[HTML][HTML] Oxidative stress-mediated, post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells
JS Harmon, R Stein, RP Robertson - Journal of biological chemistry, 2005 - ASBMB
Glucose toxicity in pancreatic islet beta cells causes loss of insulin gene expression, content,
and secretion due to loss of binding of transcription factors, most notably PDX-1 and RIPE-
3b1 activator, to the promoter region of the insulin gene. Recently, RIPE-3b1 activator was
cloned and identified as the mammalian homologue of avian MafA/Maf-L (MafA). This
enabled us to carry out more extensive studies of the role of MafA in glucotoxicity than were
hitherto possible. Northern analysis of glucotoxic HIT-T15 cells revealed normal amounts of …
and secretion due to loss of binding of transcription factors, most notably PDX-1 and RIPE-
3b1 activator, to the promoter region of the insulin gene. Recently, RIPE-3b1 activator was
cloned and identified as the mammalian homologue of avian MafA/Maf-L (MafA). This
enabled us to carry out more extensive studies of the role of MafA in glucotoxicity than were
hitherto possible. Northern analysis of glucotoxic HIT-T15 cells revealed normal amounts of …