What is it about?
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.
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Why is it important?
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-depleted and -supplemented conditions.
Perspectives
Consistent with these observations, our microarray analysis of L-Ser-depleted Phgdh KO fibroblasts revealed that the activation of a network containing the stress-response-activating transcription factor ATF4–ATF3–DNA damage-inducible transcript 3 (Ddit3) axis was most prominent among the 560 upregulated genes, and cholesterol biosynthetic process was most prominent among the 381 downregulated genes. These results imply that L-Ser deficiency causes multiple stress cascades such as integrated stress response and lipid metabolic stress in Phgdh KO fibroblasts.
Momoko Hamano
Kyushu Kogyo Daigaku
Read the Original
This page is a summary of: Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by ʟ-serine depletion, Data in Brief, June 2016, Elsevier,
DOI: 10.1016/j.dib.2016.04.052.
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