about
Epigenetic pathways and glioblastoma treatmentCasein kinase 1δ is an APC/C(Cdh1) substrate that regulates cerebellar granule cell neurogenesis.Induction of ER stress in response to oxygen-glucose deprivation of cortical cultures involves the activation of the PERK and IRE-1 pathways and of caspase-12Sigma receptor agonist 2-(4-morpholinethyl)1 phenylcyclohexanecarboxylate (Pre084) increases GDNF and BiP expression and promotes neuroprotection after root avulsion injury.Lack of a synergistic effect of a non-viral ALS gene therapy based on BDNF and a TTC fusion molecule.BET bromodomain proteins are required for glioblastoma cell proliferation.Screening of cell cycle fusion proteins to identify kinase signaling networksInhibition of WNT signaling attenuates self-renewal of SHH-subgroup medulloblastoma.GSK3 inhibitors stabilize Wee1 and reduce cerebellar granule cell progenitor proliferation.Fragment C of tetanus toxin, more than a carrier. Novel perspectives in non-viral ALS gene therapy.Valproate reduces CHOP levels and preserves oligodendrocytes and axons after spinal cord injury.Epigenetic Modifications Associated to Neuroinflammation and Neuropathic Pain After Neural Trauma.Spinal cord injury induces endoplasmic reticulum stress with different cell-type dependent responseBET protein inhibition regulates cytokine production and promotes neuroprotection after spinal cord injury.Time series modeling of cell cycle exit identifies Brd4 dependent regulation of cerebellar neurogenesis
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P50
description
researcher ORCID ID = 0000-0003-0554-3832
@en
wetenschapper
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name
Clara Penas
@ast
Clara Penas
@en
Clara Penas
@es
Clara Penas
@nl
type
label
Clara Penas
@ast
Clara Penas
@en
Clara Penas
@es
Clara Penas
@nl
prefLabel
Clara Penas
@ast
Clara Penas
@en
Clara Penas
@es
Clara Penas
@nl
P106
P1153
18038287200
P21
P31
P496
0000-0003-0554-3832