当前位置： SCI文献检索 > NEUROBIOLOGY OF DISEASE期刊下所有文献 > Infection of sympathetic and sensory neurones with herpes simplex virus does not elicit a shut-off of cellular protein synthesis: implications for viral latency and herpes vectors.

Infection of sympathetic and sensory neurones with herpes simplex virus does not elicit a shut-off of cellular protein synthesis: implications for viral latency and herpes vectors.

Abstract：

:Infection of non-neuronal cell types with herpes simplex virus type 1 (HSV-1) results in the degradation of host mRNA (Kwong & Frenkel 1987) and a shutoff in host protein synthesis (Roizman et al. 1965). This effect is mediated by a virion associated protein that is encoded by the viral vhs gene (Read & Frenkel 1983). This virion host shutoff (VHS) helps regulate viral gene expression and promotes efficient viral replication during the lytic cycle (Kwong & Frenkel 1987). Cultured sympathetic and sensory neurones, in contrast to primary rat fibroblasts, PC-12 cells, and Vero cells, showed no reduction in protein synthesis following infection with HSV-1. The resistance of neurones to VHS may be important in allowing establishment of a latent infection. In addition, this finding has a favourable impact on the idea of using HSV as a vector to deliver foreign genes into neurones.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Nichol PF,Chang JY,Johnson EM Jr,Olivo PD

doi

10.1006/nbdi.1994.0011

subject

Has Abstract

pub_date

1994-11-01 00:00:00

pages

83-94

issue

1-2

eissn

0969-9961

issn

1095-953X

pii

S0969996184700118

journal_volume

1

pub_type

杂志文章

相关文献

NEUROBIOLOGY OF DISEASE文献大全
  • Sequence of deposition of heterogeneous amyloid beta-peptides and APO E in Down syndrome: implications for initial events in amyloid plaque formation.

    abstract：:Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein. Because the neuropathological phenotype in older DS subjects...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1996.0003

    authors： Lemere CA,Blusztajn JK,Yamaguchi H,Wisniewski T,Saido TC,Selkoe DJ

    更新日期：1996-02-01 00:00:00

  • Preferential inactivation of Scn1a in parvalbumin interneurons increases seizure susceptibility.

    abstract：:Voltage-gated sodium channels (VGSCs) are essential for the generation and propagation of action potentials in electrically excitable cells. Dominant mutations in SCN1A, which encodes the Nav1.1 VGSC α-subunit, underlie several forms of epilepsy, including Dravet syndrome (DS) and genetic epilepsy with febrile seizure...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.08.012

    authors： Dutton SB,Makinson CD,Papale LA,Shankar A,Balakrishnan B,Nakazawa K,Escayg A

    更新日期：2013-01-01 00:00:00

  • Transgenic expression of an expanded (GCG)13 repeat PABPN1 leads to weakness and coordination defects in mice.

    abstract：:Oculopharyngeal muscular dystrophy (OPMD) is a late-onset disorder caused by a (GCG)n trinucleotide repeat expansion in the poly(A) binding protein nuclear-1 (PABPN1) gene, which in turn leads to an expanded polyalanine tract in the protein. We generated transgenic mice expressing either the wild type or the expanded ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.09.021

    authors： Dion P,Shanmugam V,Gaspar C,Messaed C,Meijer I,Toulouse A,Laganiere J,Roussel J,Rochefort D,Laganiere S,Allen C,Karpati G,Bouchard JP,Brais B,Rouleau GA

    更新日期：2005-04-01 00:00:00

  • Increased vulnerability of nigrostriatal terminals in DJ-1-deficient mice is mediated by the dopamine transporter.

    abstract：:Mutations in the gene for DJ-1 have been associated with early-onset autosomal recessive parkinsonism. Previous studies of null DJ-1 mice have shown alterations in striatal dopamine (DA) transmission with no DAergic cell loss. Here we characterize a new line of DJ-1-deficient mice. A subtle locomotor deficit was prese...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2007.03.014

    authors： Manning-Boğ AB,Caudle WM,Perez XA,Reaney SH,Paletzki R,Isla MZ,Chou VP,McCormack AL,Miller GW,Langston JW,Gerfen CR,Dimonte DA

    更新日期：2007-08-01 00:00:00

  • Formoterol, a β2-adrenoreceptor agonist, induces mitochondrial biogenesis and promotes cognitive recovery after traumatic brain injury.

    abstract：:Traumatic brain injury (TBI) leads to acute necrosis at the site of injury followed by a sequence of secondary events lasting from hours to weeks and often years. Targeting mitochondrial impairment following TBI has shown improvements in brain mitochondrial bioenergetics and neuronal function. Recently formoterol, a h...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2020.104866

    authors： Vekaria HJ,Hubbard WB,Scholpa NE,Spry ML,Gooch JL,Prince SJ,Schnellmann RG,Sullivan PG

    更新日期：2020-07-01 00:00:00

  • Alzheimer's disease pathology in APOE transgenic mouse models: The Who, What, When, Where, Why, and How.

    abstract：:The focus on amyloid plaques and neurofibrillary tangles has yielded no Alzheimer's disease (AD) modifying treatments in the past several decades, despite successful studies in preclinical mouse models. This inconsistency has caused a renewed focus on improving the fidelity and reliability of AD mouse models, with dis...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2020.104811

    authors： Lewandowski CT,Maldonado Weng J,LaDu MJ

    更新日期：2020-06-01 00:00:00

  • TAT-Bcl-x(L) improves survival of neuronal precursor cells in the lesioned striatum after focal cerebral ischemia.

    abstract：:Cerebral ischemia activates endogenous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus. Consecutively, SVZ-derived neural precursors migrate towards ischemic lesions. However, functional relevance of activated neurogenesis is limited by poor survival of new-born precursors. We therefore employed th...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2008.12.013

    authors： Doeppner TR,Dietz GP,El Aanbouri M,Gerber J,Witte OW,Bähr M,Weise J

    更新日期：2009-04-01 00:00:00

  • A WNT1-regulated developmental gene cascade prevents dopaminergic neurodegeneration in adult En1(+/-) mice.

    abstract：:The protracted and age-dependent degeneration of dopamine (DA)-producing neurons of the Substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) in the mammalian midbrain is a hallmark of human Parkinson's Disease (PD) and of certain genetic mouse models of PD, such as mice heterozygous for the homeodomai...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.05.015

    authors： Zhang J,Götz S,Vogt Weisenhorn DM,Simeone A,Wurst W,Prakash N

    更新日期：2015-10-01 00:00:00

  • Matrix metalloproteinase 9 regulates cell death following pilocarpine-induced seizures in the developing brain.

    abstract：:Matrix metalloproteinases (MMPs) are involved in tissue repair, cell death and morphogenesis. We investigated the role of the gelatinases MMP-2 and MMP-9 in the pathogenesis of neuronal death induced by prolonged seizures in the developing brain. Seven-day-old rats, MMP-9 knockout mice and transgenic rats overexpressi...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.06.023

    authors： Hoehna Y,Uckermann O,Luksch H,Stefovska V,Marzahn J,Theil M,Gorkiewicz T,Gawlak M,Wilczynski GM,Kaczmarek L,Ikonomidou C

    更新日期：2012-12-01 00:00:00

  • YOD1 attenuates neurogenic proteotoxicity through its deubiquitinating activity.

    abstract：:Ubiquitination, a fundamental post-translational modification of intracellular proteins, is enzymatically reversed by deubiquitinase enzymes (deubiquitinases). >90 deubiquitinases have been identified. One of these enzymes, YOD1, possesses deubiquitinase activity and is similar to ovarian tumor domain-containing prote...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.01.006

    authors： Tanji K,Mori F,Miki Y,Utsumi J,Sasaki H,Kakita A,Takahashi H,Wakabayashi K

    更新日期：2018-04-01 00:00:00

  • Perinatal human hypoxia-ischemia vulnerability correlates with brain calcification.

    abstract：:Deregulation of intracellular calcium homeostasis is widely considered as one of the underlying pathophysiological mechanisms of hypoxic-ischemic brain injury. Whether this alteration can result in cerebral calcification was investigated in basal ganglia, cerebral cortex, and hippocampus of human premature and term ne...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2000.0332

    authors： Rodríguez MJ,Ursu G,Bernal F,Cusí V,Mahy N

    更新日期：2001-02-01 00:00:00

  • MiR-146a promotes oligodendrocyte progenitor cell differentiation and enhances remyelination in a model of experimental autoimmune encephalomyelitis.

    abstract：:The death of mature oligodendrocytes (OLs) leads to demyelination in the central nervous system (CNS) and subsequently to functional deficits. Remyelination requires the differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating OLs, which in the CNS with neurodegenerative diseases such as multiple sc...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.01.019

    authors： Zhang J,Zhang ZG,Lu M,Zhang Y,Shang X,Chopp M

    更新日期：2019-05-01 00:00:00

  • Anti-NMDA receptor autoantibodies and associated neurobehavioral pathology in mice are dependent on age of first exposure to Toxoplasma gondii.

    abstract：BACKGROUND:Toxoplasma gondii is a pathogen implicated in psychiatric disorders. As elevated antibodies to T. gondii are also present in non-symptomatic individuals, we hypothesized that the age during first exposure to the pathogen may affect symptom manifestation. We tested this hypothesis by evaluating neurobehaviora...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2016.03.005

    authors： Kannan G,Crawford JA,Yang C,Gressitt KL,Ihenatu C,Krasnova IN,Cadet JL,Yolken RH,Severance EG,Pletnikov MV

    更新日期：2016-07-01 00:00:00

  • Heterogeneous expression of hydrocephalic phenotype in the hyh mice carrying a point mutation in alpha-SNAP.

    abstract：:The hyh mouse carrying a point mutation in the gene encoding for soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein alpha (alpha-SNAP) develops inherited hydrocephalus. The investigation was designed to study: (i) the clinical evolution of hyh mice; (ii) factors other than the alpha-SNAP mutation that ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.02.009

    authors： Bátiz LF,Páez P,Jiménez AJ,Rodríguez S,Wagner C,Pérez-Fígares JM,Rodríguez EM

    更新日期：2006-07-01 00:00:00

  • Neurons exposed to ammonia reproduce the differential alteration in nitric oxide modulation of guanylate cyclase in the cerebellum and cortex of patients with liver cirrhosis.

    abstract：:The activation of soluble guanylate cyclase by nitric oxide is increased in the frontal cortex but is reduced in the cerebellum of patients who died with liver cirrhosis. The aims of this work were to assess whether hyperammonemia is responsible for the region-selective alterations in guanylate cyclase modulation in l...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.12.001

    authors： Rodrigo R,Erceg S,Felipo V

    更新日期：2005-06-01 00:00:00

  • The alpha(2C)-adrenergic receptor mediates hyperactivity of coloboma mice, a model of attention deficit hyperactivity disorder.

    abstract：:Drugs that modify noradrenergic transmission such as atomoxetine and clonidine are increasingly prescribed for the treatment of attention deficit hyperactivity disorder (ADHD). However, the therapeutic targets of these compounds are unknown. Norepinephrine is also implicated in the hyperactivity exhibited by coloboma ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.05.007

    authors： Bruno KJ,Hess EJ

    更新日期：2006-09-01 00:00:00

  • Cerebrovascular pathology during the progression of experimental Alzheimer's disease.

    abstract：:Clinical and experimental evidence point to a possible role of cerebrovascular dysfunction in Alzheimer's disease (AD). The 5xFAD mouse model of AD expresses human amyloid precursor protein and presenilin genes with mutations found in AD patients. It remains unknown whether amyloid deposition driven by these mutations...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2016.01.001

    authors： Giannoni P,Arango-Lievano M,Neves ID,Rousset MC,Baranger K,Rivera S,Jeanneteau F,Claeysen S,Marchi N

    更新日期：2016-04-01 00:00:00

  • Molecular insights and therapeutic targets for blood-brain barrier disruption in ischemic stroke: critical role of matrix metalloproteinases and tissue-type plasminogen activator.

    abstract：:Blood-brain barrier (BBB) disruption, mediated through matrix metalloproteinases (MMPs) and other mechanisms, is a critical event during ischemic stroke. Tissue plasminogen activator (tPA) is the only FDA-approved thrombolytic therapy for acute ischemic stroke, but the efficacy and safety of its therapeutic applicatio...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2010.03.008

    authors： Jin R,Yang G,Li G

    更新日期：2010-06-01 00:00:00

  • Induction of apoptosis in cells expressing exogenous Hippi, a molecular partner of huntingtin-interacting protein Hip1.

    abstract：:To decipher the pathway of apoptosis induction downstream to caspase-8 activation by exogenous expression of Hippi, an interactor of huntingtin-interacting protein Hip1, we studied apoptosis in HeLa and Neuro2A cells expressing GFP-tagged Hippi. Nuclear fragmentation, caspase-1, caspase-8, caspase-9/caspase-6 and casp...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.11.003

    authors： Majumder P,Chattopadhyay B,Mazumder A,Das P,Bhattacharyya NP

    更新日期：2006-05-01 00:00:00

  • HIV-Tat-mediated Bcl-XL delivery protects retinal ganglion cells during experimental autoimmune optic neuritis.

    abstract：:In multiple sclerosis (MS), post-mortem studies of human brain tissue as well as data from animal models have shown that apoptosis of neurons occurs to a significant extent during this disease. As neurodegeneration in MS correlates with permanent neurological deficits in patients, understanding the mechanisms would be...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.03.003

    authors： Diem R,Taheri N,Dietz GP,Kuhnert A,Maier K,Sättler MB,Gadjanski I,Merkler D,Bähr M

    更新日期：2005-11-01 00:00:00

  • High-fructose intake as risk factor for neurodegeneration: Key role for carboxy methyllysine accumulation in mice hippocampal neurons.

    abstract：:Several studies indicate the involvement of advanced glycation end-products (AGEs) in neurodegenerative diseases. Moreover, the rising consumption of fructose in industrialized countries has been related to cognitive impairment, but the impact of fructose-derived AGEs on hippocampus has never been investigated. The pr...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2016.02.005

    authors： Mastrocola R,Nigro D,Cento AS,Chiazza F,Collino M,Aragno M

    更新日期：2016-05-01 00:00:00

  • Induced pluripotent stem cell lines from Huntington's disease mice undergo neuronal differentiation while showing alterations in the lysosomal pathway.

    abstract：:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by an excessive expansion of a CAG trinucleotide repeat in the gene encoding the protein huntingtin, resulting in an elongated stretch of glutamines near the N-terminus of the protein. Here we report the derivation of a collection of ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.12.032

    authors： Castiglioni V,Onorati M,Rochon C,Cattaneo E

    更新日期：2012-04-01 00:00:00

  • Bri2-23 is a potential cerebrospinal fluid biomarker in multiple sclerosis.

    abstract：:To identify potential multiple sclerosis (MS)-specific biomarkers, we used a proteomic approach to screen cerebrospinal fluid (CSF) from 40 MS patients and 13 controls. We identified seven proteins (Beta-2-microglobulin, Bri2-23, Fetuin-A, Kallikrein-6, Plasminogen, Ribonuclease-1, and Transferrin) that had significan...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.06.007

    authors： Harris VK,Diamanduros A,Good P,Zakin E,Chalivendra V,Sadiq SA

    更新日期：2010-10-01 00:00:00

  • Divergent brain changes in two audiogenic rat strains: A voxel-based morphometry and diffusion tensor imaging comparison of the genetically epilepsy prone rat (GEPR-3) and the Wistar Audiogenic Rat (WAR).

    abstract：:Acoustically evoked seizures (e.g., audiogenic seizures or AGS) are common in models of inherited epilepsy and occur in a variety of species including rat, mouse, and hamster. Two models that have been particularly well studied are the genetically epilepsy prone rat (GEPR-3) and the Wistar Audiogenic Rat (WAR) strains...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.12.014

    authors： Lee Y,Rodriguez OC,Albanese C,Santos VR,Cortes de Oliveira JA,Donatti ALF,Fernandes A,Garcia-Cairasco N,N'Gouemo P,Forcelli PA

    更新日期：2018-03-01 00:00:00

  • Cln5-deficiency in mice leads to microglial activation, defective myelination and changes in lipid metabolism.

    abstract：:CLN5 disease, late infantile variant phenotype neuronal ceroid lipofuscinosis, is a severe neurodegenerative disease caused by mutations in the CLN5 gene, which encodes a lysosomal protein of unknown function. Cln5-deficiency in mice leads to loss of thalamocortical neurons, and glial activation, but the underlying me...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.12.009

    authors： Schmiedt ML,Blom T,Blom T,Kopra O,Wong A,von Schantz-Fant C,Ikonen E,Kuronen M,Jauhiainen M,Cooper JD,Jalanko A

    更新日期：2012-04-01 00:00:00

  • beta-amyloid peptides are cytotoxic to astrocytes in culture: a role for oxidative stress.

    abstract：:beta-Amyloid is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated the cytotoxicty of beta-amyloid peptides (betaA(25-35) and betaA(1-40)) and generation of hydrogen peroxide on cortical cultured astrocytes. Twenty-four hours after a single addition of e...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2000.0313

    authors： Brera B,Serrano A,de Ceballos ML

    更新日期：2000-08-01 00:00:00

  • Pomegranate juice decreases amyloid load and improves behavior in a mouse model of Alzheimer's disease.

    abstract：:Although there are no proven ways to delay onset or slow progression of Alzheimer's disease (AD), studies suggest that diet can affect risk. Pomegranates contain very high levels of antioxidant polyphenolic substances as compared to other fruits and vegetables. Polyphenols have been shown to be neuroprotective in diff...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.08.006

    authors： Hartman RE,Shah A,Fagan AM,Schwetye KE,Parsadanian M,Schulman RN,Finn MB,Holtzman DM

    更新日期：2006-12-01 00:00:00

  • Deep brain stimulation in the treatment of refractory epilepsy: update on current data and future directions.

    abstract：:Deep brain stimulation for epilepsy has garnered attention from epileptologists due to its well-documented success in treating movement disorders and the low morbidity associated with the implantation of electrodes. Given the large proportion of patients who fail medical therapy and are not candidates for surgical ame...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2009.07.007

    authors： Lega BC,Halpern CH,Jaggi JL,Baltuch GH

    更新日期：2010-06-01 00:00:00

  • Effects of enriched environment on animal models of neurodegenerative diseases and psychiatric disorders.

    abstract：:Environmental stimulation throughout development adjusts the neurobehavioral systems involved in learning, memory and defensive responses. Environment-mediated phenotypic plasticity can be considered from two different, yet complementary, viewpoints. On one hand, the possibility that environmental interventions protec...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2008.05.001

    authors： Laviola G,Hannan AJ,Macrì S,Solinas M,Jaber M

    更新日期：2008-08-01 00:00:00

  • Psychosine induces the dephosphorylation of neurofilaments by deregulation of PP1 and PP2A phosphatases.

    abstract：:Patients with Krabbe disease, a genetic demyelinating syndrome caused by deficiency of galactosyl-ceramidase and the resulting accumulation of galactosyl-sphingolipids, develop signs of a dying-back axonopathy compounded by a deficiency of large-caliber axons. Here, we show that axonal caliber in Twitcher mice, an ani...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.01.013

    authors： Cantuti-Castelvetri L,Zhu H,Givogri MI,Chidavaenzi RL,Lopez-Rosas A,Bongarzone ER

    更新日期：2012-05-01 00:00:00