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Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by ?-serine depletion.

ABSTRACT: Inherent ?-Ser deficiency culminates in intrauterine growth retardation, severe malformation of multiple organs particularly the central nervous system, and perinatal or early postnatal death in human and mouse. To uncover the molecular mechanisms underlying the growth-arrested phenotypes of l-Ser deficiency, we compared gene expression profiles of mouse embryonic fibroblasts deficient in 3-phosphoglycerate dehydrogenase (Phgdh), the first enzyme of de novo ?-Ser synthetic pathway, between ?-Ser-depleted and -supplemented conditions. The datasets (CEL and CHP files) from this study are publicly available on the Gene Expression Omnibus repository (accession number GEO: GSE55687).

SUBMITTER: Hamano M

PROVIDER: S-EPMC4865675 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by ʟ-serine depletion.

Hamano Momoko M Sayano Tomoko T Kusada Wataru W Kato Hisanori H Furuya Shigeki S

Data in brief 20160426

Inherent ʟ-Ser deficiency culminates in intrauterine growth retardation, severe malformation of multiple organs particularly the central nervous system, and perinatal or early postnatal death in human and mouse. To uncover the molecular mechanisms underlying the growth-arrested phenotypes of l-Ser deficiency, we compared gene expression profiles of mouse embryonic fibroblasts deficient in 3-phosphoglycerate dehydrogenase (Phgdh), the first enzyme of de novo ʟ-Ser synthetic pathway, between ʟ-Ser ...[more]

PMID: 27222860

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