José R. Naranjo

Centro Nacional de Biotecnología

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Britt Mellström

Centro Nacional de Biotecnología

Carmen Valenzuela

Hospital Universitario de La Princesa

Pilar Cercós

Instituto de Química Médica

Marta Gutiérrez‐Rodríguez

Instituto de Química Médica

Paz González

Instituto de Salud Carlos III

Marcos Rivas

AbbVie (Spain)

Xosé M. Dopazo

Consejo Superior de Investigaciones Científicas

Diego A. Peraza

Universidad de Valladolid

ÁM

Ángel Manuel Carrión

Universidad Pablo de Olavide

Rosario Herranz

Instituto de Química Médica

Cooperative Institutions

Consejo Superior de Investigaciones Científicas

Universidad Autónoma de Madrid

Biomedical Research Networking Center on Neurodegenerative Diseases

Instituto de Salud Carlos III

Instituto Cajal

Centro Nacional de Biotecnología

Centro de Investigación Biomédica en Red

Centre National de la Recherche Scientifique

Universidad Complutense de Madrid

Instituto de Investigaciones Biomédicas Sols-Morreale

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Ca2+-dependent Transcriptional Control of Ca2+ Homeostasis

Journal of Biological Chemistry (2012)

José R. Naranjo Britt Mellström

Homeostasis

Transcription

10.1074/jbc.r112.384982

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Citations (67)

Co-induction of jun B and c-fos in a subset of neurons in the spinal cord.

PubMed (1991)

José R. Naranjo Britt Mellström Matilde Achaval José J. Lucas Del Rio J

c-jun

c-Fos

Lumbar Spinal Cord

Immediate early gene

Dynorphin

Source

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Citations (60)

Differential effects of D-Ala2 analogues of enkephalins on substance P-induced analgesia in rodents

European Journal of Pharmacology (1982)

José R. Naranjo Joaquı́n Del Rı́o

Differential effects

Systemic administration

10.1016/0014-2999(82)90516-7

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Citations (4)

IQM-PC332, a novel DREAM ligand with analgesic effect on experimental peripheral nerve injury- and diabetes-induced pain

Paula G. Socuéllamos Pilar Cercós Luis Alcides Olivos-Oré María Victoria Barahona Gerardo Bosch

Resumen del poster presentado en el VII Congreso de la Red Espanola de Canales Ionicos, celebrado en Caceres (Espana) del 15 al 17 de mayo de 2019.

Nerve Injury

Peripheral nerve injury

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Stimulus‐Specific Hierarchy of Enhancer Elements Within the Rat Prodynorphin Promoter

Journal of Neurochemistry (1998)

Ángel Manuel Carrión Britt Mellström Simon M. Luckman José R. Naranjo

Induction of the prodynorphin gene occurs in a tissue-specific manner following different physiological stimuli. Using electrophoretic mobility shift assays, we studied the relative activity of the five major regulatory sites in the rat prodynorphin promoter. Prodynorphin cyclic AMP-responsive element 2 (DynCRE2), DynCRE3, and the noncanonical prodynorphin AP-1 (ncDynAP-1) regulatory sites control, in a coordinated manner, prodynorphin induction in the spinal cord after noxious stimulation, whereas prodynorphin up-regulation in supraoptic neurons is regulated predominantly by the ncDynAP-1. Conversely, prodynorphin transactivation in the ovaries upon gonadotropin stimulation is controlled by DynCRE1 and DynCRE3. Our results support the idea that stimulus-specific changes in nuclear proteins establish a functional hierarchy among regulatory sites in the prodynorphin promoter and provide further insight in the molecular mechanisms that govern prodynorphin gene regulation.

Dynorphin

Stimulus (psychology)

10.1046/j.1471-4159.1998.70030914.x

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Citations (18)

Roles of CREB in the regulation of FMRP by group I metabotropic glutamate receptors in cingulate cortex

Molecular Brain (2012)

Hansen Wang Yoshikazu Morishita Daiki Miura José R. Naranjo Satoshi Kida

Fragile X syndrome is caused by lack of fragile X mental retardation protein (FMRP) due to silencing of the FMR1 gene. The metabotropic glutamate receptors (mGluRs) in the central nervous system contribute to higher brain functions including learning/memory, mental disorders and persistent pain. The transcription factor cyclic AMP-responsive element binding protein (CREB) is involved in important neuronal functions, such as synaptic plasticity and neuronal survival. Our recent study has shown that stimulation of Group I mGluRs upregulated FMRP and activated CREB in anterior cingulate cortex (ACC), a key region for brain cognitive and executive functions, suggesting that activation of Group I mGluRs may upregulate FMRP through CREB signaling pathway.In this study, we demonstrate that CREB contributes to the regulation of FMRP by Group I mGluRs. In ACC neurons of adult mice overexpressing dominant active CREB mutant, the upregulation of FMRP by stimulating Group I mGluR is enhanced compared to wild-type mice. However, the regulation of FMRP by Group I mGluRs is not altered by overexpression of Ca2+-insensitive mutant form of downstream regulatory element antagonist modulator (DREAM), a transcriptional repressor involved in synaptic transmission and plasticity.Our study has provided further evidence for CREB involvement in regulation of FMRP by Group I mGluRs in ACC neurons, and may help to elucidate the pathogenesis of fragile X syndrome.

Long-term depression

10.1186/1756-6606-5-27

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Citations (26)

Searching for a Role of NCX/NCKX Exchangers in Neurodegeneration

Molecular Neurobiology (2007)

Rosa Gómez‐Villafuertes Britt Mellström José R. Naranjo

Homeostasis

Sodium-calcium exchanger

Calcium in biology

10.1007/s12035-007-0007-0

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Citations (24)

NF-kB activation in cystic fibrosis: The dream of A20

03.02 - Airway cell biology and immunopathology (2019)

George Momtazi Amal Elbanna Sorcha Finnegan Marie Héritier Lois Lavery

Chronic, exaggerated inflammation in response to infection is characteristic for Cystic Fibrosis (CF) lung disease. Novel CF therapeutics overcome the underlying functional defect in the cystic fibrosis transmembrane conductance regulator (CFTR), but inflammatory markers in sputum remain significantly elevated. Therefore, there is still an unmet need to normalise the inflammatory response. Prolonged/heightened inflammation in CF is mediated by NF-kB and a lack of its regulator A20 (TNFAIP3). Recently, Downstream Regulatory Element Antagonist Modulator (DREAM) has been described as a transcriptional repressor of A20. We hypothesized that higher levels of A20 repressing DREAM contribute to the pro-inflammatory phenotype in CF airway cells. We used airway epithelial cells with/without CFTR mutation to determine A20 and DREAM expression (mRNA, nuclear protein, DNA binding). Results: CF epithelial cells show significantly higher DREAM expression (mRNA/protein), which was associated with significantly lowers levels of A20. We found increased nuclear DREAM protein and increased nuclear expression of the transcriptionally repressing DREAM tetramer in CF airway epithelial cells. ChIP assay confirmed increased and persistent binding of DREAM to its DNA binding site in the TNFAIP3 promoter. Knockdown of DREAM in CF airway cells (siRNA) increased lipopolysaccharide-induced A20 expression and reduced interleukin (IL)-8 release, confirming the action of DREAM. In conclusion, high expression of the repressor DREAM inhibits A20 transcription in CF epithelial cells. Our work suggests an important role of the A20-DREAM axis in (innate) inflammation, providing a new molecular target for the development of innovative anti-inflammatory therapies.

10.1183/13993003.congress-2019.pa2371

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Citations (1)

Changes in the dynamic state of brain proenkephalin‐derived peptides during amygdaloid kindling

Journal of Neuroscience Research (1986)

José R. Naranjo Michael J ladarola E. Costa

Abstract The dynamic state of the proenkephalin (PE) gene products during and after development of amygdaloid kindling was assayed by monitoring changes of the accumulation of PE mRNA and changes in proenkephalin‐related peptides. A parallel determination of PE mRNA and peptides from the same sample was conducted in this study. Electrical stimulation of the amygdala causes early increases in the PE mRNA content in that structure and in the hippocampus. Other areas related with the amygdaloid complex do not exhibit such an early increase, but this alteration occurs when the kindling process is fully established. Enkephalin content increases early in amygdala and hippocampus presumably owing to an increase in synthesis rate. Also, the enkephalin content of areas connected with amygdala and hippocampus such as the entorhinal cortex, the nucleus accumbens, and the frontal and occipital cortex exhibits an increase. A clear tendency towards normalization is observed after a recovery period of 2–3 months. Rekindling of the animals after this recovery period does not elicit a similar pattern of changes in the dynamic state of enkephalin system, even though the animals rekindle with just one single stimulation. The present data suggest that the enkephalinergic neurons participate in the development and spreading of kindling phenomena after amygdaloid stimulation, but they do not seem to play any role in mediating maintenance of the kindling state.

Proenkephalin

Entorhinal cortex

10.1002/jnr.490160108

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Citations (58)

Uncoupled changes in the expression of the jun family members during myeloid cell differentiation

European Journal of Biochemistry (1991)

Faustino Mollinedo José R. Naranjo

The differentiation into macrophages of the U937 and HL60 human cell lines induced by 4 beta-phorbol 12-myristate 13-acetate (PMA) was accompanied by induction of the expression of the proto-oncogenes c-jun, jun B and jun D. However, expression of the three jun genes was regulated differently during induction of cell differentiation in both U937 and HL60 cells, with the three jun family members being expressed distinctly at different stages of cell differentiation. Whereas jun B transcription was strongly stimulated following treatment with PMA for 30 min, jun D mRNA levels were only increased 6 h after PMA treatment and the content of c-jun mRNA was elevated maximally only 24 h after PMA treatment. The rapid induction of the jun B mRNA level suggests a putative role for this proto-oncogene in the early triggering step of U937 and HL60 cell differentiation induced by PMA. Interestingly, a weak induction of jun B and jun D mRNA levels, but no induction of the c-jun mRNA level, was detected during Me2SO-induced granulocytic HL60 differentiation. These data suggest a different role for each jun proto-oncogene in regulating gene activity and that different transcriptional complexes involving distinct jun proto-oncogenes can be formed during macrophage and granulocytic differentiation.

U937 cell

c-jun

HL60

Phorbol

10.1111/j.1432-1033.1991.tb16208.x

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Citations (17)