Data/hora: 02/06/2024 01:20:28

Provedor de dados: 	74	
País: 	Brazil	
Título: 	Expression of DLK1 and MEG3 genes in porcine tissues during postnatal development	
Autores: 	Oczkowicz,Maria; Piestrzyska-Kajtoch,Agata; Piórkowska,Katarzyna; Rejduch,Barbara; Rózycki,Marian.	
Data: 	2010-01-01	
Ano: 	2010	
Palavras-chave: 	DLK1; Imprinting; MEG3; Pigs; Polar overdominance.	
Resumo: 	The Drosophila-like homolog 1 (DLK1), a transmembrane signal protein similar to other members of the Notch/Delta/Serrate family, regulates the differentiation process in many types of mammalian cells. Callipyge sheep and DLK1 knockout mice are excellent examples of a fundamental role of the gene encoding DLK1 in muscle growth and fat deposition. DLK1 is located within co-regulated imprinted clusters (the DLK1/DIO3 domain), along with other imprinted genes. Some of these, e.g. the RNA coding MEG3 gene, presumedly interfere with DLK1 transcription. The aim of our study was to analyze DLK1 and MEG3 gene expression in porcine tissues (muscle, liver, kidney, heart, brain stem) during postnatal development. The highest expression of both DLK1 and MEG3 variant 1 (MEG3 var.1) was observed in the brain-stem and muscles, whereas that of MEG3 variant 2 (MEG3 var.2) was the most abundant in muscles and the heart. During development (between 60 and 210 days of age) expression of analyzed genes was down-regulated in all the tissues. An exception was the brain-stem, where there was no significant change in MEG3 (both variants) mRNA level, and relatively little decline (2-fold) in that of DLK1 transcription. This may indicate a distinct function of the DLK1 gene in the brain-stem, when compared with other tissues.	
Tipo: 	Info:eu-repo/semantics/other	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572010000400030	
Editor: 	Sociedade Brasileira de Genética	
Relação: 	10.1590/S1415-47572010000400030	
Formato: 	text/html	
Fonte: 	Genetics and Molecular Biology  v.33 n.4 2010	
Fonte: 	info:eu-repo/semantics/openAccess