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Knock-in AND mice

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https://www.readbyqxmd.com/read/28346489/gonadotropin-releasing-hormone-receptor-gnrhr-gene-knock-out-normal-growth-and-development-of-sensory-motor-and-spatial-orientation-behavior-but-altered-metabolism-in-neonatal-and-prepubertal-mice
#1
Ellen R Busby, Nancy M Sherwood
Gonadotropin-releasing hormone (GnRH) is important in the control of reproduction, but its actions in non-reproductive processes are less well known. In this study we examined the effect of disrupting the GnRH receptor in mice to determine if growth, metabolism or behaviors that are not associated with reproduction were affected. To minimize the effects of other hormones such as FSH, LH and sex steroids, the neonatal-prepubertal period of 2 to 28 days of age was selected. The study shows that regardless of sex or phenotype in the Gnrhr gene knockout line, there was no significant difference in the daily development of motor control, sensory detection or spatial orientation among the wildtype, heterozygous or null mice...
2017: PloS One
https://www.readbyqxmd.com/read/28346465/sept12-phosphorylation-results-in-loss-of-the-septin-ring-sperm-annulus-defective-sperm-motility-and-poor-male-fertility
#2
Yi-Ru Shen, Han-Yu Wang, Yung-Che Kuo, Shih-Chuan Shih, Chun-Hua Hsu, Yet-Ran Chen, Shang-Rung Wu, Chia-Yih Wang, Pao-Lin Kuo
Septins are critical for numerous cellular processes through the formation of heteromeric filaments and rings indicating the importance of structural regulators in septin assembly. Several posttranslational modifications (PTMs) mediate the dynamics of septin filaments in yeast. However, little is known about the role of PTMs in regulating mammalian septin assembly, and the in vivo significance of PTMs on mammalian septin assembly and function remains unknown. Here, we showed that SEPT12 was phosphorylated on Ser198 using mass spectrometry, and we generated SEPT12 phosphomimetic knock-in (KI) mice to study its biological significance...
March 27, 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28344023/cardiac-vagal-control-in-a-knock-in-mouse-model-of-dilated-cardiomyopathy-with-a-troponin-mutation
#3
Dong-Yun Zhan, Cheng-Kun Du, Tsuyoshi Akiyama, Sachio Morimoto, Shuji Shimizu, Toru Kawada, Mikiyasu Shirai, James T Pearson
The aim of this study was to evaluate cardiac vagal nerve activity and identify the abnormality of cardiac vagal control in heart failure caused by dilated cardiomyopathy (DCM) using a knock-in mouse model with a ΔK210 mutation in the cardiac troponin T gene. The effects of electrical stimulation of the cervical vagal nerve at 5 and 10Hz (peripheral vagal control) and α2-adrennoceptor stimulation by intravenous medetomidine at 0.1mg/kg (central vagal control) were examined in wild-type (WT) mice and DCM mice...
March 16, 2017: Autonomic Neuroscience: Basic & Clinical
https://www.readbyqxmd.com/read/28343944/rack1-cooperates-with-nras-q61k-to-promote-melanoma-in-vivo
#4
C Campagne, E Reyes-Gomez, M E Picco, S Loiodice, P Salaun, J Ezagal, F Bernex, P H Commère, S Pons, D Esquerre, E Bourneuf, J Estellé, U Maskos, P Lopez-Bergami, G Aubin-Houzelstein, J J Panthier, G Egidy
Melanoma is the deadliest skin cancer. RACK1 (Receptor for activated protein kinase C) protein was proposed as a biological marker of melanoma in human and domestic animal species harboring spontaneous melanomas. As a scaffold protein, RACK1 is able to coordinate the interaction of key signaling molecules implicated in both physiological cellular functions and tumorigenesis. A role for RACK1 in rewiring ERK and JNK signaling pathways in melanoma cell lines had been proposed. Here, we used a genetic approach to test this hypothesis in vivo in the mouse...
March 23, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28342750/mutation-of-the-caspase-3-cleavage-site-in-the-astroglial-glutamate-transporter-eaat2-delays-disease-progression-and-extends-lifespan-in-the-sod1-g93a-mouse-model-of-als
#5
Lauren Taylor Rosenblum, Shashirekha Shamamandri-Markandaiah, Biswarup Ghosh, Emily Foran, Angelo C Lepore, Piera Pasinelli, Davide Trotti
Downregulation in the astroglial glutamate transporter EAAT2 in amyotrophic lateral sclerosis (ALS) patients and mutant SOD1 mouse models of ALS is believed to contribute to the death of motor neurons by excitotoxicity. We previously reported that caspase-3 cleaves EAAT2 at a unique cleavage consensus site located in its c-terminus domain, a proteolytic cleavage that also occurs in vivo in the mutant SOD1 mouse model of ALS and leads to accumulation of a sumoylated EAAT2 C-Terminus fragment (CTE-SUMO1) beginning around onset of disease...
March 22, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28341460/cortical-adrenoceptor-expression-function-and-adaptation-under-conditions-of-cannabinoid-receptor-deletion
#6
B A S Reyes, A F Carvalho, P Szot, D J Kalamarides, Q Wang, L G Kirby, E J Van Bockstaele
A neurochemical target at which cannabinoids interact to have global effects on behavior is brain noradrenergic circuitry. Acute and repeated administration of a cannabinoid receptor synthetic agonist is capable of increasing multiple indices of noradrenergic activity. This includes cannabinoid-induced 1) increases in norepinephrine (NE) release in the medial prefrontal cortex (mPFC); 2) desensitization of cortical α2-adrenoceptor-mediated effects; 3) activation of c-Fos in brainstem locus coeruleus (LC) noradrenergic neurons; and 4) increases in anxiety-like behaviors...
March 21, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28339646/tgf-%C3%AE-receptor-inhibition-prevents-ventricular-fibrosis-in-a-mouse-model-of-progressive-cardiac-conduction-disease
#7
Mickael Derangeon, Jérôme Montnach, Cynthia Ore Cerpa, Benoit Jagu, Justine Patin, Gilles Toumaniantz, Aurore Girardeau, Christopher Lh Huang, William H Colledge, Andrew A Grace, Isabelle Baró, Flavien Charpentier
Loss-of-function mutations in SCN5A, the gene encoding Nav1.5 channel, have been associated with inherited progressive cardiac conduction disease (PCCD). We have proposed that Scn5a heterozygous knock-out (Scn5a+/-) mice, which are characterized by ventricular fibrotic remodeling with ageing, represent a model for PCCD. Our objectives were to identify the molecular pathway involved in fibrosis development and prevent its activation. Methods and results: Our study shows that myocardial interstitial fibrosis occurred in Scn5a+/- mice only after 45 weeks of age...
February 17, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28339401/is-huntingtin-dispensable-in-the-adult-brain
#8
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/28339026/opposite-effects-of-tumor-protein-d-tpd-52-and-tpd54-on-oral-squamous-cell-carcinoma-cells
#9
Kosuke Kato, Yoshiki Mukudai, Hiromi Motohashi, Chihiro Ito, Shinnosuke Kamoshida, Toshikazu Shimane, Seiji Kondo, Tatsuo Shirota
The tumor protein D52 (TPD52) protein family includes TPD52, -53, -54 and -55. Several reports have shown important roles for TPD52 and TPD53, and have also suggested the potential involvement of TPD54, in D52-family physiological effects. Therefore, we performed detailed expression analysis of TPD52 family proteins in oral squamous cell carcinoma (OSCC). Towards this end, TPD54-overexpressing or knocked-down cells were constructed using OSCC-derived SAS, HSC2 and HSC3 cells. tpd52 or tpd53 was expressed or co-expressed in these cells by transfection...
March 23, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28337123/analysis-of-the-serotonergic-system-in-a-mouse-model-of-rett-syndrome-reveals-unusual-upregulation-of-serotonin-receptor-5b
#10
Steffen Vogelgesang, Sabine Niebert, Ute Renner, Wiebke Möbius, Swen Hülsmann, Till Manzke, Marcus Niebert
Mutations in the transcription factor methyl-CpG-binding-protein 2 (MeCP2) cause a delayed-onset neurodevelopmental disorder known as Rett syndrome (RTT). Although alteration in serotonin levels have been reported in RTT patients, the molecular mechanisms underlying these defects are not well understood. Therefore, we chose to investigate the serotonergic system in hippocampus and brainstem of male Mecp2(-/y) knock-out mice in the B6.129P2(C)-Mecp2(tm1.1Bird) mouse model of RTT. The serotonergic system in mouse is comprised of 16 genes, whose mRNA expression profile was analyzed by quantitative RT-PCR...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28337051/a-novel-cd48-based-analysis-of-sepsis-induced-mouse-myeloid-derived-suppressor-cell-compartments
#11
Bei Jia, Chenchen Zhao, Guoli Li, Yaxian Kong, Yaluan Ma, Qiuping Wang, Beibei Wang, Hui Zeng
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous subset of cells that expands dramatically in many disease states and can suppress T-cell responses. MDSCs mainly include monocytic and granulocytic subpopulations that can be distinguished in mice by the expression of Ly6G and Ly6C cell surface markers. This identification system has been validated in experimental tumor models, but not in models of inflammation-associated conditions such as sepsis. We challenged growth factor independent 1 transcription repressor green fluorescent protein (Gfi1:GFP) knock-in reporter mice with cecal ligation and puncture surgery and found that CD11b(+)Ly6G(low)Ly6C(high) MDSCs in this sepsis model comprised both monocytic and granulocytic MDSCs...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28336343/viral-delivered-gene-therapy-to-treat-catecholamine-dependent-polymorphic-ventricular-tachycardia-cpvt2-in-mouse-models
#12
Efrat Kurtzwald-Josefson, Dor Yadin, Shiraz Harun-Khun, Maayan Waldman, Dan Aravot, Asher Shainberg, Michael Eldar, Edith Hochhauser, Michael Arad
BACKGROUND: The recessive form of catecholaminergic polymorphic ventricular tachycardia (CPVT2) is caused by mutations in cardiac calsequestrin (CASQ2), leading to protein defficiency. OBJECTIVE: To develop a viral-delivered gene therapy for CPVT2 and determine the relationship between CASQ2 expression and the antiarrhythmic efficacy in a murine model. METHODS: We used a murine model of CPVT2 caused by the D307H human mutation (CASQ2(D307H)) or CASQ2 knock-out (CASQ2(Δ/Δ))...
March 20, 2017: Heart Rhythm: the Official Journal of the Heart Rhythm Society
https://www.readbyqxmd.com/read/28334871/proteomics-insights-into-infantile-neuronal-ceroid-lipofuscinosis-cln1-point-to-the-involvement-of-cilia-pathology-in-the-disease
#13
Michal Segal-Salto, Karin Hansson, Tamar Sapir, Anna Kaplan, Talia Levy, Michaela Schwizer, Michael Frotscher, Peter James, Orly Reiner
Mutations in the depalmitoylation enzyme, palmitoyl protein thioesterase (PPT1), result in the early onset neurodegenerative disease known as Infantile Neuronal Ceroid Lipofuscinosis. Here, we provide proteomic evidence suggesting that PPT1 deficiency could be considered as a ciliopathy. Analysis of membrane proteins from brain enriched for acylated proteins from neonate Ppt1 knock out and control mice revealed a list of 88 proteins with differential expression levels. Amongst them, we identified Rab3IP, which regulates ciliogenesis in concert with Rab8 and Rab11...
March 6, 2017: Human Molecular Genetics
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
#14
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/28329117/muscle-activity-during-sleep-in-human-subjects-rats-and-mice-towards-translational-models-of-rem-sleep-without-atonia
#15
Alessandro Silvani, Raffaele Ferri, Viviana Lo Martire, Stefano Bastianini, Chiara Berteotti, Agnese Salvadè, Giuseppe Plazzi, Marco Zucconi, Luigi Ferini-Strambi, Claudio L Bassetti, Mauro Manconi, Giovanna Zoccoli
Study Objectives: rapid-eye-movement (REM) sleep without atonia (RSWA) is a marker of REM sleep behavior disorder (RBD) and is common in narcolepsy. Available techniques for electromyogram (EMG) analysis are species-specific, limiting translational research on RSWA. We developed an automated technique based on distributions of normalized EMG values (DNE) to overcome this limitation. With DNE, we tested whether the control of neck and tibialis anterior (TA) muscles during sleep in wild-type rats and mice validly models the control of submentalis (chin) and TA muscles in healthy humans...
February 22, 2017: Sleep
https://www.readbyqxmd.com/read/28328972/altered-gut-microbiome-in-a-mouse-model-of-gulf-war-illness-causes-neuroinflammation-and-intestinal-injury-via-leaky-gut-and-tlr4-activation
#16
Firas Alhasson, Suvarthi Das, Ratanesh Seth, Diptadip Dattaroy, Varun Chandrashekaran, Caitlin N Ryan, Luisa S Chan, Traci Testerman, James Burch, Lorne J Hofseth, Ronnie Horner, Mitzi Nagarkatti, Prakash Nagarkatti, Stephen M Lasley, Saurabh Chatterjee
Many of the symptoms of Gulf War Illness (GWI) that include neurological abnormalities, neuroinflammation, chronic fatigue and gastrointestinal disturbances have been traced to Gulf War chemical exposure. Though the association and subsequent evidences are strong, the mechanisms that connect exposure to intestinal and neurological abnormalities remain unclear. Using an established rodent model of Gulf War Illness, we show that chemical exposure caused significant dysbiosis in the gut that included increased abundance of phylum Firmicutes and Tenericutes, and decreased abundance of Bacteroidetes...
2017: PloS One
https://www.readbyqxmd.com/read/28327634/scleraxis-is-required-for-maturation-of-tissue-domains-for-proper-integration-of-the-musculoskeletal-system
#17
Yuki Yoshimoto, Aki Takimoto, Hitomi Watanabe, Yuji Hiraki, Gen Kondoh, Chisa Shukunami
Scleraxis (Scx) is a basic helix-loop-helix transcription factor that is expressed persistently in tendons/ligaments, but transiently in entheseal cartilage. In this study, we generated a novel Scx(Cre) knock-in (KI) allele, by in-frame replacement of most of Scx exon 1 with Cre recombinase (Cre), to drive Cre expression using Scx promoter and to inactivate the endogenous Scx. Reflecting the intensity and duration of endogenous expression, Cre-mediated excision occurs in tendinous and ligamentous tissues persistently expressing Scx...
March 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28326932/a-critical-role-of-spinal-shank2-proteins-in-nmda-induced-pain-hypersensitivity
#18
Seo-Yeon Yoon, Soon-Gu Kwon, Yong Ho Kim, Ji-Hee Yeo, Hyoung-Gon Ko, Dae-Hyun Roh, Bong-Kiun Kaang, Alvin J Beitz, Jang-Hern Lee, Seog Bae Oh
Background Self-injurious behaviors (SIBs) are devastating traits in autism spectrum disorder (ASD). Although deficits in pain sensation might be one of the contributing factors underlying the development of SIBs, the mechanisms have yet to be addressed. Recently, the Shank2 synaptic protein has been considered to be a key component in ASD, and mutations of SHANK2 gene induce the dysfunction of N-methyl-D-aspartate (NMDA) receptors, suggesting a link between Shank2 and NMDA receptors in ASD. Given that spinal NMDA receptors play a pivotal role in pain hypersensitivity, we investigated the possible role of Shank2 in nociceptive hypersensitivity by examining changes in spontaneous pain following intrathecal NMDA injection in S hank2-/- ( Shank2 knock-out, KO) mice...
January 2017: Molecular Pain
https://www.readbyqxmd.com/read/28325753/mouse-model-for-inherited-renal-fibrosis-associated-with-endoplasmic-reticulum-stress
#19
Sian E Piret, Eric Olinger, Anita A C Reed, M Andrew Nesbit, Tertius A Hough, Liz Bentley, Olivier Devuyst, Roger Cox, Rajesh V Thakker
Renal fibrosis is a common feature of renal failure resulting from multiple aetiologies, including diabetic nephropathy, hypertension and inherited renal disorders. However, the mechanisms of renal fibrosis are incompletely understood and we therefore explored these by establishing a mouse model for a renal tubular disorder, referred to as autosomal dominant tubulointerstitial kidney disease (ADTKD) due to missense uromodulin (UMOD) mutations (ADTKD-UMOD). ADTKD-UMOD, which is associated with retention of mutant uromodulin in the endoplasmic reticulum (ER) of renal thick ascending limb cells, is characterized by hyperuricemia, interstitial fibrosis, inflammation, and renal failure, and we used targeted homologous recombination to generate a knock-in mouse model with an ADTKD-causing missense cysteine to arginine uromodulin mutation (C125R)...
March 21, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28325281/systemic-antisense-therapeutics-for-dystrophin-and-myostatin-exon-splice-modulation-improve-muscle-pathology-of-adult-mdx-mice
#20
Ngoc Lu-Nguyen, Alberto Malerba, Linda Popplewell, Fred Schnell, Gunnar Hanson, George Dickson
Antisense-mediated exon skipping is a promising approach for the treatment of Duchenne muscular dystrophy (DMD), a rare life-threatening genetic disease due to dystrophin deficiency. Such an approach can restore the disrupted reading frame of dystrophin pre-mRNA, generating a truncated form of the protein. Alternatively, antisense therapy can be used to induce destructive exon skipping of myostatin pre-mRNA, knocking down myostatin expression to enhance muscle strength and reduce fibrosis. We have reported previously that intramuscular or intraperitoneal antisense administration inducing dual exon skipping of dystrophin and myostatin pre-mRNAs was beneficial in mdx mice, a mouse model of DMD, although therapeutic effects were muscle type restricted, possibly due to the delivery routes used...
March 17, 2017: Molecular Therapy. Nucleic Acids
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