Methylpyridinium (MPP(+))- and nerve growth factor-induced changes in pro- and anti-apoptotic signaling pathways in SH-SY5Y neuroblastoma cells (Q30310043)

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English	Methylpyridinium (MPP(+))- and nerve growth factor-induced changes in pro- and anti-apoptotic signaling pathways in SH-SY5Y neuroblastoma cells	scientific article

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scholarly article

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Europe PubMed Central

PubMed publication ID

16 June 2017

Methylpyridinium (MPP(+))- and nerve growth factor-induced changes in pro- and anti-apoptotic signaling pathways in SH-SY5Y neuroblastoma cells (English)

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Europe PubMed Central

PubMed publication ID

16 June 2017

apoptotic process

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author name string

Erik M Halvorsen

1

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Europe PubMed Central

PubMed publication ID

16 June 2017

Jameel Dennis

2

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Europe PubMed Central

PubMed publication ID

16 June 2017

Paula Keeney

3

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Europe PubMed Central

PubMed publication ID

16 June 2017

Thomas W Sturgill

4

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Europe PubMed Central

PubMed publication ID

16 June 2017

Jeremy B Tuttle

5

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Europe PubMed Central

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16 June 2017

James B Bennett

6

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Europe PubMed Central

PubMed publication ID

16 June 2017

language of work or name

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publication date

1 October 2002

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Europe PubMed Central

PubMed publication ID

16 June 2017

number of pages

13

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based on heuristic

inferred from page(s)

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Europe PubMed Central

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16 June 2017

952

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Europe PubMed Central

PubMed publication ID

16 June 2017

1

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Europe PubMed Central

PubMed publication ID

16 June 2017

98-110

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Europe PubMed Central

PubMed publication ID

16 June 2017

Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms

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Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease

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Protein kinase B (c-Akt) in phosphatidylinositol-3-OH kinase signal transduction

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Elevated reactive oxygen species and antioxidant enzyme activities in animal and cellular models of Parkinson's disease

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An evaluation of the role of mitochondria in neurodegenerative diseases: mitochondrial mutations and oxidative pathology, protective nuclear responses, and cell death in neurodegeneration

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Interaction among mitochondria, mitogen-activated protein kinases, and nuclear factor-kappaB in cellular models of Parkinson's disease

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Mammalian MAP kinase signalling cascades

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Raf-1 promotes cell survival by antagonizing apoptosis signal-regulating kinase 1 through a MEK-ERK independent mechanism

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Dopaminergic cell death induced by MPP(+), oxidant and specific neurotoxicants shares the common molecular mechanism

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Serine/threonine protein kinases and apoptosis.

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Akt is a direct target of the phosphatidylinositol 3-kinase. Activation by growth factors, v-src and v-Ha-ras, in Sf9 and mammalian cells

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Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery

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Cellular survival: a play in three Akts

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Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt

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Novel role for JNK as a stress-activated Bcl2 kinase

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Akt, a target of phosphatidylinositol 3-kinase, inhibits apoptosis in a differentiating neuronal cell line

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Characterization and time course of MPP+ -induced apoptosis in human SH-SY5Y neuroblastoma cells

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Regulation of BAD phosphorylation at serine 112 by the Ras-mitogen-activated protein kinase pathway

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Mechanism of protein kinase B activation by insulin/insulin-like growth factor-1 revealed by specific inhibitors of phosphoinositide 3-kinase--significance for diabetes and cancer

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p38 MAP kinase mediates bax translocation in nitric oxide-induced apoptosis in neurons

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The 90-kDa Ribosomal S6 Kinase (pp90rsk) Phosphorylates the N-terminal Regulatory Domain of IκBα and Stimulates Its Degradation in Vitro

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Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells

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p75-mediated NF-kappaB activation enhances the survival response of developing sensory neurons to nerve growth factor

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Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A

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Caspase-3: A vulnerability factor and final effector in apoptotic death of dopaminergic neurons in Parkinson's disease.

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Neuroprotection by brain-derived neurotrophic factor is mediated by extracellular signal-regulated kinase and phosphatidylinositol 3-kinase.

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Transgenic activation of Ras in neurons promotes hypertrophy and protects from lesion-induced degeneration

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Cell death mechanisms in Parkinson's disease

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Neurotrophin signal transduction in the nervous system

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The beginning of the end: IkappaB kinase (IKK) and NF-kappaB activation

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Protein phosphatases and the regulation of mitogen-activated protein kinase signalling.

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Akt is more than just a Bad kinase

1 reference

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Caspase-3 activation induced by inhibition of mitochondrial complex I is facilitated by glycogen synthase kinase-3beta and attenuated by lithium

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Withdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell death

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Apoptosis overrides survival signals through a caspase-mediated dominant-negative NF-kappa B loop

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Akt suppresses apoptosis by stimulating the transactivation potential of the RelA/p65 subunit of NF-kappaB.

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The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event

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Roles of nuclear factor kappaB in neuronal survival and plasticity

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Rel/NF-kappa B and I kappa B proteins: an overview

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Ras regulates sympathetic neuron survival by suppressing the p53-mediated cell death pathway

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Mitogenic Activation, Phosphorylation, and Nuclear Translocation of Protein Kinase Bβ

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JNK and p38 stresskinases--degenerative effectors of signal-transduction-cascades in the nervous system

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Dimerization properties of human BAD. Identification of a BH-3 domain and analysis of its binding to mutant BCL-2 and BCL-XL proteins

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NF-kappaB activation by tumour necrosis factor requires the Akt serine-threonine kinase

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Activation of nuclear transcription factor kappa B (NF-kappaB) is essential for dopamine-induced apoptosis in PC12 cells

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Insulin-like Growth Factor 1 Inhibits Apoptosis Using the Phosphatidylinositol 3′-Kinase and Mitogen-activated Protein Kinase Pathways

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Tumor necrosis factor induces phosphorylation and translocation of BAD through a phosphatidylinositide-3-OH kinase-dependent pathway

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Phosphoinositide 3-OH kinase (PI3K) and PKB/Akt delay the onset of p53-mediated, transcriptionally dependent apoptosis

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MPTP activates c-Jun NH(2)-terminal kinase (JNK) and its upstream regulatory kinase MKK4 in nigrostriatal neurons in vivo

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Regulation of bad phosphorylation and association with Bcl-x(L) by the MAPK/Erk kinase

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Ikappa Balpha is a target for the mitogen-activated 90kDa ribosomal S6 kinase

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Nerve growth factor prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced cell death via the Akt pathway by suppressing caspase-3-like activity using PC12 cells: relevance to therapeutical application for Parkinson's disease

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Origin and functional consequences of the complex I defect in Parkinson's disease

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Increased caspase 3 and Bax immunoreactivity accompany nuclear GAPDH translocation and neuronal apoptosis in Parkinson's disease

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Depolarization and neurotrophins converge on the phosphatidylinositol 3-kinase-Akt pathway to synergistically regulate neuronal survival

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Structure and function of phosphoinositide 3-kinases.

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Gene transfer of the JNK interacting protein-1 protects dopaminergic neurons in the MPTP model of Parkinson's disease

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The Ras/phosphatidylinositol 3-kinase and Ras/ERK pathways function as independent survival modules each of which inhibits a distinct apoptotic signaling pathway in sympathetic neurons

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p38 mitogen-activated protein kinase mediates bid cleavage, mitochondrial dysfunction, and caspase-3 activation during apoptosis induced by singlet oxygen but not by hydrogen peroxide

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Identifiers

10.1016/S0006-8993(02)03216-X

1 reference

Europe PubMed Central

PubMed publication ID

16 June 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

16 June 2017

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