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Equivocal roles of tissue-type plasminogen activator in stroke-induced injury.Lysine acetyltransferases CBP and p300 as therapeutic targets in cognitive and neurodegenerative disorders.Histone H3 lysine methylation in cognition and intellectual disability disorders.Can changes in histone acetylation contribute to memory formation?Lack of IL-1R8 in neurons causes hyperactivation of IL-1 receptor pathway and induces MECP2-dependent synaptic defectsHistone acetylation deficits in lymphoblastoid cell lines from patients with Rubinstein-Taybi syndrome.Arginine 260 of the amino-terminal domain of NR1 subunit is critical for tissue-type plasminogen activator-mediated enhancement of N-methyl-D-aspartate receptor signaling.Is tissue-type plasminogen activator a neuromodulator?Brain size regulations by cbp haploinsufficiency evaluated by in-vivo MRI based volumetry.Blocking miRNA Biogenesis in Adult Forebrain Neurons Enhances Seizure Susceptibility, Fear Memory, and Food Intake by Increasing Neuronal Responsiveness.Selective boosting of transcriptional and behavioral responses to drugs of abuse by histone deacetylase inhibition.2,7-Bis-(4-amidinobenzylidene)-cycloheptan-1-one dihydrochloride, tPA stop, prevents tPA-enhanced excitotoxicity both in vitro and in vivo.Specific promoter deacetylation of histone H3 is conserved across mouse models of Huntington's disease in the absence of bulk changes.Toward safer thrombolytic agents in stroke: molecular requirements for NMDA receptor-mediated neurotoxicity.Tissue-type plasminogen activator crosses the intact blood-brain barrier by low-density lipoprotein receptor-related protein-mediated transcytosis.The brain-specific tissue-type plasminogen activator inhibitor, neuroserpin, protects neurons against excitotoxicity both in vitro and in vivo.Loss of Kdm5c Causes Spurious Transcription and Prevents the Fine-Tuning of Activity-Regulated Enhancers in Neurons.Development and maintenance of the brain's immune toolkit: Microglia and non-parenchymal brain macrophages.Recombinant Desmodus rotundus salivary plasminogen activator crosses the blood-brain barrier through a low-density lipoprotein receptor-related protein-dependent mechanism without exerting neurotoxic effects.Anti-NR1 N-terminal-domain vaccination unmasks the crucial action of tPA on NMDA-receptor-mediated toxicity and spatial memory.Tissue-type plasminogen activator rescues neurones from serum deprivation-induced apoptosis through a mechanism independent of its proteolytic activity.Loss of neuronal 3D chromatin organization causes transcriptional and behavioural deficits related to serotonergic dysfunction.Cbp-dependent histone acetylation mediates axon regeneration induced by environmental enrichment in rodent spinal cord injury modelsEcdysone-Induced 3D Chromatin Reorganization Involves Active Enhancers Bound by Pipsqueak and Polycomb
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description
researcher ORCID ID = 0000-0001-6064-7584
@en
wetenschapper
@nl
name
Jose P Lopez-Atalaya
@ast
Jose P Lopez-Atalaya
@en
Jose P Lopez-Atalaya
@nl
type
label
Jose P Lopez-Atalaya
@ast
Jose P Lopez-Atalaya
@en
Jose P Lopez-Atalaya
@nl
prefLabel
Jose P Lopez-Atalaya
@ast
Jose P Lopez-Atalaya
@en
Jose P Lopez-Atalaya
@nl
P106
P21
P31
P496
0000-0001-6064-7584