergic (5-HT) signaling. Fibromyalgia (FM) is a chronic pain syndrome, characterized by widespread musculoskeletal pain and reduced exercise-induced hypoalgesia (EIH). In this study, we assessed the effects of three functional genetic polymorphisms on EIH in 130 patients with FM and 132 healthy controls (HC). Subjects were genotyped regarding the mu-opioid receptor (OPRM1) gene (rs1799971), the serotonin transporter (5-HTT) gene (5-HTTLPR/rs25531) and the serotonin-1a receptor (5-HT1a) gene (rs6296)...
March 7, 2017: Pain
https://www.readbyqxmd.com/read/28274274/a-novel-form-of-necrosis-triad-occurs-in-human-huntington-s-disease
#16
Emiko Yamanishi, Kazuko Hasegawa, Kyota Fujita, Shizuko Ichinose, Saburo Yagishita, Miho Murata, Kazuhiko Tagawa, Takumi Akashi, Yoshinobu Eishi, Hitoshi Okazawa
We previously reported transcriptional repression-induced atypical cell death of neuron (TRIAD), a new type of necrosis that is mainly regulated by Hippo pathway signaling and distinct from necroptosis regulated by RIP1/3 pathway. Here, we examined the ultrastructural and biochemical features of neuronal cell death in the brains of human HD patients in parallel with the similar analyses using mutant Htt-knock-in (Htt-KI) mice. LATS1 kinase, the critical regulator and marker of TRIAD, is actually activated in cortical neurons of postmortem human HD and of Htt-KI mouse brains, while apoptosis promoter kinase Plk1 was inactivated in human HD brains...
March 8, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28272473/vesicle-mir-195-derived-from-endothelial-cells-inhibits-expression-of-serotonin-transporter-in-vessel-smooth-muscle-cells
#17
Junzhong Gu, Huiyuan Zhang, Bingyang Ji, Hui Jiang, Tao Zhao, Rongcai Jiang, Zhiren Zhang, Shengjiang Tan, Asif Ahmed, Yuchun Gu
Serotonin or 5-hydroxytryptamine (5-HT) has been shown to be essential in lots of physiological and pathological processes. It is well known that 5-HT and 5-HT transporter (5-HTT) play important roles in the pulmonary artery in pulmonary hypertension. However, little is known about the function of 5-HTT in other arteries. In this study we found that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype could be reversed by knocking-down of 5-HTT or endothelial cells conditional medium (EC-CM)...
March 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28270748/huntingtin-is-required-for-neural-but-not-cardiac-pancreatic-progenitor-differentiation-of-mouse-embryonic-stem-cells-in-vitro
#18
Man Shan Yu, Naoko Tanese
Mutation in the huntingtin (HTT) gene causes Huntington's disease (HD). It is an autosomal dominant trinucleotide-repeat expansion disease in which CAG repeat sequence expands to >35. This results in the production of mutant HTT protein with an increased stretch of glutamines near the N-terminus. The wild type HTT gene encodes a 350 kD protein whose function remains elusive. Mutant HTT protein has been implicated in transcription, axonal transport, cytoskeletal structure/function, signal transduction, and autophagy...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28266655/intact-sensory-motor-network-structure-and-function-in-far-from-onset-premanifest-huntington-s-disease
#19
Martin Gorges, Hans-Peter Müller, Isabella Maria Sophie Mayer, Gesa Sophie Grupe, Thomas Kammer, Georg Grön, Jan Kassubek, G Bernhard Landwehrmeyer, Robert Christian Wolf, Michael Orth
Structural and functional changes attributable to the neurodegenerative process in Huntington's disease (HD) may be evident in HTT CAG repeat expansion carriers before the clinical manifestations of HD. It remains unclear, though, how far from motor onset a consistent signature of the neurodegenerative process in HD can be detected. Twelve far from onset preHD and 22 age-matched healthy control participants underwent volumetric structural magnetic resonance imaging (MRI), diffusion tensor imaging (DTI), and resting-state functional MRI (11 preHD, 22 controls) as well as electrophysiological measurements (12 preHD, 13 controls)...
March 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28263187/aggregation-of-scaffolding-protein-disc1-dysregulates-phosphodiesterase-4-in-huntington-s-disease
#20
Motomasa Tanaka, Koko Ishizuka, Yoko Nekooki-Machida, Ryo Endo, Noriko Takashima, Hideyuki Sasaki, Yusuke Komi, Amy Gathercole, Elaine Huston, Kazuhiro Ishii, Kelvin Kai-Wan Hui, Masaru Kurosawa, Sun-Hong Kim, Nobuyuki Nukina, Eiki Takimoto, Miles D Houslay, Akira Sawa
Huntington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansion of the polyQ tract in Huntingtin (HTT). While motor impairment mediated by polyQ-expanded HTT has been intensively studied, molecular mechanisms for nonmotor symptoms in HD, such as psychiatric manifestations, remain elusive. Here we have demonstrated that HTT forms a ternary protein complex with the scaffolding protein DISC1 and cAMP-degrading phosphodiesterase 4 (PDE4) to regulate PDE4 activity. We observed pathological cross-seeding between DISC1 and mutant HTT aggregates in the brains of HD patients as well as in a murine model that recapitulates the polyQ pathology of HD (R6/2 mice)...
March 6, 2017: Journal of Clinical Investigation
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