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APOF  -  apolipoprotein F

Homo sapiens

Synonyms: Apo-F, Apolipoprotein F, LTIP, Lipid transfer inhibitor protein
 
 
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Disease relevance of APOF

 

High impact information on APOF

  • Lipid transfer inhibitor protein defines the participation of high density lipoprotein subfractions in lipid transfer reactions mediated by cholesterol ester transfer protein (CETP) [2].
  • In this study, we report the purification of LTIP and the expression of its cDNA in cultured cells [3].
  • Suppression of lipid transfer inhibitor protein activity by oleate. A novel mechanism of cholesteryl ester transfer protein regulation by plasma free fatty acids [4].
  • Based on these studies, we proposed that LTIP activity is an important determinant of lipoprotein size and composition, which leads to a stimulation of reverse cholesterol transport [5].
  • LTIP activity was completely blocked by approximately 10 microM oleate but only mildly suppressed by acetylation [6].
 

Biological context of APOF

 

Anatomical context of APOF

  • This association does not appear to reflect decreased LTIP synthesis, inasmuch as conditions that stimulate TG synthesis and secretion (200 micromol/L oleate) do not reduce LTIP secretion by SW872 or Caco-2 cells [1].
 

Associations of APOF with chemical compounds

  • The CETP inhibitor activity of recombinant apoF possessed the same LDL specificity, oleate sensitivity, and dependence on lipoprotein concentration as previously noted for LTIP [3].
  • Markedly elevated lipid transfer inhibitor protein in hypercholesterolemic subjects is mitigated by plasma triglyceride levels [1].
  • These data further suggested that palmitate has greater LTIP suppressive activity than oleate [8].
  • The effects of increasing amounts of a given NEFA on LTIP activity correlated well with the increase in LDL negative charge induced by that NEFA, yet this relationship was unique for each NEFA, especially stearate [8].
  • In contrast, linoleate and myristate were poor inhibitors of LTIP activity [8].
 

Regulatory relationships of APOF

  • Although LTIP inhibits CETP activity among different lipoprotein classes, it preferentially suppresses transfer events involving low density lipoprotein (LDL), whereas transfers involving high density lipoprotein as donor are less affected [3].
 

Other interactions of APOF

  • LpF:A-I:A-II was found to contain ApoF, ApoA-I, and ApoA-II in an apparent 2:1:1 molar ratio [7].
  • We also searched for polymorphisms within the APOM and APOF by dHPLC [9].
 

Analytical, diagnostic and therapeutic context of APOF

References

  1. Markedly elevated lipid transfer inhibitor protein in hypercholesterolemic subjects is mitigated by plasma triglyceride levels. Morton, R.E., Nunes, V., Izem, L., Quintão, E. Arterioscler. Thromb. Vasc. Biol. (2001) [Pubmed]
  2. Lipid transfer inhibitor protein defines the participation of high density lipoprotein subfractions in lipid transfer reactions mediated by cholesterol ester transfer protein (CETP). Paromov, V.M., Morton, R.E. J. Biol. Chem. (2003) [Pubmed]
  3. Molecular cloning and expression of lipid transfer inhibitor protein reveals its identity with apolipoprotein F. Wang, X., Driscoll, D.M., Morton, R.E. J. Biol. Chem. (1999) [Pubmed]
  4. Suppression of lipid transfer inhibitor protein activity by oleate. A novel mechanism of cholesteryl ester transfer protein regulation by plasma free fatty acids. Morton, R.E., Greene, D.J. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
  5. Lipid transfer inhibitor protein activity deficiency in normolipidemic uremic patients on continuous ambulatory peritoneal dialysis. Serdyuk, A.P., Morton, R.E. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
  6. CETP and lipid transfer inhibitor protein are uniquely affected by the negative charge density of the lipid and protein domains of LDL. Morton, R.E., Greene, D.J. J. Lipid Res. (2003) [Pubmed]
  7. Isolation and characterization of simple and complex lipoproteins containing apolipoprotein F from human plasma. Koren, E., McConathy, W.J., Alaupovic, P. Biochemistry (1982) [Pubmed]
  8. The capacity of various non-esterified fatty acids to suppress lipid transfer inhibitor protein activity is related to their perturbation of the lipoprotein surface. Morton, R.E., Greene, D.J. Biochim. Biophys. Acta (2000) [Pubmed]
  9. Exclusion of CYP46 and APOM as candidate genes for Alzheimer's disease in a French population. Kabbara, A., Payet, N., Cottel, D., Frigard, B., Amouyel, P., Lambert, J.C. Neurosci. Lett. (2004) [Pubmed]
  10. Purification and molecular cloning of human apolipoprotein F. Day, J.R., Albers, J.J., Gilbert, T.L., Whitmore, T.E., McConathy, W.J., Wolfbauer, G. Biochem. Biophys. Res. Commun. (1994) [Pubmed]
  11. Regulation of lipid transfer between lipoproteins by an endogenous plasma protein: selective inhibition among lipoprotein classes. Morton, R.E., Greene, D.J. J. Lipid Res. (1994) [Pubmed]
 
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