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Gene Review

JPH3  -  junctophilin 3

Homo sapiens

Synonyms: CAGL237, HDL2, JP-3, JP3, Junctophilin type 3, ...
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Disease relevance of JPH3


Psychiatry related information on JPH3


High impact information on JPH3


Chemical compound and disease context of JPH3

  • After adjustment for age, sex, obesity, and smoking, plasma vitamin C was directly associated with HDL- (P = 0.01) and HDL2 cholesterol (P = 0.0002) [13].
  • In conclusion, obesity is associated with dyslipidaemia in Chinese men, characterised by increased plasma triglyceride, apo B, LDL/HDL, apo B/LDL, and decreased HDL, HDL2 and apo A-I concentrations [14].
  • HDL and HDL2 cholesterol also were positively associated with estradiol regardless of adjustment for obesity and other covariates [15].
  • As previously shown, plasma cholesterol, LDL-C, HDL-C, HDL2, and apolipoproteins A-I, A-II, and B all fell significantly following probucol treatment [16].
  • HDL and HDL2 cholesterol were unrelated to either total or free testosterone in the univariate analysis, but negatively associated with free, not total, testosterone after adjustment for obesity [15].

Biological context of JPH3

  • LCAT and apoE contents of CETP-D HDL-2 were markedly increased compared with control HDL-2, and increased cholesterol esterification activity resided within the apoE-HDL fraction [17].
  • Competition studies indicated that the HDL binding sites recognized either HDL3 or HDL2 but interacted weakly with low density lipoprotein (LDL) [18].
  • The turnover of apoA-I and apoA-II was substantially slower in both HDL2 and HDL3 in the CETP-deficient homozygotes than in controls [19].
  • Additional adjustments for alcohol consumption, cigarettes smoked daily, smoking years, and leisure time energy expenditure reduced these excess risks associated with low HDL, HDL2, and HDL3 cholesterol levels by another 26%, 24% and 21%, respectively [20].
  • Expression of the transgene resulted in a dramatic reduction in the level of large high density lipoproteins (HDL1 and HDL2) as well as dense HDL3 [21].

Anatomical context of JPH3

  • The body-mass index, total percentage of body fat, maximal oxygen uptake, diet, and sex were not significant predictors of the HDL2 level when added to this model, whereas the original variables remained significant predictors [12].
  • Also, HDL2, HDL3, and VHDL competed similarly for binding of 125I-HDL3 to LDL receptor-negative fibroblasts [22].
  • CETP-D HDL-2 caused a 2- to 3-fold stimulation of net cholesterol efflux compared with control HDL-2 in LXR-activated macrophages, due primarily to an increase in lecithin:cholesterol acyltransferase-mediated (LCAT-mediated) cholesteryl ester formation in media [17].
  • Apolipoprotein AI was also ineffective in preventing monocyte transmigration while phosphatidylcholine liposomes were as effective as HDL2 suggesting that lipid components of HDL2 may have been responsible for its action [23].
  • Changes in serum mass concentrations of low-density lipoproteins (LDL; flotation rate 0-12), very-low-density lipoproteins (VLDL; flotation rate 20-400), high-density lipoproteins (HDL), and the HDL2 and HDL3 subfractions did not differ significantly between men with and without definite progression of coronary artery disease [24].

Associations of JPH3 with chemical compounds

  • Resumption of drinking increased the levels of HDL cholesterol and HDL3 mass (P less than or equal to 0.05) without affecting HDL2 mass [1].
  • Although plasma lipid levels were normal in most subjects with this trait, levels of plasma apoprotein B and triglyceride were higher and levels of apoprotein AI and HDL2 lower than in unaffected family members [25].
  • MEASUREMENTS: Plasma lipids, including high-density lipoprotein (HDL) subfractions HDL2 and HDL3, apoprotein A1, and serum levels of gonadotropins, estradiol, and testosterone were measured before, during, and after treatment [4].
  • Human high density lipoprotein (HDL) and its subfractions (HDL2 and HDL3) were separated by ultracentrifugation and the molar ratio of the two major polypeptide chains apo-Gln-I and apo-Gln-II was determined by fluorescence tagging of sodium dodecyl sulfate-denatured proteins combined with polyacrylamide disc gel electrophoresis [26].
  • In conclusion, compared with glibenclamide, insulin treatment (independent of variations in glucose control) is able to decrease significantly plasma triglycerides, to increase HDL2 cholesterol, and to reduce only the concentration of the larger VLDL subfractions, with a consequent redistribution of their profile [27].

Other interactions of JPH3

  • The HDL genes PRNP and JPH3, encoding the prion protein and junctophilin-3, respectively, were screened for repeat expansions in these patients [28].
  • Huntington's disease-like phenotype due to trinucleotide repeat expansions in the TBP and JPH3 genes [6].
  • RA patients also had significantly higher levels of small, dense LDL-1 (P < 0.05) and lower levels of small HDL-2 particles (P < 0.001) compared with controls [29].
  • Lipid and apoprotein composition of HDL-2, HDL-3 and LDL were unchanged [30].
  • Genetic deficiency or inhibition of cholesteryl ester transfer protein (CETP) leads to a marked increase in plasma levels of large HDL-2 particles [17].

Analytical, diagnostic and therapeutic context of JPH3

  • The distribution of the HDL subfractions HDL2, HDL3, and HDL3D, as determined by zonal ultracentrifugation, was normal in black and abnormal in white men receiving hemodialysis [31].
  • The HDL2 cholesterol level in subjects at the 25th percentile for waist-to-hip ratio was 153 percent of that in subjects at the 75th percentile [12].
  • CONCLUSIONS: From this large case-control study, it is concluded that the presence of PAOD is predicted by parameters of LDL, triglyceride, and HDL2 metabolism, whereas the extent of PAOD is related to HDL3 and nonlipid risk factors [32].
  • Distribution of cholesterol over the lipoprotein subclasses changed by ligation: levels in low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) were increased 2-fold and 5-fold, respectively, and were decreased in HDL 2-fold. rHDL treatment did not affect cholesterol distribution [33].
  • Fractionation of plasma by vertical gradient density centrifugation revealed apoJ-HDL in HDL2 (d 1.063-1.125 g/ml) with the majority overlapping HDL3 (d 1.125-1.21 g/ml) and very high density lipoprotein (d 1.21-1.25 g/ml) [34].


  1. The effect of cessation and resumption of moderate alcohol intake on serum high-density-lipoprotein subfractions. A controlled study. Haskell, W.L., Camargo, C., Williams, P.T., Vranizan, K.M., Krauss, R.M., Lindgren, F.T., Wood, P.D. N. Engl. J. Med. (1984) [Pubmed]
  2. Lipoprotein lipase. A multifunctional enzyme relevant to common metabolic diseases. Eckel, R.H. N. Engl. J. Med. (1989) [Pubmed]
  3. Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. Gaziano, J.M., Buring, J.E., Breslow, J.L., Goldhaber, S.Z., Rosner, B., VanDenburgh, M., Willett, W., Hennekens, C.H. N. Engl. J. Med. (1993) [Pubmed]
  4. Physiologic testosterone levels in normal men suppress high-density lipoprotein cholesterol levels. Bagatell, C.J., Knopp, R.H., Vale, W.W., Rivier, J.E., Bremner, W.J. Ann. Intern. Med. (1992) [Pubmed]
  5. Associations of the HDL2 and HDL3 cholesterol subfractions with the development of ischemic heart disease in British men. The Caerphilly and Speedwell Collaborative Heart Disease Studies. Sweetnam, P.M., Bolton, C.H., Yarnell, J.W., Bainton, D., Baker, I.A., Elwood, P.C., Miller, N.E. Circulation (1994) [Pubmed]
  6. Huntington's disease-like phenotype due to trinucleotide repeat expansions in the TBP and JPH3 genes. Stevanin, G., Fujigasaki, H., Lebre, A.S., Camuzat, A., Jeannequin, C., Dode, C., Takahashi, J., San, C., Bellance, R., Brice, A., Durr, A. Brain (2003) [Pubmed]
  7. Lifestyle determinants of HDL2- and HDL3-cholesterol levels in a hypercholesterolemic male population. Mänttäri, M., Koskinen, P., Manninen, V., Tenkanen, L., Huttunen, J.K. Atherosclerosis (1991) [Pubmed]
  8. Serum lipids and lipoproteins in postmenopausal women receiving transdermal oestrogen in combination with a levonorgestrel-releasing intrauterine device. Raudaskoski, T.H., Tomás, E.I., Paakkari, I.A., Kauppila, A.J., Laatikainen, T.J. Maturitas. (1995) [Pubmed]
  9. A repeat expansion in the gene encoding junctophilin-3 is associated with Huntington disease-like 2. Holmes, S.E., O'Hearn, E., Rosenblatt, A., Callahan, C., Hwang, H.S., Ingersoll-Ashworth, R.G., Fleisher, A., Stevanin, G., Brice, A., Potter, N.T., Ross, C.A., Margolis, R.L. Nat. Genet. (2001) [Pubmed]
  10. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. Brown, B.G., Zhao, X.Q., Chait, A., Fisher, L.D., Cheung, M.C., Morse, J.S., Dowdy, A.A., Marino, E.K., Bolson, E.L., Alaupovic, P., Frohlich, J., Albers, J.J. N. Engl. J. Med. (2001) [Pubmed]
  11. A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. Stampfer, M.J., Sacks, F.M., Salvini, S., Willett, W.C., Hennekens, C.H. N. Engl. J. Med. (1991) [Pubmed]
  12. The ratio of waist-to-hip circumference, plasma insulin level, and glucose intolerance as independent predictors of the HDL2 cholesterol level in older adults. Ostlund, R.E., Staten, M., Kohrt, W.M., Schultz, J., Malley, M. N. Engl. J. Med. (1990) [Pubmed]
  13. High plasma vitamin C associated with high plasma HDL- and HDL2 cholesterol. Hallfrisch, J., Singh, V.N., Muller, D.C., Baldwin, H., Bannon, M.E., Andres, R. Am. J. Clin. Nutr. (1994) [Pubmed]
  14. The association between dyslipidaemia and obesity in Chinese men after adjustment for insulin resistance. Ko, G.T., Chan, J.C., Cockram, C.S. Atherosclerosis (1998) [Pubmed]
  15. Behavioral correlates of plasma sex hormones and their relationships with plasma lipids and lipoproteins in Japanese men. Handa, K., Ishii, H., Kono, S., Shinchi, K., Imanishi, K., Mihara, H., Tanaka, K. Atherosclerosis (1997) [Pubmed]
  16. Probucol treatment in hypercholesterolemic patients: effects on lipoprotein composition, HDL particle size, and cholesteryl ester transfer. Bagdade, J.D., Kaufman, D., Ritter, M.C., Subbaiah, P.V. Atherosclerosis (1990) [Pubmed]
  17. HDL from CETP-deficient subjects shows enhanced ability to promote cholesterol efflux from macrophages in an apoE- and ABCG1-dependent pathway. Matsuura, F., Wang, N., Chen, W., Jiang, X.C., Tall, A.R. J. Clin. Invest. (2006) [Pubmed]
  18. Regulation of high density lipoprotein receptor activity in cultured human skin fibroblasts and human arterial smooth muscle cells. Oram, J.F., Brinton, E.A., Bierman, E.L. J. Clin. Invest. (1983) [Pubmed]
  19. Delayed catabolism of high density lipoprotein apolipoproteins A-I and A-II in human cholesteryl ester transfer protein deficiency. Ikewaki, K., Rader, D.J., Sakamoto, T., Nishiwaki, M., Wakimoto, N., Schaefer, J.R., Ishikawa, T., Fairwell, T., Zech, L.A., Nakamura, H. J. Clin. Invest. (1993) [Pubmed]
  20. HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men. Salonen, J.T., Salonen, R., Seppänen, K., Rauramaa, R., Tuomilehto, J. Circulation (1991) [Pubmed]
  21. Overexpression of hepatic lipase in transgenic rabbits leads to a marked reduction of plasma high density lipoproteins and intermediate density lipoproteins. Fan, J., Wang, J., Bensadoun, A., Lauer, S.J., Dang, Q., Mahley, R.W., Taylor, J.M. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  22. Specific high-affinity binding of high density lipoproteins to cultured human skin fibroblasts and arterial smooth muscle cells. Biesbroeck, R., Oram, J.F., Albers, J.J., Bierman, E.L. J. Clin. Invest. (1983) [Pubmed]
  23. Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. Navab, M., Imes, S.S., Hama, S.Y., Hough, G.P., Ross, L.A., Bork, R.W., Valente, A.J., Berliner, J.A., Drinkwater, D.C., Laks, H. J. Clin. Invest. (1991) [Pubmed]
  24. Intermediate-density lipoproteins and progression of coronary artery disease in hypercholesterolaemic men. Krauss, R.M., Lindgren, F.T., Williams, P.T., Kelsey, S.F., Brensike, J., Vranizan, K., Detre, K.M., Levy, R.I. Lancet (1987) [Pubmed]
  25. Genetic control of low-density-lipoprotein subclasses. Austin, M.A., Krauss, R.M. Lancet (1986) [Pubmed]
  26. The molar ratio of the two major polypeptide components of human high density lipoprotein. Friedberg, S.J., Reynolds, J.A. J. Biol. Chem. (1976) [Pubmed]
  27. Insulin and sulfonylurea therapy in NIDDM patients. Are the effects on lipoprotein metabolism different even with similar blood glucose control? Romano, G., Patti, L., Innelli, F., Di Marino, L., Annuzzi, G., Iavicoli, M., Coronel, G.A., Riccardi, G., Rivellese, A.A. Diabetes (1997) [Pubmed]
  28. Exclusion of mutations in the PRNP, JPH3, TBP, ATN1, CREBBP, POU3F2 and FTL genes as a cause of disease in Portuguese patients with a Huntington-like phenotype. Costa, M.d.o. .C., Teixeira-Castro, A., Constante, M., Magalhães, M., Magalhães, P., Cerqueira, J., Vale, J., Passão, V., Barbosa, C., Robalo, C., Coutinho, P., Barros, J., Santos, M.M., Sequeiros, J., Maciel, P. J. Hum. Genet. (2006) [Pubmed]
  29. Elevated levels of small, low-density lipoprotein with high affinity for arterial matrix components in patients with rheumatoid arthritis: possible contribution of phospholipase A2 to this atherogenic profile. Hurt-Camejo, E., Paredes, S., Masana, L., Camejo, G., Sartipy, P., Rosengren, B., Pedreno, J., Vallve, J.C., Benito, P., Wiklund, O. Arthritis Rheum. (2001) [Pubmed]
  30. Changes in lipoprotein composition in women receiving two low-dose oral contraceptives containing ethinylestradiol and gonane progestins. Harvengt, C., Desager, J.P., Gaspard, U., Lepot, M. Contraception. (1988) [Pubmed]
  31. Racial differences in plasma high-density lipoproteins in patients receiving hemodialysis. A possible mechanism for accelerated atherosclerosis in white men. Goldberg, A.P., Harter, H.R., Patsch, W., Schechtman, K.B., Province, M., Weerts, C., Kuisk, I., McCrate, M.M., Schonfeld, G. N. Engl. J. Med. (1983) [Pubmed]
  32. Predictors of the presence and extent of peripheral arterial occlusive disease. Drexel, H., Steurer, J., Muntwyler, J., Meienberg, S., Schmid, H.R., Schneider, E., Gröchenig, E., Amann, F.W. Circulation (1996) [Pubmed]
  33. Endotoxin-induced mortality in bile duct-ligated rats after administration of reconstituted high-density lipoprotein. Sewnath, M.E., Levels, H.H., Oude Elferink, R., van Noorden, C.J., ten Kate, F.J., van Deventer, S.J., Gouma, D.J. Hepatology (2000) [Pubmed]
  34. A 70-kDa apolipoprotein designated ApoJ is a marker for subclasses of human plasma high density lipoproteins. de Silva, H.V., Stuart, W.D., Duvic, C.R., Wetterau, J.R., Ray, M.J., Ferguson, D.G., Albers, H.W., Smith, W.R., Harmony, J.A. J. Biol. Chem. (1990) [Pubmed]
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