Placental endoplasmic reticulum stress by administration of Tun causes downregulation of Slc2a1(GLUT1) and upregulation of Slc2a3(GLUT3) mRNA expression.
Recruitment of Creb1-Mecp2 by glut3-(m)CpG contributes towards transactivation formulating an escape from (m)CpG-induced gene suppression and thereby promoting developmental neuronal glut3 gene transcription and expression.
These observations collectively support a temporal contribution by transcription toward ensuring adequate tissue-specific developmental (placenta and embryonic brain) and postnatal hypoxic brain GLUT3 expression.
Both transcripts and protein synthesis of the glucose transporters Glut1 and Glut3 were reduced in blastocysts cultured in the presence of either 25 or 55 mM glucose
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