当前位置： SCI文献检索 > NEUROBIOLOGY OF DISEASE期刊下所有文献 > Interaction of ASK1 and the beta-amyloid precursor protein in a stress-signaling complex.

Interaction of ASK1 and the beta-amyloid precursor protein in a stress-signaling complex.

Abstract：

:The amyloid precursor protein (APP) is a type I transmembrane protein translocated to neuronal terminals, whose function is still unknown. The C-terminus of APP mediates its interaction with cellular adaptor and signaling proteins, some of which signal to the stress-activated protein kinase (SAPK) pathway. Here we show that ASK1, a MAPKKK that activates two SAPKs, c-Jun N-terminal-kinase (JNK) and p38, is present in a complex containing APP, phospho-MKK6, JIP1 and JNK1. In primary neurons deprived of growth factors, as well as in brains of (FAD)APP-transgenic mice, ASK1 was upregulated in neuronal projections, where it interacted with APP. In non-transgenic brains, ASK1 and APP associated mainly in the ER. Our results indicate that recruitment of ASK1 to stress-signaling complexes assembled with APP may be triggered and enhanced by cellular stress. Thus, ASK1 may be the apical MAPKKK in a signaling complex assembled with APP as a response to stress.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Galvan V,Banwait S,Spilman P,Gorostiza OF,Peel A,Ataie M,Crippen D,Huang W,Sidhu G,Ichijo H,Bredesen DE

doi

10.1016/j.nbd.2007.06.017

subject

Has Abstract

pub_date

2007-10-01 00:00:00

pages

65-75

issue

1

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(07)00134-9

journal_volume

28

pub_type

杂志文章

相关文献

NEUROBIOLOGY OF DISEASE文献大全
  • Cystamine and intrabody co-treatment confers additional benefits in a fly model of Huntington's disease.

    abstract：:Huntington's disease (HD) is a lethal, neurodegenerative disorder caused by expansion of the polyglutamine repeat in the Huntingtin gene (HTT), leading to mutant protein misfolding, aggregation, and neuronal death. Feeding a Drosophila HD model cystamine, or expressing a transgene encoding the anti-htt intracellular a...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.04.007

    authors： Bortvedt SF,McLear JA,Messer A,Ahern-Rindell AJ,Wolfgang WJ

    更新日期：2010-10-01 00:00:00

  • Progressive neuroanatomical changes caused by Grin1 loss-of-function mutation.

    abstract：:NMDA receptor dysfunction is central to the encephalopathies caused by missense mutations in the NMDA receptor subunit genes. Missense variants of GRIN1, GRIN2A, and GRIN2B cause similar syndromes with varying severity of intellectual impairment, autism, epilepsy, and motor dysfunction. To gain insight into possible b...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.104527

    authors： Intson K,van Eede MC,Islam R,Milenkovic M,Yan Y,Salahpour A,Henkelman RM,Ramsey AJ

    更新日期：2019-12-01 00:00:00

  • Erythropoietin promotes hippocampal neurogenesis in in vitro models of neonatal stroke.

    abstract：:The hippocampus is often injured in neonatal stroke. We have investigated the effect of erythropoietin (EPO) on oxygen-glucose deprived hippocampal slices and hypoxic progenitor cells. EPO improved survival of the organotypic hippocampal slices with significantly less cell death in the dentate gyrus and an increased n...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.01.015

    authors： Osredkar D,Sall JW,Bickler PE,Ferriero DM

    更新日期：2010-05-01 00:00:00

  • High t-PA release by neonate brain microvascular endothelial cells under glutamate exposure affects neuronal fate.

    abstract：:Glutamate excitotoxicity is a consolidated hypothesis in neonatal brain injuries and tissue plasminogen activator (t-PA) participates in the processes through proteolytic and receptor mediated effects. In brain microvascular endothelial cell (nBMEC) cultures from neonates, t-PA content and release upon glutamate are h...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.10.020

    authors： Henry VJ,Lecointre M,Laudenbach V,Ali C,Macrez R,Jullienne A,Berezowski V,Carmeliet P,Vivien D,Marret S,Gonzalez BJ,Leroux P

    更新日期：2013-02-01 00:00:00

  • Local insulin and the rapid regrowth of diabetic epidermal axons.

    abstract：:Insulin deficiency may contribute toward the neurological deficits of diabetic polyneuropathy (DPN). In particular, the unique trophic properties of insulin, acting on sensory neuron and axon receptors offer an approach toward reversing loss of skin axons that develops during diabetes. Here we examined how local cutan...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.04.012

    authors： Guo G,Kan M,Martinez JA,Zochodne DW

    更新日期：2011-08-01 00:00:00

  • BDNF regulates the expression of fragile X mental retardation protein mRNA in the hippocampus.

    abstract：:Both fragile X mental retardation protein (FMRP) and brain-derived neurotrophic factor (BDNF) are implicated in the maturation of neurons and in the higher cognitive functions. We have investigated whether FMRP and BDNF are reciprocally regulated in neurons. Exposure of cultured hippocampal neurons to BDNF, but not to...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2002.0544

    authors： Castrén M,Lampinen KE,Miettinen R,Koponen E,Sipola I,Bakker CE,Oostra BA,Castrén E

    更新日期：2002-10-01 00:00:00

  • Fluoxetine in adulthood normalizes GABA release and rescues hippocampal synaptic plasticity and spatial memory in a mouse model of Down syndrome.

    abstract：:Down syndrome (DS) is the most common genetic disorder associated with mental retardation. It has been repeatedly shown that Ts65Dn mice, the major animal model for DS, have severe cognitive and synaptic plasticity dysfunctions caused by excessive inhibition in their temporal lobe structures. Here we employed a multid...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.11.010

    authors： Begenisic T,Baroncelli L,Sansevero G,Milanese M,Bonifacino T,Bonanno G,Cioni G,Maffei L,Sale A

    更新日期：2014-03-01 00:00:00

  • Hereditary deficiencies in complement C5 are associated with intensified neurodegenerative responses that implicate new roles for the C-system in neuronal and astrocytic functions.

    abstract：:Possible roles of the complement (C) system in the normal and injured brain were explored with inbred mice that carried a frameshift mutation in the C5 gene. A congenic pair was used: the C5-sufficient (C5+) B10.D2/nSnJ strain with the functional allele (Hc1) from the C57BL/10J donor strain was compared with the C5-de...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1996.0020

    authors： Pasinetti GM,Tocco G,Sakhi S,Musleh WD,DeSimoni MG,Mascarucci P,Schreiber S,Baudry M,Finch CE

    更新日期：1996-01-01 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

  • Forebrain knock-out of torsinA reduces striatal free-water and impairs whole-brain functional connectivity in a symptomatic mouse model of DYT1 dystonia.

    abstract：:Multiple lines of evidence implicate striatal dysfunction in the pathogenesis of dystonia, including in DYT1, a common inherited form of the disease. The impact of striatal dysfunction on connected motor circuits and their interaction with other brain regions is poorly understood. Conditional knock-out (cKO) of the DY...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.06.015

    authors： DeSimone JC,Pappas SS,Febo M,Burciu RG,Shukla P,Colon-Perez LM,Dauer WT,Vaillancourt DE

    更新日期：2017-10-01 00:00:00

  • Increased glial glutamate transporter EAAT2 expression reduces epileptogenic processes following pilocarpine-induced status epilepticus.

    abstract：:Several lines of evidence indicate that glutamate plays a crucial role in the initiation of seizures and their propagation; abnormal glutamate release causes synchronous firing of large populations of neurons, leading to seizures. In the present study, we investigated whether enhanced glutamate uptake by increased gli...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.03.032

    authors： Kong Q,Takahashi K,Schulte D,Stouffer N,Lin Y,Lin CL

    更新日期：2012-08-01 00:00:00

  • A human single-chain Fv intrabody preferentially targets amino-terminal Huntingtin's fragments in striatal models of Huntington's disease.

    abstract：:Amino-terminal fragments of huntingtin (htt) appear to result from proteolytic processing of the full-length protein in Huntington's disease (HD), and fragments containing pathological expansions of polyglutamine elicit toxicity in model systems. Such fragments are sequestered into insoluble aggregates, which may init...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.11.003

    authors： Miller TW,Zhou C,Gines S,MacDonald ME,Mazarakis ND,Bates GP,Huston JS,Messer A

    更新日期：2005-06-01 00:00:00

  • Lack of nigral pathology in transgenic mice expressing human alpha-synuclein driven by the tyrosine hydroxylase promoter.

    abstract：:alpha-Synuclein has been identified as a major component of Lewy body inclusions, which are one of the pathologic hallmarks of idiopathic Parkinson's disease. Mutations in alpha-synuclein have been found to be responsible for rare familial cases of Parkinsonism. To test whether overexpression of human alpha-synuclein ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2001.0392

    authors： Matsuoka Y,Vila M,Lincoln S,McCormack A,Picciano M,LaFrancois J,Yu X,Dickson D,Langston WJ,McGowan E,Farrer M,Hardy J,Duff K,Przedborski S,Di Monte DA

    更新日期：2001-06-01 00:00:00

  • Poloxamer 188 decreases membrane toxicity of mutant SOD1 and ameliorates pathology observed in SOD1 mouse model for ALS.

    abstract：:Here we report a gain in function for mutant (mt) superoxide dismutase I (SOD1), a cause of familial amyotrophic lateral sclerosis (FALS), wherein small soluble oligomers of mtSOD1 acquire a membrane toxicity. Phosphatidylglycerol (PG) lipid domains are selectively targeted, which could result in membrane damage or "t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.03.014

    authors： Riehm JJ,Wang L,Ghadge G,Teng M,Correa AM,Marks JD,Roos RP,Allen MJ

    更新日期：2018-07-01 00:00:00

  • Cellular distribution of NMDA glutamate receptor subunit mRNAs in the human cerebellum.

    abstract：:We have used a quantitative in situ hybridization method with human ribonucleotide probes to examine the regional and cellular distribution of N-methyl-D-aspartate receptor (NMDAR) subunit mRNAs in the human cerebellum. Purkinje cells showed very dense labeling for NMDAR1 mRNA, dense labeling for NMDAR2A mRNA, and mod...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1997.0136

    authors： Scherzer CR,Landwehrmeyer GB,Kerner JA,Standaert DG,Hollingsworth ZR,Daggett LP,Veliçelebi G,Penney JB Jr,Young AB

    更新日期：1997-01-01 00:00:00

  • Prenatal stress elicits regionally selective changes in basal FGF-2 gene expression in adulthood and alters the adult response to acute or chronic stress.

    abstract：:Exposure to stress during pregnancy influences the trajectory of brain development resulting in permanent alterations that may contribute to increased susceptibility to subsequent cognitive or neuropsychiatric disorders. In this manuscript, we examined the effects of prenatal stress on the expression of basic fibrobla...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.05.005

    authors： Fumagalli F,Bedogni F,Slotkin TA,Racagni G,Riva MA

    更新日期：2005-12-01 00:00:00

  • Proteomic signatures of brain regions affected by tau pathology in early and late stages of Alzheimer's disease.

    abstract：BACKGROUND:Alzheimer's disease (AD) is the most common neurodegenerative disorder. Depositions of amyloid β peptide (Aβ) and tau protein are among the major pathological hallmarks of AD. Aβ and tau burden follows predictable spatial patterns during the progression of AD. Nevertheless, it remains obscure why certain bra...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.104509

    authors： Mendonça CF,Kuras M,Nogueira FCS,Plá I,Hortobágyi T,Csiba L,Palkovits M,Renner É,Döme P,Marko-Varga G,Domont GB,Rezeli M

    更新日期：2019-10-01 00:00:00

  • Silencing of the Charcot-Marie-Tooth disease-associated gene GDAP1 induces abnormal mitochondrial distribution and affects Ca2+ homeostasis by reducing store-operated Ca2+ entry.

    abstract：:GDAP1 is an outer mitochondrial membrane protein that acts as a regulator of mitochondrial dynamics. Mutations of the GDAP1 gene cause Charcot-Marie-Tooth (CMT) neuropathy. We show that GDAP1 interacts with the vesicle-organelle trafficking proteins RAB6B and caytaxin, which suggests that GDAP1 may participate in the ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.03.010

    authors： Pla-Martín D,Rueda CB,Estela A,Sánchez-Piris M,González-Sánchez P,Traba J,de la Fuente S,Scorrano L,Renau-Piqueras J,Alvarez J,Satrústegui J,Palau F

    更新日期：2013-07-01 00:00:00

  • Identification of gene expression changes in transgenic C. elegans overexpressing human alpha-synuclein.

    abstract：:Alpha-synuclein containing cellular inclusions are a hallmark of Parkinson Disease, Lewy Body Dementia, and Multiple System Atrophy. A genome wide expression screen was performed in C. elegans overexpressing both wild-type and A53T human alpha-synuclein. 433 genes were up- and 67 genes down-regulated by statistical an...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.12.021

    authors： Vartiainen S,Pehkonen P,Lakso M,Nass R,Wong G

    更新日期：2006-06-01 00:00:00

  • Role of the pituitary–adrenal axis in granulocyte-colony stimulating factor-induced neuroprotection against hypoxia–ischemia in neonatal rats.

    abstract：:Several reports indicate that the activity of the hypothalamic–pituitary–adrenal axis (HPA) is increased after a brain insult and that its down-regulation can improve detrimental outcomes associated with ischemic brain injuries.Granulocyte-colony stimulating factor (G-CSF) is a neuroprotective drug shown in the naïve ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.03.021

    authors： Charles MS,Ostrowski RP,Manaenko A,Duris K,Zhang JH,Tang J

    更新日期：2012-07-01 00:00:00

  • Triptolide protects dopaminergic neurons from inflammation-mediated damage induced by lipopolysaccharide intranigral injection.

    abstract：:Converging lines of evidence suggest that neuroinflammatory processes may account for the progressive death of dopaminergic neurons in Parkinson's disease (PD). Therefore, anti-inflammatory strategies have attracted much interest for their potential to prevent further deterioration of PD. Our previous study showed tha...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.12.005

    authors： Zhou HF,Liu XY,Niu DB,Li FQ,He QH,Wang XM

    更新日期：2005-04-01 00:00:00

  • Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Abeta levels.

    abstract：:Transgenic mice expressing mutant human amyloid precursor protein (APP) develop an age-dependent amyloid pathology and memory deficits, but no overt neuronal loss. Here, in mice overexpressing wild-type human APP (hAPP(wt)) we found an early memory impairment, particularly in the water maze and to a lesser extent in t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2008.11.005

    authors： Simón AM,Schiapparelli L,Salazar-Colocho P,Cuadrado-Tejedor M,Escribano L,López de Maturana R,Del Río J,Pérez-Mediavilla A,Frechilla D

    更新日期：2009-03-01 00:00:00

  • Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease.

    abstract：:Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). Apolipoprotein ε4 (APOE4) is the most common genetic risk factor for both familial AD (FAD) and sporadic AD; it accelerates Aβ aggregation ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.02.014

    authors： Ma QL,Teng E,Zuo X,Jones M,Teter B,Zhao EY,Zhu C,Bilousova T,Gylys KH,Apostolova LG,LaDu MJ,Hossain MA,Frautschy SA,Cole GM

    更新日期：2018-06-01 00:00:00

  • Involvement of oxidative stress on the impairment of energy metabolism induced by A beta peptides on PC12 cells: protection by antioxidants.

    abstract：:Alzheimer's disease is widely held to be associated with oxidative stress due, in part, to the membrane action of amyloid beta-peptide (A beta) aggregates. In this study, the involvement of oxidative stress on A beta-induced energy metabolism dysfunction was evaluated on PC12 cells. It was shown that A beta peptides (...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1999.0241

    authors： Pereira C,Santos MS,Oliveira C

    更新日期：1999-06-01 00:00:00

  • Benefits and risks of intranigral transplantation of GABA-producing cells subsequent to the establishment of kindling-induced seizures.

    abstract：:Neural transplantation has been investigated experimentally and clinically for the purpose of developing new treatment options for intractable epilepsy. In the present study we assessed the anticonvulsant efficacy and safety of bilateral allotransplantation of genetically engineered striatal GABAergic rat cell lines i...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2008.05.010

    authors： Nolte MW,Löscher W,Herden C,Freed WJ,Gernert M

    更新日期：2008-09-01 00:00:00

  • Degenerative and regenerative mechanisms governing spinal cord injury.

    abstract：:Spinal cord injury (SCI) is a major cause of disability, and at present, there is no universally accepted treatment. The functional decline following SCI is contributed to both direct mechanical injury and secondary pathophysiological mechanisms that are induced by the initial trauma. These mechanisms initially involv...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2003.11.015

    authors： Profyris C,Cheema SS,Zang D,Azari MF,Boyle K,Petratos S

    更新日期：2004-04-01 00:00:00

  • Early changes in the hypothalamic region in prodromal Huntington disease revealed by MRI analysis.

    abstract：:Huntington disease (HD) is a fatal neurodegenerative disorder caused by an expanded CAG repeat. Its length can be used to estimate the time of clinical diagnosis, which is defined by overt motor symptoms. Non-motor symptoms begin before motor onset, and involve changes in hypothalamus-regulated functions such as sleep...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,多中心研究

    doi：10.1016/j.nbd.2010.07.013

    authors： Soneson C,Fontes M,Zhou Y,Denisov V,Paulsen JS,Kirik D,Petersén A,Huntington Study Group PREDICT-HD investigators.

    更新日期：2010-12-01 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

  • Functional genomics, genetic risk profiling and cell phenotypes in neurodegenerative disease.

    abstract：:Human genetics provides unbiased insights into the causes of human disease, which can be used to create a foundation for effective ways to more accurately diagnose patients, stratify patients for more successful clinical trials, discover and develop new therapies, and ultimately help patients choose the safest and mos...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2020.105088

    authors： Finkbeiner S

    更新日期：2020-12-01 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