JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death. - Test2 - elhamkhani - TriplyDB

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

http://www.wikidata.org/entity/Q42030670

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Neuronal endoplasmic reticulum stress in axon injury and neurodegeneration Endothelin-Mediated Changes in Gene Expression in Isolated Purified Rat Retinal Ganglion Cells Dual leucine zipper kinase-dependent PERK activation contributes to neuronal degeneration following insult.Involvement of the MEK-ERK/p38-CREB/c-fos signaling pathway in Kir channel inhibition-induced rat retinal Müller cell gliosis Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1.DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury Role of endoplasmic reticulum stress in the loss of retinal ganglion cells in diabetic retinopathy.Tumor necrosis factor alpha has an early protective effect on retinal ganglion cells after optic nerve crush.Design and synthesis of highly potent and isoform selective JNK3 inhibitors: SAR studies on aminopyrazole derivatives.Activation of TLR3 promotes the degeneration of retinal ganglion cells by upregulating the protein levels of JNK3 Structural basis and biological consequences for JNK2/3 isoform selective aminopyrazoles.Involvement of AP-1 and C/EBPβ in upregulation of endothelin B (ETB) receptor expression in a rodent model of glaucoma Molecular and bioenergetic differences between cells with African versus European inherited mitochondrial DNA haplogroups: implications for population susceptibility to diseases.Caspase-7: a critical mediator of optic nerve injury-induced retinal ganglion cell death The Bcl-2 family member BIM has multiple glaucoma-relevant functions in DBA/2J mice dMyc is required in retinal progenitors to prevent JNK-mediated retinal glial activation.Enhanced Functional Genomic Screening Identifies Novel Mediators of Dual Leucine Zipper Kinase-Dependent Injury Signaling in Neurons.Combined HDAC1 and HDAC2 Depletion Promotes Retinal Ganglion Cell Survival After Injury Through Reduction of p53 Target Gene Expression Novel axon projection after stress and degeneration in the Dscam mutant retina Functional genomic screening identifies dual leucine zipper kinase as a key mediator of retinal ganglion cell death.DLK initiates a transcriptional program that couples apoptotic and regenerative responses to axonal injury.In vitro and in vivo neuroprotective effects of cJun N-terminal kinase inhibitors on retinal ganglion cells.Quantitative measurement of retinal ganglion cell populations via histology-based random forest classification.Evaluation of the percentage of ganglion cells in the ganglion cell layer of the rodent retina 3-MCPD 1-Palmitate Induced Tubular Cell Apoptosis In Vivo via JNK/p53 Pathways.JNK-mediated phosphorylation of DLK suppresses its ubiquitination to promote neuronal apoptosis.Mobile zinc increases rapidly in the retina after optic nerve injury and regulates ganglion cell survival and optic nerve regeneration.The cell and molecular biology of glaucoma: mechanisms of retinal ganglion cell death.Programmed cell death during neuronal development: the sympathetic neuron model.Strong Correlation of Genome-Wide Expression after Traumatic Brain Injury In Vitro and In Vivo Implicates a Role for SORLA.BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.Attenuation of Axonal Degeneration by Calcium Channel Inhibitors Improves Retinal Ganglion Cell Survival and Regeneration After Optic Nerve Crush.JUN is important for ocular hypertension-induced retinal ganglion cell degeneration.Intracellular disulfide reduction by phosphine-borane complexes: Mechanism of action for neuroprotection A feed-forward regulation of endothelin receptors by c-Jun in human non-pigmented ciliary epithelial cells and retinal ganglion cells.Can a death signal half-life be used to sense the distance to a lesion site in axons?BCL2L1 (BCL-X) promotes survival of adult and developing retinal ganglion cells.Together JUN and DDIT3 (CHOP) control retinal ganglion cell death after axonal injury.JUN regulates early transcriptional responses to axonal injury in retinal ganglion cells.KLF9 and JNK3 Interact to Suppress Axon Regeneration in the Adult CNS.

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P2860

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

http://www.wikidata.org/entity/Q42030670

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@en

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@nl

type

label

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@en

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@nl

prefLabel

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@en

JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

@nl

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J.NBD.2012.02.003

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Neurobiology of Disease

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JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.

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Abbot F Clark

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Iok-Hou Pang

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Jeffrey M Harder

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Kimberly A Fernandes

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Laura B Fornarola

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Richard T Libby

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Robert S Freeman

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Simon W M John

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P2860

Promoting axon regeneration in the adult CNS by modulation of the PTEN/mTOR pathway

Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage

Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation

Signal transduction by the JNK group of MAP kinases

The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1

POU domain factor Brn-3b is essential for retinal ganglion cell differentiation and survival but not for initial cell fate specification

Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene

dp5/HRK is a c-Jun target gene and required for apoptosis induced by potassium deprivation in cerebellar granule neurons

Dominant-negative c-Jun promotes neuronal survival by reducing BIM expression and inhibiting mitochondrial cytochrome c release

Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain

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393-401

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10.1016/J.NBD.2012.02.003

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2

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46

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221850462

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22353563

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3323666

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