Disease relevance of APOF

• In summary, LTIP levels are markedly elevated by hypercholesterolemia; however, plasma TG levels attenuate this response [1].

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

• It is suggested that ApoF-containing lipoproteins may be involved in transport and/or esterification of cholesterol [7].
• CETP and lipid transfer inhibitor protein are uniquely affected by the negative charge density of the lipid and protein domains of LDL [6].

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

• Molecular cloning and expression of lipid transfer inhibitor protein reveals its identity with apolipoprotein F [3].
• On Western blots, peptide-specific antibodies raised against synthetic fragments of apoF reacted with the same 33-kDa protein in LTIP-containing fractions purified from LDL and from lipoprotein-deficient plasma [3].
• Northern blot analysis indicates that apolipoprotein F mRNA is detected only in liver for the tissues examined [10].
• Lipid transfer inhibitor protein activity deficiency in normolipidemic uremic patients on continuous ambulatory peritoneal dialysis [5].
• Consistent with the preferential inhibition of transfer events involving LDL, LTIP was shown by gel filtration studies to associate primarily with LDL in plasma [11].

References