Experts and Doctors on ldl receptors in New York, United States

Summary

Locale: New York, United States
Topic: ldl receptors

Top Publications

  1. Shachter N. Apolipoproteins C-I and C-III as important modulators of lipoprotein metabolism. Curr Opin Lipidol. 2001;12:297-304 pubmed
    ..Variation in the expression of apoC-III has been credibly documented to have an important role in hypertriglyceridemia. Variation in the expression of apoC-I may also be important for hypertriglyceridemia under certain circumstances. ..
  2. Gotto A, Moon J. Pitavastatin for the treatment of primary hyperlipidemia and mixed dyslipidemia. Expert Rev Cardiovasc Ther. 2010;8:1079-90 pubmed publisher
    ..Its safety and adverse event profile is similar to that of other available statins, and it has an established history of use in Asia indicating tolerability and safety for treatment lasting up to 7 years. ..
  3. Vikramadithyan R, Hu Y, Noh H, Liang C, Hallam K, Tall A, et al. Human aldose reductase expression accelerates diabetic atherosclerosis in transgenic mice. J Clin Invest. 2005;115:2434-43 pubmed
    ..Thus, hAR increases atherosclerosis in diabetic mice. Inhibitors of AR or other enzymes that mediate glucose toxicity could be useful in the treatment of diabetic atherosclerosis. ..
  4. Grant B, Hirsh D. Receptor-mediated endocytosis in the Caenorhabditis elegans oocyte. Mol Biol Cell. 1999;10:4311-26 pubmed
    ..We describe a new member of the low-density lipoprotein receptor superfamily, RME-2, identified in our screens for endocytosis defective mutants. We show that RME-2 is the C. elegans yolk receptor. ..
  5. Hoang B, Kubo T, Healey J, Sowers R, Mazza B, Yang R, et al. Expression of LDL receptor-related protein 5 (LRP5) as a novel marker for disease progression in high-grade osteosarcoma. Int J Cancer. 2004;109:106-11 pubmed
    ..These results showed that expression of LRP5 is a common event in OS and strongly suggest a role for LRP and Wnt signaling in the pathobiology and progression of this disease. ..
  6. Siri P, Candela N, Zhang Y, Ko C, Eusufzai S, Ginsberg H, et al. Post-transcriptional stimulation of the assembly and secretion of triglyceride-rich apolipoprotein B lipoproteins in a mouse with selective deficiency of brown adipose tissue, obesity, and insulin resistance. J Biol Chem. 2001;276:46064-72 pubmed
    ..This rodent model should prove useful in exploring mechanisms underlying the regulation of apoB secretion in the context of insulin resistance. ..
  7. Jeong T, Schissel S, Tabas I, Pownall H, Tall A, Jiang X. Increased sphingomyelin content of plasma lipoproteins in apolipoprotein E knockout mice reflects combined production and catabolic defects and enhances reactivity with mammalian sphingomyelinase. J Clin Invest. 1998;101:905-12 pubmed
    ..The increased SM content in slowly cleared remnant lipoproteins may enhance their susceptibility to arterial wall SMase and increase their atherogenic potential. ..
  8. Devlin C, Leventhal A, Kuriakose G, Schuchman E, Williams K, Tabas I. Acid sphingomyelinase promotes lipoprotein retention within early atheromata and accelerates lesion progression. Arterioscler Thromb Vasc Biol. 2008;28:1723-30 pubmed publisher
    ..0005). These findings support a causal role for acid SMase in lipoprotein retention and lesion progression and provides further support for the response-to-retention model of atherogenesis. ..
  9. Teupser D, Persky A, Breslow J. Induction of atherosclerosis by low-fat, semisynthetic diets in LDL receptor-deficient C57BL/6J and FVB/NJ mice: comparison of lesions of the aortic root, brachiocephalic artery, and whole aorta (en face measurement). Arterioscler Thromb Vasc Biol. 2003;23:1907-13 pubmed
    ..LDLR-/-) and FVB/NJ (FVB.LDLR-/-) backgrounds...

More Information

Publications49

  1. Culi J, Mann R. Boca, an endoplasmic reticulum protein required for wingless signaling and trafficking of LDL receptor family members in Drosophila. Cell. 2003;112:343-54 pubmed
    ..Consequently, boca is an essential component of the Wingless pathway but is more generally required for the activities of multiple LDL receptor family members. ..
  2. Song L, Leung C, Schindler C. Lymphocytes are important in early atherosclerosis. J Clin Invest. 2001;108:251-9 pubmed
    ..Differences in lesion area did not correlate with any significant alterations in plasma lipid levels. These studies suggest that lymphocytes play an important role early in atherogenesis. ..
  3. Sehayek E, Ono J, Duncan E, Batta A, Salen G, Shefer S, et al. Hyodeoxycholic acid efficiently suppresses atherosclerosis formation and plasma cholesterol levels in mice. J Lipid Res. 2001;42:1250-6 pubmed
    ..These results suggest that HDCA might have beneficial effects in the treatment of increased plasma cholesterol levels and atherosclerosis. ..
  4. McCaffrey T, Fu C, Du B, Eksinar S, Kent K, Bush H, et al. High-level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis. J Clin Invest. 2000;105:653-62 pubmed
    ..Thus, induction of Egr-1 by atherogenic factors may be a key step in coordinating the cellular events that result in vascular lesions. ..
  5. Carter M, Chen X, Slowinska B, Minnerath S, Glickstein S, Shi L, et al. Crooked tail (Cd) model of human folate-responsive neural tube defects is mutated in Wnt coreceptor lipoprotein receptor-related protein 6. Proc Natl Acad Sci U S A. 2005;102:12843-8 pubmed
    ..The Lrp6 mutation in Cd mice provides evidence for a functional connection between Wnt signaling and folate rescue of neural tube defects. ..
  6. Liu G, Bafico A, Aaronson S. The mechanism of endogenous receptor activation functionally distinguishes prototype canonical and noncanonical Wnts. Mol Cell Biol. 2005;25:3475-82 pubmed
    ..These findings provide a novel mechanism by which the same receptor can be switched between distinct signaling pathways depending on the differential recruitment of a coreceptor by members of the same ligand family. ..
  7. Masucci Magoulas L, Goldberg I, Bisgaier C, Serajuddin H, Francone O, Breslow J, et al. A mouse model with features of familial combined hyperlipidemia. Science. 1997;275:391-4 pubmed
    ..This mouse model may provide clues to the origin of human FCHL. ..
  8. Elder G, Cho J, English D, Franciosi S, Schmeidler J, Sosa M, et al. Elevated plasma cholesterol does not affect brain Abeta in mice lacking the low-density lipoprotein receptor. J Neurochem. 2007;102:1220-31 pubmed
    ..ApoE protein levels in brain were, however, elevated, in LDLR-/- mice by post-transcriptional mechanisms. Collectively, these studies argue that plasma cholesterol levels do not normally regulate production of brain Abeta. ..
  9. Thorp E, Li G, Seimon T, Kuriakose G, Ron D, Tabas I. Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP. Cell Metab. 2009;9:474-81 pubmed publisher
    ..These data provide direct evidence for a causal link between the ER stress effector CHOP and plaque necrosis and suggest that interventions weakening this arm of the UPR may lessen plaque progression. ..
  10. Welch C, Bretschger S, Latib N, Bezouevski M, Guo Y, Pleskac N, et al. Localization of atherosclerosis susceptibility loci to chromosomes 4 and 6 using the Ldlr knockout mouse model. Proc Natl Acad Sci U S A. 2001;98:7946-51 pubmed
    ..Athsq1 and Athsq2 represent candidate susceptibility loci for human atherosclerosis, most likely residing on chromosomes 1p36--32 and 12p13--12, respectively. ..
  11. Masson D, Koseki M, Ishibashi M, Larson C, Miller S, King B, et al. Increased HDL cholesterol and apoA-I in humans and mice treated with a novel SR-BI inhibitor. Arterioscler Thromb Vasc Biol. 2009;29:2054-60 pubmed publisher
    ..This suggests that pharmacological inhibition of SR-BI has the potential to raise HDL-C and apoA-I levels without adverse effects on VLDL/LDL cholesterol levels in humans. ..
  12. Yagyu H, Lutz E, Kako Y, Marks S, Hu Y, Choi S, et al. Very low density lipoprotein (VLDL) receptor-deficient mice have reduced lipoprotein lipase activity. Possible causes of hypertriglyceridemia and reduced body mass with VLDL receptor deficiency. J Biol Chem. 2002;277:10037-43 pubmed
    ..Therefore, the VLDLr is required for normal LpL regulation in vivo, and the disruption of VLDLr results in hypertriglyceridemia associated with decreased LpL activity. ..
  13. Li S, Sun Y, Liang C, Thorp E, Han S, Jehle A, et al. Defective phagocytosis of apoptotic cells by macrophages in atherosclerotic lesions of ob/ob mice and reversal by a fish oil diet. Circ Res. 2009;105:1072-82 pubmed publisher
  14. Deborde S, Perret E, Gravotta D, Deora A, Salvarezza S, Schreiner R, et al. Clathrin is a key regulator of basolateral polarity. Nature. 2008;452:719-23 pubmed publisher
    ..Our results demonstrate a broad requirement for clathrin in basolateral protein trafficking in epithelial cells...
  15. Jehle A, Gardai S, Li S, Linsel Nitschke P, Morimoto K, Janssen W, et al. ATP-binding cassette transporter A7 enhances phagocytosis of apoptotic cells and associated ERK signaling in macrophages. J Cell Biol. 2006;174:547-56 pubmed
    ..These studies reveal a major role of ABCA7 and not -A1 in the clearance of apoptotic cells and therefore suggest that ABCA7 is an authentic orthologue of CED-7...
  16. Wu L, Vikramadithyan R, Yu S, Pau C, Hu Y, Goldberg I, et al. Addition of dietary fat to cholesterol in the diets of LDL receptor knockout mice: effects on plasma insulin, lipoproteins, and atherosclerosis. J Lipid Res. 2006;47:2215-22 pubmed
    ..Our data suggest that when lipoprotein profiles are similar, addition of fat to a cholesterol-rich diet does not increase atherosclerotic lesion formation in Ldlr(-/-) mice. ..
  17. Teupser D, Tan M, Persky A, Breslow J. Atherosclerosis quantitative trait loci are sex- and lineage-dependent in an intercross of C57BL/6 and FVB/N low-density lipoprotein receptor-/- mice. Proc Natl Acad Sci U S A. 2006;103:123-8 pubmed
    ..Awareness of these complexities may have major consequences for the identification of atherosclerosis susceptibility genes by quantitative trait locus mapping. ..
  18. Zhou X, He W, Huang Z, Gotto A, Hajjar D, Han J. Genetic deletion of low density lipoprotein receptor impairs sterol-induced mouse macrophage ABCA1 expression. A new SREBP1-dependent mechanism. J Biol Chem. 2008;283:2129-38 pubmed
  19. Yvan Charvet L, Welch C, Pagler T, Ranalletta M, Lamkanfi M, Han S, et al. Increased inflammatory gene expression in ABC transporter-deficient macrophages: free cholesterol accumulation, increased signaling via toll-like receptors, and neutrophil infiltration of atherosclerotic lesions. Circulation. 2008;118:1837-47 pubmed publisher
    ..This study was undertaken to elucidate the mechanisms and consequences of enhanced inflammatory gene expression in ABC transporter-deficient macrophages...
  20. Nakaya H, Summers B, Nicholson A, Gotto A, Hajjar D, Han J. Atherosclerosis in LDLR-knockout mice is inhibited, but not reversed, by the PPARgamma ligand pioglitazone. Am J Pathol. 2009;174:2007-14 pubmed publisher
    ..These findings have implications for the analysis of therapeutic agents in murine models of atherosclerosis and the use of pioglitazone in patients with established atherosclerosis. ..
  21. Seidelmann S, Kuo C, Pleskac N, Molina J, Sayers S, Li R, et al. Athsq1 is an atherosclerosis modifier locus with dramatic effects on lesion area and prominent accumulation of versican. Arterioscler Thromb Vasc Biol. 2008;28:2180-6 pubmed publisher
    ..These studies confirm the proatherogenic activity of a novel gene(s) in the MOLF-derived Athsq1 locus and provide in vivo evidence for a causative role of versican in lesion development. ..
  22. Vikramadithyan R, Kako Y, Chen G, Hu Y, Arikawa Hirasawa E, Yamada Y, et al. Atherosclerosis in perlecan heterozygous mice. J Lipid Res. 2004;45:1806-12 pubmed
    ..Although this might be attributable to a decrease in lipoprotein retention, it should be noted that perlecan might mediate multiple other processes that could, in sum, accelerate atherosclerosis. ..
  23. Kim N, Stiegler A, Cameron T, Hallock P, Gomez A, Huang J, et al. Lrp4 is a receptor for Agrin and forms a complex with MuSK. Cell. 2008;135:334-42 pubmed publisher
    ..Here, we report that Lrp4, a member of the LDLR family, is a receptor for Agrin, forms a complex with MuSK, and mediates MuSK activation by Agrin. ..
  24. Lim W, Timmins J, Seimon T, Sadler A, Kolodgie F, Virmani R, et al. Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo. Circulation. 2008;117:940-51 pubmed publisher
    ..These findings suggest a potentially important role for STAT1-mediated macrophage apoptosis in atherosclerotic plaque progression. ..
  25. Han S, Liang C, Westerterp M, Senokuchi T, Welch C, Wang Q, et al. Hepatic insulin signaling regulates VLDL secretion and atherogenesis in mice. J Clin Invest. 2009;119:1029-41 pubmed publisher
    ..These findings suggest a dual action of hepatic IR on lipoprotein levels, in which the ability to increase VLDL apoB and lipid secretion via AKT/GSK is offset by upregulation of Ldlr. ..
  26. Khan Z, Vijayakumar S, de la Torre T, Rotolo S, Bafico A. Analysis of endogenous LRP6 function reveals a novel feedback mechanism by which Wnt negatively regulates its receptor. Mol Cell Biol. 2007;27:7291-301 pubmed
    ..In light of the direct role that the Wnt pathway plays in human bone diseases and malignancies, our findings may support the development of novel therapeutic approaches that target Wnt signaling through LRP6. ..
  27. Lane R, Raines S, Steele J, Ehrlich M, Lah J, Small S, et al. Diabetes-associated SorCS1 regulates Alzheimer's amyloid-beta metabolism: evidence for involvement of SorL1 and the retromer complex. J Neurosci. 2010;30:13110-5 pubmed publisher
    ..003) in the brains of female Sorcs1 hypomorphic mice. From these data, we propose that dysfunction of SorCS1 may contribute to both the APP/A? disturbance underlying AD and the insulin/glucose disturbance underlying DM. ..
  28. Weatherbee S, Anderson K, Niswander L. LDL-receptor-related protein 4 is crucial for formation of the neuromuscular junction. Development. 2006;133:4993-5000 pubmed
    ..The identification of Lrp4 as a crucial factor for NMJ formation may have implications for human neuromuscular diseases such as myasthenia syndromes. ..
  29. Ranalletta M, Wang N, Han S, Yvan Charvet L, Welch C, Tall A. Decreased atherosclerosis in low-density lipoprotein receptor knockout mice transplanted with Abcg1-/- bone marrow. Arterioscler Thromb Vasc Biol. 2006;26:2308-15 pubmed
    ..Recent studies indicate that the ATP-binding cassette transporter ABCG1 can promote cholesterol efflux from macrophages to high-density lipoprotein. This study was designed to assess the in vivo role of macrophage ABCG1 in atherosclerosis...
  30. Maxwell K, Fisher E, Breslow J. Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment. Proc Natl Acad Sci U S A. 2005;102:2069-74 pubmed
    ..These results indicate that overexpression of PCSK9 induces the degradation of the LDLR by a nonproteasomal mechanism in a post-endoplasmic reticulum compartment. ..
  31. Angeli V, Llodra J, Rong J, Satoh K, Ishii S, Shimizu T, et al. Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization. Immunity. 2004;21:561-74 pubmed
    ..In this context, HDL and PAFAH maintain a normally functional DC compartment. ..
  32. González Sancho J, Brennan K, Castelo Soccio L, Brown A. Wnt proteins induce dishevelled phosphorylation via an LRP5/6- independent mechanism, irrespective of their ability to stabilize beta-catenin. Mol Cell Biol. 2004;24:4757-68 pubmed
    ..Our data also present Dvl phosphorylation as a general biochemical assay for Wnt protein function, including those Wnts that do not activate the Wnt/beta-catenin pathway. ..
  33. Hoang B, Kubo T, Healey J, Yang R, Nathan S, Kolb E, et al. Dickkopf 3 inhibits invasion and motility of Saos-2 osteosarcoma cells by modulating the Wnt-beta-catenin pathway. Cancer Res. 2004;64:2734-9 pubmed
    ..Taken together, these results support a possible role for Wnt signaling in the pathobiology and progression of human OS. ..
  34. Brennan K, González Sancho J, Castelo Soccio L, Howe L, Brown A. Truncated mutants of the putative Wnt receptor LRP6/Arrow can stabilize beta-catenin independently of Frizzled proteins. Oncogene. 2004;23:4873-84 pubmed
    ..In light of these models, our data imply that LRP5/6/Arrow proteins constitute the distal signal-initiating component of these receptors. The results also support the notion that LRP5/6 are candidate oncogenes. ..
  35. Abe E, Marians R, Yu W, Wu X, Ando T, Li Y, et al. TSH is a negative regulator of skeletal remodeling. Cell. 2003;115:151-62 pubmed
    ..These studies define a role for TSH as a single molecular switch in the independent control of both bone formation and resorption. ..
  36. Liu G, Bafico A, Harris V, Aaronson S. A novel mechanism for Wnt activation of canonical signaling through the LRP6 receptor. Mol Cell Biol. 2003;23:5825-35 pubmed
    ..Thus, Wnt canonical signaling through LRP6 establishes a novel mechanism for receptor activation which is opposite to the general paradigm of ligand-induced receptor oligomerization. ..
  37. Gan Y, McGraw T, Rodriguez Boulan E. The epithelial-specific adaptor AP1B mediates post-endocytic recycling to the basolateral membrane. Nat Cell Biol. 2002;4:605-9 pubmed
    ..Targeting and recycling assays in LLC-PK1 cells, before and after transfection with mu 1B, and in MDCK cells, which express mu 1B constitutively, suggest that AP1B sorts basolateral proteins post-endocytically...
  38. Merkel M, Velez Carrasco W, Hudgins L, Breslow J. Compared with saturated fatty acids, dietary monounsaturated fatty acids and carbohydrates increase atherosclerosis and VLDL cholesterol levels in LDL receptor-deficient, but not apolipoprotein E-deficient, mice. Proc Natl Acad Sci U S A. 2001;98:13294-9 pubmed
  39. Bafico A, Liu G, Yaniv A, Gazit A, Aaronson S. Novel mechanism of Wnt signalling inhibition mediated by Dickkopf-1 interaction with LRP6/Arrow. Nat Cell Biol. 2001;3:683-6 pubmed
  40. Plump A, Masucci Magoulas L, Bruce C, Bisgaier C, Breslow J, Tall A. Increased atherosclerosis in ApoE and LDL receptor gene knock-out mice as a result of human cholesteryl ester transfer protein transgene expression. Arterioscler Thromb Vasc Biol. 1999;19:1105-10 pubmed
    ..However, apoA1 overexpression has more dramatic protective effects on atherosclerosis in apoE0 mice, which are not significantly reversed by concomitant expression of CETP. ..