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https://www.readbyqxmd.com/read/29145453/the-antiviral-drug-tenofovir-an-inhibitor-of-pannexin-1-mediated-atp-release-prevents-liver-and-skin-fibrosis-by-downregulating-adenosine-levels-in-the-liver-and-skin
#1
Jessica L Feig, Aranzazu Mediero, Carmen Corciulo, Hailing Liu, Jin Zhang, Miguel Perez-Aso, Laura Picard, Tuere Wilder, Bruce Cronstein
BACKGROUND: Fibrosing diseases are a leading cause of morbidity and mortality worldwide and, therefore, there is a need for safe and effective antifibrotic therapies. Adenosine, generated extracellularly by the dephosphorylation of adenine nucleotides, ligates specific receptors which play a critical role in development of hepatic and dermal fibrosis. Results of recent clinical trials indicate that tenofovir, a widely used antiviral agent, reverses hepatic fibrosis/cirrhosis in patients with chronic hepatitis B infection...
2017: PloS One
https://www.readbyqxmd.com/read/29136128/the-proton-activated-receptor-gpr4-modulates-intestinal-inflammation
#2
Yu Wang, Cheryl de Vallière, Pedro H Imenez Silva, Irina Leonardi, Sven Gruber, Alexandra Gerstgrasser, Hassan Melham, Achim Weber, Katharina Leucht, Lutz Wolfram, Martin Hausmann, Carsten Krieg, Koray Thomasson, Onur Boyman, Isabelle Frey-Wagner, Gerhard Rogler, Carsten A Wagner
BACKGROUND AND AIMS: During active inflammation tissue intraluminal intestinal pH is decreased in patients with inflammatory bowel disease (IBD). Acidic pH may play a role in IBD pathophysiology. Recently, proton sensing G-protein coupled receptors were identified, including GPR4, OGR1 (GPR68), and TDAG8 (GPR65). We investigated whether GPR4 is involved in intestinal inflammation. METHODS: The role of GPR4 was assessed in murine colitis models: chronic dextran sulphate sodium (DSS) administration and by crossbreeding into an IL-10 deficient background for development of spontaneous colitis...
November 9, 2017: Journal of Crohn's & Colitis
https://www.readbyqxmd.com/read/29133847/female-mice-lacking-pald1-exhibit-endothelial-cell-apoptosis-and-emphysema
#3
Isabel Egaña, Hiroshi Kaito, Anja Nitzsche, Lore Becker, Carolina Ballester-Lopez, Colin Niaudet, Milena Petkova, Wei Liu, Michael Vanlandewijck, Alexandra Vernaleken, Thomas Klopstock, Helmut Fuchs, Valerie Gailus-Durner, Martin Hrabe de Angelis, Helge Rask-Andersen, Henrik J Johansson, Janne Lehtiö, Liqun He, Ali Ö Yildirim, Mats Hellström
Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype...
November 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29133437/abnormal-microglia-and-enhanced-inflammation-related-gene-transcription-in-mice-with-conditional-deletion-of-ctcf-in-camk2a-cre-expressing-neurons
#4
Bryan E McGill, Ruteja A Barve, Susan E Maloney, Amy Strickland, Nicholas Rensing, Peter Wang, Michael Wong, Richard Head, David F Wozniak, Jeffrey Milbrandt
CCCTC-binding factor (CTCF) is an 11 zinc finger DNA-binding domain protein that regulates gene expression by modifying three dimensional chromatin structure. Human mutations in CTCF cause intellectual disability and autistic features. Knocking out Ctcf in mouse embryonic neurons is lethal by neonatal age, but the effects of CTCF deficiency in postnatal neurons are less well studied. We knocked out Ctcf postnatally in glutamatergic forebrain neurons under the control of Camk2a-CreCtcf(loxP/loxP) ;Camk2a-Cre+ (Ctcf CKO) mice of both sexes were viable and exhibited profound deficits in spatial learning/memory, impaired motor co-ordination, and decreased sociability by 4 months of age...
November 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29133249/immunomodulation-of-dual-specificity-phosphatase-4-during-visceral-leishmaniasis
#5
Shabina Parveen, Atish Roy Chowdhury, Junaid Jibran Jawed, Suchandra Bhattacharyya Majumdar, Bhaskar Saha, Subrata Majumdar
DUSP4, an inducible protein has a substrate specificity toward ERK1/2, a component of MAP kinase which is enhanced during Leishmania infection. The DUSP4(-/-) mice show increased susceptibility towards the infection caused by Toxoplasma gondii and Leishmania mexicana. These observations emphatically established the fact that unlike DUSP1, DUSP4 has host protective role. In our study, it has been Leishmania donovani, the causative agent of visceral leishmaniasis (VL) significantly reduced the expression of DUSP4 during infection...
November 10, 2017: Microbes and Infection
https://www.readbyqxmd.com/read/29132416/distinct-functional-consequences-of-ecel1-dine-missense-mutations-in-the-pathogenesis-of-congenital-contracture-disorders
#6
Kenichi Nagata, Mika Takahashi, Sumiko Kiryu-Seo, Hiroshi Kiyama, Takaomi C Saido
Endothelin-converting enzyme-like 1 (ECEL1, also termed DINE in rodents), a membrane-bound metalloprotease, has been identified as a gene responsible for distal arthrogryposis (DA). ECEL1-mutated DA is generally characterized by ocular phenotypes in addition to the congenital limb contractures that are common to all DA subtypes. Until now, the consequences of the identified pathogenic mutations have remained incompletely understood because of a lack of detailed phenotypic analyses in relevant mouse models. In this study, we generated a new knock-in mouse strain that carries an ECEL1/DINE pathogenic G607S missense mutation, based on a previous study reporting atypical DA hindlimb phenotypes in two siblings with the mutation...
November 13, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29125827/early-cerebellar-deficits-in-mitochondrial-biogenesis-and-respiratory-chain-complexes-in-the-kiko-mouse-model-of-friedreich-ataxia
#7
Hong Lin, Jordi Magrane, Amy Rattelle, Anna Stepanova, Alexander Galkin, Elisia M Clark, Yi Na Dong, Sarah M Halawani, David R Lynch
Friedreich ataxia (FRDA), the most common recessive inherited ataxia, results from deficiency of frataxin, a small mitochondrial protein crucial for iron-sulphur cluster formation and ATP production. Frataxin deficiency is associated with mitochondrial dysfunction in FRDA patients and animal models; however, early mitochondrial pathology in FRDA cerebellum remains elusive. Using frataxin knock-in/knockout (KIKO) mice and KIKO mice carrying the mitoDendra transgene, we show early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in this FRDA model...
November 1, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29125462/systematic-proteomic-analysis-of-lrrk2-mediated-rab-gtpase-phosphorylation-establishes-a-connection-to-ciliogenesis
#8
Martin Steger, Federico Diez, Herschel S Dhekne, Pawel Lis, Raja S Nirujogi, Ozge Karayel, Francesca Tonelli, Terina N Martinez, Esben Lorentzen, Suzanne R Pfeffer, Dario R Alessi, Matthias Mann
We previously reported that Parkinson's disease (PD) kinase LRRK2 phosphorylates a subset of Rab GTPases on a conserved residue in their switch-II domains (Steger, Tonelli et al., 2016) (PMID: 26824392). Here, we systematically analyzed the Rab protein family and found 14 of them (Rab3A/B/C/D, Rab5A/B/C, Rab8A/B, Rab10, Rab12, Rab29, Rab35 and Rab43) to be specifically phosphorylated by LRRK2, with evidence for endogenous phosphorylation for ten of them (Rab3A/B/C/D, Rab8A/B, Rab10, Rab12, Rab35 and Rab43)...
November 10, 2017: ELife
https://www.readbyqxmd.com/read/29124919/location-and-expression-of-juno-in-mice-oocytes-during-maturation
#9
Banri Suzuki, Yukou Sugano, Jun Ito, Haruka Saito, Sueo Niimura, Hideaki Yamashiro
OBJECTIVE: Oocyte-sperm interaction is the essential step in fertilization. Juno, which has been known as Folate receptor 4, is the Izumo1 receptor expressed on the oocyte membrane. This study aims to investigate the location and expression of Juno in mice oocytes during maturation. METHODS: To confirm the stage at which Juno expression begins in the mice oocytes and its location pattern, we performed immunostaining methods. Next, we evaluated Juno mRNA expression by a half quantitative RT-PCR...
November 10, 2017: JBRA Assisted Reproduction
https://www.readbyqxmd.com/read/29124664/downhill-exercise-alters-immunoproteasome-content-in-mouse-skeletal-muscle
#10
Cory W Baumann, Dongmin Kwak, Deborah A Ferrington, LaDora V Thompson
Content of the immunoproteasome, the inducible form of the standard proteasome, increases in atrophic muscle suggesting it may be associated with skeletal muscle remodeling. However, it remains unknown if the immunoproteasome responds to stressful situations that do not promote large perturbations in skeletal muscle proteolysis. The purpose of this study was to determine how an acute bout of muscular stress influences immunoproteasome content. To accomplish this, wild-type (WT) and immunoproteasome knockout lmp7 (-/-) /mecl1 (-/-) (L7M1) mice were run downhill on a motorized treadmill...
November 9, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/29120956/protein-kinase-c%C3%AE-deletion-causes-hypotension-and-decreased-vascular-contractility
#11
Brandi M Wynne, Cameron G McCarthy, Theodora Szasz, Patrick A Molina, Arlene B Chapman, R Clinton Webb, Janet D Klein, Robert S Hoover
AIM: Protein kinase Cα (PKCα) is a critical regulator of multiple cell signaling pathways including gene transcription, posttranslation modifications and activation/inhibition of many signaling kinases. In regards to the control of blood pressure, PKCα causes increased vascular smooth muscle contractility, while reducing cardiac contractility. In addition, PKCα has been shown to modulate nephron ion transport. However, the role of PKCα in modulating mean arterial pressure (MAP) has not been investigated...
November 8, 2017: Journal of Hypertension
https://www.readbyqxmd.com/read/29120944/targeted-genotyping-identifies-susceptibility-locus-in-brain-derived-neurotrophic-factor-gene-for-chronic-postsurgical-pain
#12
Yuanyuan Tian, Xiaodong Liu, Mingzhong Jia, Hui Yu, Peter Lichtner, Yujian Shi, Zhaoyu Meng, Shanglong Kou, Idy H T Ho, Bo Jia, Benny C P Cheng, Carmen K M Lam, Sharon Tsang, Sunny H Wong, Jun Yu, Christopher H K Cheng, Tony Gin, William K K Wu, Zheyu Chen, Matthew T V Chan
BACKGROUND: The purpose of this study was to evaluate the association between single-nucleotide polymorphisms and chronic postsurgical pain. METHODS: Using GoldenGate genotyping assays, we genotyped 638 polymorphisms within 54 pain-related genes in 1,152 surgical patients who were enrolled in our Persistent Pain after Surgery Study. Patients were contacted by phone to determine whether they had chronic postsurgical pain at 12 months. Polymorphisms identified were validated in a matched cohort of 103 patients with chronic postsurgical pain and 103 patients who were pain free...
November 9, 2017: Anesthesiology
https://www.readbyqxmd.com/read/29118110/cellular-functions-of-the-autism-risk-factor-ptchd1-in-mice
#13
David Tora, Andrea M Gomez, Jean-Francois Michaud, Patricia T Yam, Frédéric Charron, Peter Scheiffele
The gene PTCHD1 is mutated in patients with autism spectrum disorders (ASD) and intellectual disabilities (ID) and has been hypothesized to contribute to Sonic hedgehog (Shh) signaling and synapse formation. We identify a panel of Ptchd1 interacting proteins that include postsynaptic density proteins and the retromer complex, revealing a link to critical regulators of dendritic and postsynaptic trafficking. Ptchd1 knock-out male mice exhibit cognitive alterations, including defects in a novel object recognition task...
November 8, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29116166/multiple-behavior-phenotypes-of-the-fragile-x-syndrome-mouse-model-respond-to-chronic-inhibition-of-phosphodiesterase-4d-pde4d
#14
Mark E Gurney, Patricia Cogram, Robert M Deacon, Christopher Rex, Michael Tranfaglia
Fragile-X syndrome (FXS) patients display intellectual disability and autism spectrum disorder due to silencing of the X-linked, fragile-X mental retardation-1 (FMR1) gene. Dysregulation of cAMP metabolism is a consistent finding in patients and in the mouse and fly FXS models. We therefore explored if BPN14770, a prototypic phosphodiesterase-4D negative allosteric modulator (PDE4D-NAM) in early human clinical trials, might provide therapeutic benefit in the mouse FXS model. Daily treatment of adult male fmr1 C57Bl6 knock-out mice with BPN14770 for 14 days reduced hyperarousal, improved social interaction, and improved natural behaviors such as nesting and marble burying as well as dendritic spine morphology...
November 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29115049/generation-and-characterization-of-an-estrogen-receptor-alpha-icre-knock-in-mouse
#15
Chan Jin Park, Guanglin Chen, Yongbum Koo, Po-Ching P Lin, Joseph A Cacioppo, Hailey Prohaska, CheMyong J Ko
Two estrogen receptors, ESR1 and ESR2, are responsible for the classical actions of estrogens in mammalian species. They display different spatiotemporal expression patterns and non-overlapping functions in various tissues and physiological conditions. In this study, a novel knock-in mouse line that expresses codon-improved Cre recombinase (iCre) under regulation of the natural Esr1 promoter (Esr1-iCre) was developed. Functional characterization of iCre expression by crossing them with reporter lines (ROSA26-lacZ or Ai9-RFP) showed that iCre is faithfully expressed in Esr1-lineage cells...
November 8, 2017: Genesis: the Journal of Genetics and Development
https://www.readbyqxmd.com/read/29113822/lack-of-tnf-%C3%AE-signaling-through-p55-makes-the-mice-more-susceptible-to-acute-infection-but-does-not-alter-state-of-latency-and-reactivation-of-hsv-1
#16
Aditi Mohankrishnan, Rajesh Parmar, Vishakha Bhurani, Sarat Kumar Dalai
TNF-α has been shown to play an important role in pathogenesis and latency of HSV-1 infections. TNF-α signals through TNFR1 (p55) and TNFR2 (p75), and signaling through p55 generally results in gene activation leading to induction of inflammatory responses. Here, we studied the role of TNF-α signaling in latent virus reactivation in p55-knock out (KO) mouse model of ocular HSV-1 infection. We found that KO mice are more susceptible to HSV-1 infection compared to wild type C57Bl/6 mice. While the absence of TNFRI signaling enhanced the ganglion latent DNA content by two folds, there was no difference in the maintenance and reactivation of latent HSV-1...
November 4, 2017: Virus Research
https://www.readbyqxmd.com/read/29113787/nox4-genetic-inhibition-in-experimental-hypertension-and-metabolic-syndrome
#17
Ghina Bouabout, Estelle Ayme-Dietrich, Hugues Jacob, Marie-France Champy, Marie-Christine Birling, Guillaume Pavlovic, Lola Madeira, Lahcen El Fertak, Benoit Petit-Demoulière, Tania Sorg, Yann Herault, John Mudgett, Laurent Monassier
BACKGROUND: Metabolic syndrome is a combination of symptoms including obesity, dyslipidaemia, glucose intolerance and hypertension. Oxidative stress appears to be a pathophysiological factor that links these signs and encourages progression towards heart failure and diabetes. Nox4 is a hydrogen peroxide nicotinamide adenine dinucleotide phosphate (NADPH) oxidase isoform - found in various cardiovascular cells and tissues, but also in tissues such as the liver - which is involved in glucose and lipid homeostasis...
November 4, 2017: Archives of Cardiovascular Diseases
https://www.readbyqxmd.com/read/29113169/lentivirus-mediated-rna-interference-inhibits-the-tumorigenicity-of-cluster-of-differentiation-44-tumor-cells-in-hypopharyngeal-cancer
#18
Chenling Shen, Bin Ye, Haixia Hu, Chen Nie, Yan Ma, Jingrong Lv, Hao Wu, Mingliang Xiang
The present study aimed to investigate whether the inhibition of cluster of differentiation (CD)44 expression reduces the tumorigenicity of CD44(+) cancer stem cells in hypopharyngeal cancer. To assess this, effective recombinant CD44 short hairpin RNA-expressing lentiviruses were produced. Lentivirus-mediated RNA interference (RNAi) was then used to knockdown CD44 gene expression in the hypopharyngeal cancer FaDu cell line. The viability of FaDu cells in the two control groups and the RNAi group (RNAi-CD44 lentiviral vector) was detected using an MTT assay in vitro...
November 2017: Oncology Letters
https://www.readbyqxmd.com/read/29111973/otoferlin-acts-as-a-ca-2-sensor-for-vesicle-fusion-and-vesicle-pool-replenishment-at-auditory-hair-cell-ribbon-synapses
#19
Nicolas Antoine Michalski, Juan D Goutman, Sarah Marie Auclair, Jacques Boutet de Monvel, Margot Tertrais, Alice Emptoz, Alexandre Parrin, Sylvie Nouaille, Marc Guillon, Martin Sachse, Danica Ciric, Amel Bahloul, Jean-Pierre Hardelin, Roger Bryan Sutton, Paul Avan, Shyam S Krishnakumar, James E Rothman, Didier Dulon, Saaid Safieddine, Christine Petit
Hearing relies on rapid, temporally precise, and sustained neurotransmitter release at the ribbon synapses of sensory cells, the inner hair cells (IHCs). This process requires otoferlin, a six C2-domain, Ca(2+)-binding transmembrane protein of synaptic vesicles. To decipher the role of otoferlin in the synaptic vesicle cycle, we produced knock-in mice (Otof(Ala515,Ala517/Ala515,Ala517)) with lower Ca(2+)-binding affinity of the C2C domain. The IHC ribbon synapse structure, synaptic Ca(2+) currents, and otoferlin distribution were unaffected in these mutant mice, but auditory brainstem response wave-I amplitude was reduced...
November 7, 2017: ELife
https://www.readbyqxmd.com/read/29111385/jnk1-inhibition-by-licochalcone-a-leads-to-neuronal-protection-against-excitotoxic-insults-derived-of-kainic-acid
#20
Oriol Busquets, Miren Ettcheto, Ester Verdaguer, Rubén Dario, Carme Auladell, Carlos Beas-Zarate, Jaume Folch, Antoni Camins
The mitogen-activated protein kinase family (MAPK) is an important group of enzymes involved in cellular responses to diverse external stimuli. One of the members of this family is the c-Jun-N-terminal kinase (JNK). The activation of the JNK pathway has been largely associated with the pathogenesis that occurs in epilepsy and neurodegeneration. Kainic acid (KA) administration in rodents is an experimental approach that induces status epilepticus (SE) and replicates many of the phenomenological features of human temporal lobe epilepsy (TLE)...
October 27, 2017: Neuropharmacology
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