Associated Papers
Prader-Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review.
Butler MG
International Journal of Molecular Sciences, 2023
Prader-Willi syndrome, deletion subtypes, and magnesium: Potential impact on clinical findings.
Butler MG et al.
American Journal of Medical Genetics. Part A, 2022
The absence of NIPA2 enhances neural excitability through BK (big potassium) channels.
Liu NN et al.
Cns Neuroscience & Therapeutics, 2019
Magnesium Supplement and the 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome: A Potential Treatment?
Butler MG
International Journal of Molecular Sciences, 2019
Does variation in NIPA2 contribute to genetic generalized epilepsy?
Hildebrand MS et al.
Human Genetics, 2014
NIPA2 mutations are correlative with childhood absence epilepsy in the Han Chinese population.
Jiang Y et al.
Human Genetics, 2014
Functional study of NIPA2 mutations identified from the patients with childhood absence epilepsy.
Xie H et al.
Plos One, 2014
NIPA2 located in 15q11.2 is mutated in patients with childhood absence epilepsy.
Jiang Y et al.
Human Genetics, 2012
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