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RTL1 is a retrotransposon-derived, paternally expressed imprinted gene that is highly expressed at the late fetal stage in both the fetus and placenta. De plus, nous expédions et beaucoup plus de produits pour cette protéine.
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Data suggest that DNA is differentially methylated (hypomethylated) at a gene locus associated with regulation of expression of RTL1 and miR136 in type 1 diabetes; these studies were conducted using tissue bank placentas and whole blood cell DNA from children with type 1 diabetes. (RTL1 = retrotransposon-like protein 1; miR136 = microRNA 136)
We find that placental expression of DIO3 and RTL1) correlates with prenatal growth. Combined, these findings suggest that epigenetic programming and gene expression within the DLK1-DIO3 imprinted domain influence both prenatal and postnatal growth.
The results of this study suggest that hyperactive retrotransposition of L1 in neurons triggered by environmental and/or genetic risk factors may contribute to the susceptibility and pathophysiology of schizophrenia.
In addition to identifying Rtl1 as a novel driver of HCC, our study represents one of the first direct in vivo demonstrations of a role for such a co-opted genetic element in promoting carcinogenesis.
RTL1, a paternally expressed gene in a cluster of imprinted genes on chromosome 14q32.2, is associated with upd(14)pat-like and upd(14)mat-like phenotypes.
Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice show mid- to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality
miR-127 is an essential regulator of Rtl1, mediated by a trans-homologue interaction between reciprocally imprinted genes on the maternally and paternally inherited chromosomes
Rtl1, an imprinted gene with preferential expression from the paternal allele, is essential for maintenance of the fetal capillaries.
Despite the coordinate down-regulation of Dlk1 and Rtl1 mRNA levels, Rtl1 over-expression did not affect the time course of adipogenesis or Dlk1 expression
These data support a role for mir-127 and mir-136 in the epigenetic reprogramming of the Rtl1 imprinting process.
This gene is a retrotransposon-derived, paternally expressed imprinted gene that is highly expressed at the late fetal stage in both the fetus and placenta. It has an overlapping maternally expressed antisense transcript, which contains several microRNAs targeting the transcripts of this gene through an RNA interference (RNAi) mechanism. This gene is essential for maintenance of the fetal capillaries.
mammalian retrotransposon derived protein 1
, paternally expressed gene 11 protein
, retrotransposon-derived protein PEG11
, retrotransposon-like protein 1
, paternally expressed gene 11 protein homolog