Multiple proteins bind the insulin response element in the human IGFBP-1 promoter
References (30)
- et al.
Insulin-like growth factor binding protein-1 response to insulin during suppression of endogenous insulin secretion
Metabolism
(1993) - et al.
Insulin inhibits transcription of the human gene for insulin-like growth factor binding protein-1
J Biol Chem.
(1991) - et al.
Glucocorticoids and insulin regulate expression of the human gene for insulin-like growth factor binding protein-1 through proximal promoter elements
J Biol Chem.
(1994) - et al.
Glucocorticoids regulate the induction of phosphoenolpyruvate carboxykinase (GTP) gene transcription during diabetes
J Biol Chem.
(1993) - et al.
DBP, a liver-enriched transcriptional activator, is expressed late in ontogeny and its tissue specificity is determined post-transcriptionally
Cell
(1990) - et al.
The liver-enriched transcription factor D-site binding protein activates the promoter of the phosphoenolpyruvate carboxykinase gene in hepatoma cells
J Biol Chem.
(1992) - et al.
Mechanisms of transcriptional synergism between distinct virus-inducible enhancer elements
Cell
(1993) - et al.
Phosphorylation by cdc2 kinase modulates DNA binding activity of high mobility group I nonhistone chromatin protein
J Biol Chem.
(1991) - et al.
HNF3β as a regulator of floor plate development
Cell
(1994) - et al.
The promoter of the human gene for insulin-like growth factor binding protein-1
J Biol Chem.
(1990)
Sequencing end-labeled DNA with base-specific chemical cleavages
Methods Enzymol.
An active tissue-specific enhancer and bound transcription factors existing in a precisely positioned nucleosomal array
Cell
Hepatic nuclear factor-3 (HNF-3) binds to the insulin response sequence in the insulin-like growth factor binding protein-1 (IGFBP-1) promoter and enhances promoter function
Biochem Biophys Res Commun.
Consensus sequences as substrate specificity determinants for protein kinases and protein phosphates
J Biol Chem.
Interplay of the liver-enriched transacting factors, DBP and HNF1, in the transactivation of human IGFBP-1 promoter
Biochem Biophys Res Commun.
Cited by (26)
Distinct post-transcriptional regulation of Igfbp1 gene by hypoxia in lowland mouse and Qinghai-Tibet plateau root vole Microtus oeconomus
2013, Molecular and Cellular EndocrinologyCitation Excerpt :IGFBP1 is released from the liver into the circulation and binds to IGF1 with high affinity to govern its bioavailability and action (Rajpathak et al., 2009; Wheatcroft and Kearney, 2009). Furthermore, the igfbp1 gene is known to be modulated through transcriptional regulation by many factors, including insulin, glucocorticoids, cAMP, and hypoxia (Lee et al., 1997; Powell et al., 1995; Sugawara et al., 2000). The root vole (Microtus oeconomus Pallas, 1776) belongs to the species-rich genus Microtus, and is widely distributed in the north of Europe, Asia and North America (Brunhoff et al., 2003), and particularly lives on the Qinghai-Tibet plateau of China, exposed to cold and hypoxia at altitudes of 3000–4500 m.
Aerobic exercise training increases circulating insulin-like growth factor binding protein-1 concentration, but does not attenuate the reduction in circulating insulin-like growth factor binding protein-1 after a high-fat meal
2012, Metabolism: Clinical and ExperimentalCitation Excerpt :Future prospective studies will be necessary to address the interactive effects of regular aerobic exercise and chronic dietary habits (both macronutrient composition and caloric intake) on IGFBP-1 concentrations. Insulin has been the most investigated regulator of IGFBP-1 expression to date because it suppresses IGFBP-1 expression and secretion by the liver [32]. Changes in insulin levels may be partially responsible for the changes we observe in IGFBP-1 concentrations after aerobic exercise training.
Gene- and activation-specific mechanisms for insulin inhibition of basal and glucocorticoid-induced insulin-like growth factor binding protein-1 and phosphoenolpyruvate carboxykinase transcription. Roles of forkhead and insulin response sequences
2001, Journal of Biological ChemistryCitation Excerpt :The location of the PEPCK IRS within AF2 of the GRU suggested that insulin inhibition of glucocorticoid-induced transcription could be mediated by regulation of an IRS-associated factor (32, 33). The IRSs present in PEPCK, IGFBP-1, and other genes are highly homologous and have been shown to bind FKHR, HNF3, and other related factors (18, 29,32, 36, 37, 39) of the Fox(o) subgroup (61) of the forkhead/winged helix family. FKHR regulates insulin inhibition of basal IGFBP-1 activity by binding to the IRSs (38, 41).
Serum insulin-like growth factor binding protein-1 at 16 weeks and subsequent preeclampsia
2000, Obstetrics and Gynecology