Associated Papers
Hyperprolinemia type I caused by homozygous p.T466M mutation in PRODH.
Hama R et al.
Human Genome Variation, 2021
Rare Tumor-Normal Matched Whole Exome Sequencing Identifies Novel Genomic Pathogenic Germline and Somatic Aberrations.
Sprissler R et al.
Cancers, 2020
32570879 (PubMed )
Supplement: cancers-12-01618-s001.zip › cancers-817200-Supplementary_Materials3 › Supplementary_Table_S2.xlsx › Somatic_TSG_allVariants_
PRODH polymorphisms, cortical volumes and thickness in schizophrenia.
Ota VK et al.
Plos One, 2014
Identification of PRODH mutations in Korean neonates with type I hyperprolinemia.
Jang MA et al.
Annals of Clinical and Laboratory Science, 2013
Functional polymorphisms in PRODH are associated with risk and protection for schizophrenia and fronto-striatal structure and function.
Kempf L et al.
Plos Genetics, 2008
Type I hyperprolinemia and proline dehydrogenase (PRODH) mutations in four Italian children with epilepsy and mental retardation.
Di Rosa G et al.
Psychiatric Genetics, 2008
Association study of the G-protein signaling 4 (RGS4) and proline dehydrogenase (PRODH) genes with schizophrenia: a meta-analysis.
Li D et al.
European Journal of Human Genetics : Ejhg, 2006
Hyperprolinemia is a risk factor for schizoaffective disorder.
Jacquet H et al.
Molecular Psychiatry, 2005
Functional consequences of PRODH missense mutations.
Bender HU et al.
American Journal of Human Genetics, 2005
PRODH mutations and hyperprolinemia in a subset of schizophrenic patients.
Jacquet H et al.
Human Molecular Genetics, 2002
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