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Mlxipl  -  MLX interacting protein-like

Mus musculus

Synonyms: Carbohydrate-responsive element-binding protein, ChREBP, MLX interactor, MLX-interacting protein-like, Mio, ...
 
 
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Disease relevance of Mlxipl

  • Carbohydrate response element-binding protein (ChREBP) is a rat homolog of human Williams-Beuren syndrome region 14 and a member of the basic helix-loop-helix leucine zipper transcription factor family [1].
  • As a consequence, insulin signaling was improved in liver, skeletal muscles, and white adipose tissue, and overall glucose tolerance and insulin sensitivity were restored in ob/ob mice after a 7-day treatment with the recombinant adenovirus expressing shRNA against ChREBP [2].
  • To investigate ChREBP's role in the development of obesity and obesity-associated metabolic dysregulation, ChREBP-deficient mice were intercrossed with ob/ob mice [3].
 

High impact information on Mlxipl

  • The aim of our study was to assess the role of ChREBP in the control of L-PK and FAS gene expression by PUFAs [4].
  • Polyunsaturated fatty acids suppress glycolytic and lipogenic genes through the inhibition of ChREBP nuclear protein translocation [4].
  • Since glucose metabolism via the pentose phosphate pathway is determinant for ChREBP nuclear translocation, the decrease in xylulose 5-phosphate concentrations caused by a PUFA diet favors a PUFA-mediated inhibition of ChREBP translocation [4].
  • Carbohydrate response element (ChRE)-binding protein (ChREBP) is a recently discovered transcription factor that is activated in response to high glucose concentrations in liver independently of insulin [5].
  • Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis [6].
 

Biological context of Mlxipl

  • Our studies also reveal that the loss of glucose effect observed in hGK-KO hepatocytes is associated with a decreased in the carbohydrate responsive element-binding protein (ChREBP) gene expression, a transcription factor suggested to mediate glucose signaling in liver [7].
  • We show that T0901317 treatment of mice is associated with up-regulation of the ChREBP target gene, liver-type pyruvate kinase [8].
  • In contrast, reporters containing non-glucose-responsive E box elements were not activated by ChREBP-Mlx expression [9].
  • The ChREBP promoter contains functional LXR-binding sites that confer receptor-dependent binding and transactivation [8].
  • When a plasmid expressing either Mlx or ChREBP was cotransfected with a ChoRE-containing reporter plasmid into human embryonic kidney 293 cells, no increase in promoter activity was observed [9].
 

Anatomical context of Mlxipl

 

Associations of Mlxipl with chemical compounds

 

Other interactions of Mlxipl

  • Together these results support a model whereby both SREBP-1c and glucose metabolism, acting via ChREBP, are necessary for the dietary induction of glycolytic and lipogenic gene expression in liver [7].
  • We have recently demonstrated that carbohydrate responsive element-binding protein (ChREBP) plays a key role in the control of lipogenesis through the transcriptional regulation of lipogenic genes, including acetyl-CoA carboxylase and fatty acid synthase [2].
  • Here, we demonstrated that (i) nuclear localization signal and basic helix-loop-helix/leucine-zipper domains of ChREBP were essential for the transcription, and (ii) these domains were the targets of regulation by cAMP and glucose [11].

References

  1. Modulation of carbohydrate response element-binding protein gene expression in 3T3-L1 adipocytes and rat adipose tissue. He, Z., Jiang, T., Wang, Z., Levi, M., Li, J. Am. J. Physiol. Endocrinol. Metab. (2004) [Pubmed]
  2. Liver-specific inhibition of ChREBP improves hepatic steatosis and insulin resistance in ob/ob mice. Dentin, R., Benhamed, F., Hainault, I., Fauveau, V., Foufelle, F., Dyck, J.R., Girard, J., Postic, C. Diabetes (2006) [Pubmed]
  3. Deficiency of carbohydrate-activated transcription factor ChREBP prevents obesity and improves plasma glucose control in leptin-deficient (ob/ob) mice. Iizuka, K., Miller, B., Uyeda, K. Am. J. Physiol. Endocrinol. Metab. (2006) [Pubmed]
  4. Polyunsaturated fatty acids suppress glycolytic and lipogenic genes through the inhibition of ChREBP nuclear protein translocation. Dentin, R., Benhamed, F., Pégorier, J.P., Foufelle, F., Viollet, B., Vaulont, S., Girard, J., Postic, C. J. Clin. Invest. (2005) [Pubmed]
  5. Carbohydrate response element binding protein directly promotes lipogenic enzyme gene transcription. Ishii, S., Iizuka, K., Miller, B.C., Uyeda, K. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  6. Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis. Iizuka, K., Bruick, R.K., Liang, G., Horton, J.D., Uyeda, K. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  7. Hepatic glucokinase is required for the synergistic action of ChREBP and SREBP-1c on glycolytic and lipogenic gene expression. Dentin, R., Pégorier, J.P., Benhamed, F., Foufelle, F., Ferré, P., Fauveau, V., Magnuson, M.A., Girard, J., Postic, C. J. Biol. Chem. (2004) [Pubmed]
  8. The Liver X Receptor (LXR) and Hepatic Lipogenesis: THE CARBOHYDRATE-RESPONSE ELEMENT-BINDING PROTEIN IS A TARGET GENE OF LXR. Cha, J.Y., Repa, J.J. J. Biol. Chem. (2007) [Pubmed]
  9. Mlx is the functional heteromeric partner of the carbohydrate response element-binding protein in glucose regulation of lipogenic enzyme genes. Stoeckman, A.K., Ma, L., Towle, H.C. J. Biol. Chem. (2004) [Pubmed]
  10. ChREBP rather than USF2 regulates glucose stimulation of endogenous L-pyruvate kinase expression in insulin-secreting cells. Wang, H., Wollheim, C.B. J. Biol. Chem. (2002) [Pubmed]
  11. Glucose and cAMP regulate the L-type pyruvate kinase gene by phosphorylation/dephosphorylation of the carbohydrate response element binding protein. Kawaguchi, T., Takenoshita, M., Kabashima, T., Uyeda, K. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
 
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