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This study primarily reveals that a selective magnesium transporter NIPA2 may play a role in the pathogenesis of CAE.
mutations in NIPA2 gene were associated with childhood absence epilepsy (CAE), which indicated that the haploinsufficiency of NIPA2 might be a candidate mechanism underlying the IGE/CAE phenotypes caused by 15q11.2 microdeletions or rare mutations in NIPA2
located in the genomic domain between break points 1 and 2 on chromosome 15, of the Prader-Willi/Angelman syndromes
quantitated mRNA levels of NIPA2, NIPA2,l CYFIP1, and GCP5 in Prader-Willi syndrome and correlated levels with psychological and behavior scales
Altered mRNA expression is associated with prostate cancer recurrence.
indentification on mouse chromosome 7C
The isolation and characterization of Nipa2 in mouse distal convoluted tubule cells are reported.
This gene encodes a possible magnesium transporter. This gene is located adjacent to the imprinted domain in the Prader-Willi syndrome deletion region of chromosome 15. Alternate splicing results in multiple transcript variants. Pseudogenes of this gene are found on chromosomes 3, 7 and 21.
magnesium transporter NIPA2
, non-imprinted in Prader-Willi/Angelman syndrome 2
, non-imprinted in Prader-Willi/Angelman syndrome region protein 2
, non-imprinted in Prader-Willi/Angelman syndrome region protein 2 homolog
, non imprinted in Prader-Willi/Angelman syndrome 2 homolog