about
Alterations in mammalian target of rapamycin signaling pathways after traumatic brain injuryA necessity for MAP kinase activation in mammalian spatial learning.Post-traumatic seizure susceptibility is attenuated by hypothermia therapy.Proinflammatory cytokine regulation of cyclic AMP-phosphodiesterase 4 signaling in microglia in vitro and following CNS injury.Mild hyperthermia worsens the neuropathological damage associated with mild traumatic brain injury in ratsPosttraumatic hypothermia increases doublecortin expressing neurons in the dentate gyrus after traumatic brain injury in the ratPostinjury treatment with rolipram increases hemorrhage after traumatic brain injuryModulation of the cAMP signaling pathway after traumatic brain injury.Phosphodiesterase isoform-specific expression induced by traumatic brain injury.Traumatic Brain Injury Upregulates Phosphodiesterase Expression in the Hippocampus.Age-dependent alterations in cAMP signaling contribute to synaptic plasticity deficits following traumatic brain injuryChronic Cognitive Dysfunction after Traumatic Brain Injury Is Improved with a Phosphodiesterase 4B Inhibitor.Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia.Effects of early rolipram treatment on histopathological outcome after controlled cortical impact injury in mice.Cytoplasmic polyadenylation element binding protein-dependent protein synthesis is regulated by calcium/calmodulin-dependent protein kinase II.Bidirectional regulation of cytoplasmic polyadenylation element-binding protein phosphorylation by Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 1 during hippocampal long-term potentiation.Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury.Regulation of myelin basic protein phosphorylation by mitogen-activated protein kinase during increased action potential firing in the hippocampus.Mutation of the Angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation.Activated c-Jun N-terminal kinase is required for axon formation.Activation of calcium/calmodulin-dependent protein kinases after traumatic brain injury.An important role of neural activity-dependent CaMKIV signaling in the consolidation of long-term memory.STAT3 signaling after traumatic brain injury.Fluid-percussion brain injury induces changes in aquaporin channel expressionPositive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
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description
hulumtuese
@sq
researcher
@en
wetenschapper
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հետազոտող
@hy
name
Coleen M. Atkins
@ast
Coleen M. Atkins
@en
Coleen M. Atkins
@es
Coleen M. Atkins
@nl
Coleen M. Atkins
@sl
type
label
Coleen M. Atkins
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Coleen M. Atkins
@en
Coleen M. Atkins
@es
Coleen M. Atkins
@nl
Coleen M. Atkins
@sl
prefLabel
Coleen M. Atkins
@ast
Coleen M. Atkins
@en
Coleen M. Atkins
@es
Coleen M. Atkins
@nl
Coleen M. Atkins
@sl
P106
P1153
7102789660
P21
P31
P496
0000-0003-4718-7493