Significados de genomic imprinting em inglês

Recent studies highlight cross-talk between pathways controlling the cell cycle and genomic imprinting.

The inheritance pattern of the disease suggests that PGL undergoes maternal genomic imprinting.

Mechanisms governing genomic imprinting are just beginning to be understood.

Errors in genomic imprinting have been implicated in some diseases such as Angelman syndrome.

Background: The evolution of genomic imprinting, the parental-origin specific expression of genes, is the subject of much debate.

Understanding properties of maternally and paternally inherited imprints provides insight into the mechanisms and evolution of genomic imprinting.

Recently, evidence has been presented for the role of methylation and genomic imprinting in the expression of the disease.

Genes subject to genomic imprinting exist in large chromosomal domains, probably reflecting coordinate regulation of the genes within a cluster.

Parent-of-origin effects have been reported for type 2 diabetes and PCOS, thus implicating a role for genomic imprinting in these phenotypes.

We suggest that the signals governing genomic imprinting are rapidly evolving and that disruptions in the process may contribute to mammalian speciation.

Mammalian development to adulthood typically requires both maternal and paternal genomes, because genomic imprinting places stringent limitations on mammalian development, strictly precluding parthenogenesis.

These deletions are exclusively of maternal origin in AS but of paternal origin in PWS indicating that the 15q11-q13 region is subject to genomic imprinting.

We focused on 11p15, a chromosome band harboring at least 25 known genes and associated with the Beckwith-Wiedemann syndrome, several childhood tumors, and genomic imprinting.

Genomic imprinting has played a significant part in both of these developments.

Genomic imprinting is characterized by allele-specific expression of genes within chromosomal domains.

Genomic imprinting is a process that involves one gene copy turned-off in a parent-of-origin-dependent manner.