Idioma:

The estrogen receptor α colocalizes with proopiomelanocortin in hypothalamic neurons and binds to a conserved motif present in the neuron-specific enhancer nPE2

de Souza, Flávio S.J. ; Nasif, Sofia ; López-Leal, Rodrigo ; Levi, Diego H. ; Low, Malcolm J. ; Rubinsten, Marcelo

European journal of pharmacology, 2011-06, Vol.660 (1), p.181-187 [Periódico revisado por pares]

Amsterdam: Elsevier B.V

Texto completo disponível

Citações Citado por

Enviar para

Título:
The estrogen receptor α colocalizes with proopiomelanocortin in hypothalamic neurons and binds to a conserved motif present in the neuron-specific enhancer nPE2
Autor: de Souza, Flávio S.J. ; Nasif, Sofia ; López-Leal, Rodrigo ; Levi, Diego H. ; Low, Malcolm J. ; Rubinsten, Marcelo
Assuntos: adulthood ; Animals ; Arcuate nucleus ; Base Sequence ; Biological and medical sciences ; Conserved Sequence ; Embryos ; Energy balance ; Enhancer Elements, Genetic - genetics ; Enhancers ; Estrogen receptor ; Estrogen Receptor alpha - metabolism ; Estrogen receptors ; Female ; females ; fluorescent antibody technique ; gene expression ; Gene Expression Regulation, Developmental ; Humans ; Hypothalamus ; Hypothalamus - cytology ; Immunofluorescence ; Male ; males ; Medical sciences ; Melanocortin ; Mice ; Molecular Sequence Data ; Neurons ; Neurons - metabolism ; Nuclear receptors ; Pain ; peptides ; pharmacology ; Pharmacology. Drug treatments ; Phylogeny ; Pituitary ; Pituitary (anterior) ; pro-opiomelanocortin ; Pro-Opiomelanocortin - genetics ; Pro-Opiomelanocortin - metabolism ; Proopiomelanocortin ; Protein Binding ; Protein Transport ; Reporter gene ; reporter genes ; screening ; Transcription factors ; Transcriptional enhancer ; Transcriptional regulation ; Transgenic mice
É parte de: European journal of pharmacology, 2011-06, Vol.660 (1), p.181-187
Notas: http://dx.doi.org/10.1016/j.ejphar.2010.10.114
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
Descrição: The gene encoding the prohormone proopiomelanocortin (POMC) is mainly expressed in two regions in vertebrates, namely corticotrophs and melanotrophs in the pituitary and a small population of neurons in the arcuate nucleus of the hypothalamus. In this latter region, POMC-derived peptides participate in the control of energy balance and sensitivity to pain. Neuronal expression of POMC is conferred by two enhancers, nPE1 and nPE2, which are conserved in most mammals, but no transcription factors are yet known to bind to these enhancers. In this work, by means of a one-hybrid screening, we identify that nPE2 possesses an element recognized by transcription factors of the nuclear receptor superfamily. This element, named NRBE, is conserved in all known nPE2 enhancers and is necessary to confer full enhancer strength to nPE2-driven reporter gene expression in transgenic mice assays, indicating that the phylogenetic conservation of the element is indicative of its functional importance. In a search for candidate nuclear receptors that might control POMC we observed that estrogen receptor alpha (ESR1) – a known regulator of energy balance at the hypothalamic level – can bind to the NRBE element in vitro. In addition we observed by immunofluorescence that ESR1 is coexpressed with POMC in around 25–30% of hypothalamic neurons of males and females during late embryonic stages and adulthood. Thus, our results indicate that hypothalamic expression of POMC is controlled by nuclear receptors and establish ESR1 as a candidate regulator of POMC.
Editor: Amsterdam: Elsevier B.V
Idioma: Inglês

Links

Voltar para lista de resultados

Anterior Resultado 7 Avançar Ir para próxima página

Realização: Logos de Redes Sociais:

The estrogen receptor α colocalizes with proopiomelanocortin in hypothalamic neurons and binds to a conserved motif present in the neuron-specific enhancer nPE2

de Souza, Flávio S.J. ; Nasif, Sofia ; López-Leal, Rodrigo ; Levi, Diego H. ; Low, Malcolm J. ; Rubinsten, Marcelo

Amsterdam: Elsevier B.V

Buscando em bases de dados remotas. Favor aguardar.