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Valentín Ceña

Researcher at University of Castilla–La Mancha

Publications -  133
Citations -  11040

Valentín Ceña is an academic researcher from University of Castilla–La Mancha. The author has contributed to research in topics: Apoptosis & Chromaffin cell. The author has an hindex of 40, co-authored 127 publications receiving 9864 citations. Previous affiliations of Valentín Ceña include National Institutes of Health & French Institute of Health and Medical Research.

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HIF-1α is neuroprotective during the early phases of mild hypoxia in rat cortical neurons.

TL;DR: Results indicate that HIF-1α is neuroprotective in the early phases of hypoxia, and lentiviral-mediated overexpression of HIF -1α increased lactate dehydrogenase (LDH) A, one of the target genes for Hif-1 α, but did not show protective actions on Hypoxia-mediated neuronal death, indicating that the level of endogenous HIF
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Acetaminophen potentiates staurosporine‐induced death in a human neuroblastoma cell line

TL;DR: The aim of the present work was to investigate a possible relationship between cyclo‐oxygenase pathway and stauroporine‐induced apoptosis in the neuroblastoma cell line SH‐SY5Y.
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Chromostatin receptors control calcium channel activity in adrenal chromaffin cells.

TL;DR: The results together with the patch-clamp experiments support the idea that chromaffin cells possess specific chromostatin receptors and that activation of such receptors leads to the inhibition of L-type voltage-sensitive calcium channels through an intracellular second messenger pathway.
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Bcl-x(L) blocks a mitochondrial inner membrane channel and prevents Ca2+ overload-mediated cell death.

TL;DR: It is found that Bcl-xL neuroprotective actions take place at mitochondria where this antiapoptotic protein delays both mitochondrial potential collapse and opening of the permeability transition pore by preventing Ca2+-mediated mitochondrial multiple conductance channel opening.
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Acetaminophen induces human neuroblastoma cell death through NFKB activation.

TL;DR: The results presented here suggest that AAP activates the intrinsic death pathway in neuroblastoma cells through a mechanism involving NFkB and IL-1β.