Protracted lithium treatment protects against the ER stress elicited by thapsigargin in rat PC12 cells: roles of intracellular calcium, GRP78 and Bcl-2. (Q45236966)

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scientific article published in January 2005

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English	Protracted lithium treatment protects against the ER stress elicited by thapsigargin in rat PC12 cells: roles of intracellular calcium, GRP78 and Bcl-2.	scientific article published in January 2005

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scholarly article

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Europe PubMed Central

11 December 2017

Protracted lithium treatment protects against the ER stress elicited by thapsigargin in rat PC12 cells: roles of intracellular calcium, GRP78 and Bcl-2. (English)

1 reference

Europe PubMed Central

11 December 2017

author name string

Hiroi T

1

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Europe PubMed Central

11 December 2017

Wei H

2

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Europe PubMed Central

11 December 2017

Hough C

3

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Europe PubMed Central

11 December 2017

Leeds P

4

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Europe PubMed Central

11 December 2017

Chuang DM

5

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Europe PubMed Central

11 December 2017

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1 January 2005

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11 December 2017

The Pharmacogenomics Journal

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Europe PubMed Central

11 December 2017

5

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Europe PubMed Central

11 December 2017

102-111

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Europe PubMed Central

11 December 2017

2

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Europe PubMed Central

11 December 2017

https://scigraph.springernature.com/pub.10.1038/sj.tpj.6500296

0 references

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The mammalian endoplasmic reticulum as a sensor for cellular stress

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A trip to the ER: coping with stress

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Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta

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Endoplasmic reticulum chaperones GRP78 and calreticulin prevent oxidative stress, Ca2+ disturbances, and cell death in renal epithelial cells

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Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

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BH-3-only BIK functions at the endoplasmic reticulum to stimulate cytochrome c release from mitochondria

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Calcium signaling in the ER: its role in neuronal plasticity and neurodegenerative disorders

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Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases

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Endoplasmic reticulum: a primary target in various acute disorders and degenerative diseases of the brain

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Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

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Lithium protection against glutamate excitotoxicity in rat cerebral cortical neurons: involvement of NMDA receptor inhibition possibly by decreasing NR2B tyrosine phosphorylation.

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beta-amyloid peptide-induced death of PC 12 cells and cerebellar granule cell neurons is inhibited by long-term lithium treatment

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Glycogen synthase kinase-3beta facilitates staurosporine- and heat shock-induced apoptosis. Protection by lithium

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Valproic acid inhibits histone deacetylase activity and suppresses excitotoxicity-induced GAPDH nuclear accumulation and apoptotic death in neurons

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Evaluation of neuroprotection by lithium and valproic acid against ouabain-induced cell damage

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Lithium induces apoptosis in immature cerebellar granule cells but promotes survival of mature neurons.

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Lithium protects cultured neurons against beta-amyloid-induced neurodegeneration.

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Long-term lithium treatment prevents neurotoxic effects of beta-bungarotoxin in primary cultured neurons.

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Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats

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Postinsult treatment with lithium reduces brain damage and facilitates neurological recovery in a rat ischemia/reperfusion model

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Chronic treatment with a low dose of lithium protects the brain against ischemic injury by reducing apoptotic death

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Lithium suppresses excitotoxicity-induced striatal lesions in a rat model of Huntington's disease

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Short-term lithium treatment promotes neuronal survival and proliferation in rat striatum infused with quinolinic acid, an excitotoxic model of Huntington's disease

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Effects of chronic lithium treatment on ornithine decarboxylase induction and excitotoxic neuropathology in the rat.

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Lithium induces brain-derived neurotrophic factor and activates TrkB in rodent cortical neurons: an essential step for neuroprotection against glutamate excitotoxicity.

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Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons

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Chronic lithium treatment antagonizes glutamate-induced decrease of phosphorylated CREB in neurons via reducing protein phosphatase 1 and increasing MEK activities

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A molecular mechanism for the effect of lithium on development

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Regulation of Akt and glycogen synthase kinase-3 beta phosphorylation by sodium valproate and lithium

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Inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3) in response to lithium. Evidence for autoregulation of GSK-3.

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Lithium-induced inhibition of Src tyrosine kinase in rat cerebral cortical neurons: a role in neuroprotection against N-methyl-D-aspartate receptor-mediated excitotoxicity

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Central role of glycogen synthase kinase-3beta in endoplasmic reticulum stress-induced caspase-3 activation

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Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase

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Presenilin-1 mutations downregulate the signalling pathway of the unfolded-protein response

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The endoplasmic reticulum stress-responsive protein GRP78 protects neurons against excitotoxicity and apoptosis: suppression of oxidative stress and stabilization of calcium homeostasis.

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Induction of Bip mRNA upon programmed cell death of differentiated PC12 cells as well as rat sympathetic neurons

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Involvement of c-Fos in signaling grp78 induction following ER calcium release.

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Lithium augments fos protoonocogene expression in PC12 pheochromocytoma cells: implications for therapeutic action of lithium.

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Long-term biphasic effects of lithium treatment on phospholipase C-coupled M3-muscarinic acetylcholine receptors in cultured cerebellar granule cells.

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Evidence that BCL-2 represses apoptosis by regulating endoplasmic reticulum-associated Ca2+ fluxes

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Maintenance of calcium homeostasis in the endoplasmic reticulum by Bcl-2

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Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity

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The mood-stabilizing agents lithium and valproate robustly increase the levels of the neuroprotective protein bcl-2 in the CNS

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Lithium inhibits Abeta-induced stress in endoplasmic reticulum of rabbit hippocampus but does not prevent oxidative damage and tau phosphorylation

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Regulation of c-Jun N-terminal kinase, p38 kinase and AP-1 DNA binding in cultured brain neurons: roles in glutamate excitotoxicity and lithium neuroprotection

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10.1038/SJ.TPJ.6500296

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Europe PubMed Central

11 December 2017

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Europe PubMed Central

11 December 2017

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