The phenotype of multiple congenital anomalies‐hypotonia‐seizures syndrome 1: Report and review
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J. Berg | K. Wilhelmsen | C. Powell | K. Crooks | A. K. Foreman | M. Roche | K. Weck | N. Strande | Maheer M. Masood | N. Couser | Mei Lu | J. Evans | Natario L. Couser
[1] N. Matsumoto,et al. PIGA mutations cause early-onset epileptic encephalopathies and distinctive features , 2014, Neurology.
[2] Yasuhiro Suzuki,et al. PIGN mutations cause congenital anomalies, developmental delay, hypotonia, epilepsy, and progressive cerebellar atrophy , 2014, neurogenetics.
[3] V. Kalscheuer,et al. Early Frameshift Mutation in PIGA Identified in a Large XLID Family Without Neonatal Lethality , 2014, Human mutation.
[4] E. Cuppen,et al. Expanding the spectrum of phenotypes associated with germline PIGA mutations: A child with developmental delay, accelerated linear growth, facial dysmorphisms, elevated alkaline phosphatase, and progressive CNS abnormalities , 2014, American journal of medical genetics. Part A.
[5] O. Mäkitie,et al. A novel intellectual disability syndrome caused by GPI anchor deficiency due to homozygous mutations in PIGT , 2013, Journal of Medical Genetics.
[6] G. Rechavi,et al. Multiple congenital anomalies-hypotonia-seizures syndrome is caused by a mutation in PIGN , 2011, Journal of Medical Genetics.
[7] H. Riezman,et al. Pig-n, a Mammalian Homologue of Yeast Mcd4p, Is Involved in Transferring Phosphoethanolamine to the First Mannose of the Glycosylphosphatidylinositol* , 1999, The Journal of Biological Chemistry.
[8] S. Reed,et al. MCD4 encodes a conserved endoplasmic reticulum membrane protein essential for glycosylphosphatidylinositol anchor synthesis in yeast. , 1999, Molecular biology of the cell.