Expression of Concern: Glycogen synthase kinase 3β (GSK3β) mediates 6‐ hydroxydopamine‐induced neuronal death

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GSK3 takes centre stage more than 20 years after its discovery

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Trk receptors: mediators of neurotrophin action

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An Unfolded Putative Transmembrane Polypeptide, which Can Lead to Endoplasmic Reticulum Stress, Is a Substrate of Parkin

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GSK3 takes centre stage more than 20 years after its discovery

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Inactivation of glycogen synthase kinase-3β by phosphorylation: new kinase connections in insulin and growth-factor signalling

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An Endoplasmic Reticulum Stress-specific Caspase Cascade in Apoptosis

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Role of Glycogen Synthase Kinase-3β in Neuronal Apoptosis Induced by Trophic Withdrawal

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First Non-ATP Competitive Glycogen Synthase Kinase 3 β (GSK-3β) Inhibitors: Thiadiazolidinones (TDZD) as Potential Drugs for the Treatment of Alzheimer's Disease

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Glycogen synthase kinase-3 is rapidly inactivated in response to insulin and phosphorylates eukaryotic initiation factor eIF-2B

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Central Role of Glycogen Synthase Kinase-3β in Endoplasmic Reticulum Stress-induced Caspase-3 Activation

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Two distinct mechanisms are involved in 6-hydroxydopamine- and MPP+-induced dopaminergic neuronal cell death: Role of caspases, ROS, and JNK

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Presenilins, the Endoplasmic Reticulum, and Neuronal Apoptosis in Alzheimer's Disease

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Endoplasmic reticulum dysfunction – a common denominator for cell injury in acute and degenerative diseases of the brain?

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Insulin Transiently Increases Tau Phosphorylation

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Dopamine, 6-hydroxydopamine, iron, and dioxygen — their mutual interactions and possible implication in the development of Parkinson's disease

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Proapoptotic Stimuli Induce Nuclear Accumulation of Glycogen Synthase Kinase-3β

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Rescue from death but not from functional impairment: caspase inhibition protects dopaminergic cells against 6-hydroxydopamine-induced apoptosis but not against the loss of their terminals

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N‐Methyl‐4‐phenylpyridine (MMP⁺ together with 6‐hydroxydopamine or dopamine stimulates Ca²⁺ release from mitochondria

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6-Hydroxydopamine increases ubiquitin-conjugates and protein degradation: implications for the pathogenesis of Parkinson's disease.

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Medial nigral dopamine neurons have rich neurotrophin support in humans

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Calretinin-containing axons and neurons are resistant to an intrastriatal 6-hydroxydopamine lesion

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Signaling Pathways Mediate the Neuroprotective Effects of GDNF

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Rescue from death but not from functional impairment: caspase inhibition protects dopaminergic cells against 6‐hydroxydopamine‐induced apoptosis but not against the loss of their terminals

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Therapeutic options for Parkinson's disease

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