Ube3a imprinting impairs circadian robustness in Angelman syndrome models.
AUTHORS
Shi
SQ ,
Bichell
TJ ,
Ihrie
RA ,
Johnson
CH ,
. Current biology : CB. primary| primary| primary| primary 3 2; 25(5). 537-45
- PMID: 25660546 [PubMed].
- PMCID: PMC4348236.
- NIHMSID: NIHMS651675
ABSTRACT
The paternal allele of Ube3a is silenced by imprinting in neurons, and Angelman syndrome (AS) is a disorder arising from a deletion or mutation of the maternal Ube3a allele, which thereby eliminates Ube3a neuronal expression. Sleep disorders such as short sleep duration and increased sleep onset latency are very common in AS.