cDNA Cloning of a New Low-Density Lipoprotein Receptor-Related Protein and Mapping of Its Gene (LRP3) to Chromosome Bands 19q12–q13.2

Ishii, Hiroki; Kim, Dong Ho; Fujita, Teizo; Endo, Yuichi; Saeki, Shigeru; Yamamoto, Tokuo

doi:10.1006/geno.1998.5339

Cited by 42 publications

(31 citation statements)

References 11 publications

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“…The function of the LRP3 Evidence for a QTL on chromosome 19 influencing LDL-C M Beekman et al remains unclear, but as a family member of LDLR a role in lipid metabolism is assumed. 13 INSR and LIPE are candidates for influencing triglyceride levels, but not for LDL-C levels. 11,12 Near the LDLR locus, the ATHS locus has been mapped involved in atherogenic lipoprotein phenotype pattern B, which is characterized by small, dense LDL particles, increased levels of triglycerides and decreased levels of HDL-C. 41 Since we have no indication for linkage with levels of triglycerides and HDL-C, we assume that the ATHS locus is a different locus than our LDL-C QTL.…”

Section: Discussionmentioning

confidence: 96%

“…13 Compatible with this wealth of candidate genes, evidence for linkage with plasma levels of total cholesterol was found in Pima Indians and with LDL cholesterol levels in Hutterites. 14,15 In contrast to the findings in these genetic isolates, however, no significant linkage with LDL-C levels on chromosome 19 was found in genome scans among outbred Caucasians.…”

Section: Introductionmentioning

confidence: 99%

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Evidence for a QTL on chromosome 19 influencing LDL cholesterol levels in the general population

et al. 2003

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The genetic basis of cardiovascular disease (CVD) with its complex etiology is still largely elusive. Plasma levels of lipids and apolipoproteins are among the major quantitative risk factors for CVD and are well-established intermediate traits that may be more accessible to genetic dissection than clinical CVD end points. Chromosome 19 harbors multiple genes that have been suggested to play a role in lipid metabolism and previous studies indicated the presence of a quantitative trait locus (QTL) for cholesterol levels in genetic isolates. To establish the relevance of genetic variation at chromosome 19 for plasma levels of lipids and apolipoproteins in the general, out-bred Caucasian population, we performed a linkage study in four independent samples, including adolescent Dutch twins and adult Dutch, Swedish and Australian twins totaling 493 dizygotic twin pairs. The average spacing of short-tandem-repeat markers was 6-8 cM. In the three adult twin samples, we found consistent evidence for linkage of chromosome 19 with LDL cholesterol levels (maximum LOD scores of 4.5, 1.7 and 2.1 in the Dutch, Swedish and Australian sample, respectively); no indication for linkage was observed in the adolescent Dutch twin sample. The QTL effects in the three adult samples were not significantly different and a simultaneous analysis of the samples increased the maximum LOD score to 5.7 at 60 cM pter. Bivariate analyses indicated that the putative LDL-C QTL also contributed to the variance in ApoB levels, consistent with the high genetic correlation between these phenotypes. Our study provides strong evidence for the presence of a QTL on chromosome 19 with a major effect on LDL-C plasma levels in outbred Caucasian populations.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Evidence for a QTL on chromosome 19 influencing LDL cholesterol levels in the general population

et al. 2003

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“…Wnt canonical signaling plays an important role in osteoblast differentiation both during embryogenesis and in adult life (50). However, there are several novel members in the LDLR family such as, LRP3, LRP10 and LRP12 (25,29,40), which are uncertain if they are receptors for apoE.…”

Section: Discussionmentioning

confidence: 99%

“…There are several novel members in the LDLR family including LRP3, LRP10 and LRP12 (25,29,40), which are uncertain if they are receptors for apoE. Interestingly, either in the saline group or in E2 treated group, LRP3, LRP10 and LRP12 genes were all induced at day 5 and 25 of differentiation ( Figures 5A, 5D, and 5G, p < 0.05, p < 0.01, p < 0.001).…”

Section: Regulation Of Other Novel Members In Ldlr Family By E2 Durinmentioning

confidence: 97%

“…ApoE has a strong affinity for and is the main ligand for members of the LDLR family. The LDLR family is a highly conserved receptor family with diverse functions in cellular physiology (shown in Table 1) (17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32). LDLR is the prototype of the entire family, and members of this family are structurally and functionally related to it.…”

Section: Introductionmentioning

confidence: 99%

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Multifarious effects of 17-β-estradiol on apolipoprotein E receptors gene expression during osteoblast differentiation <i>in vitro </i>

Gui

Duan

Tang

et al. 2016

BST

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Differential Expression of LR11 during Proliferation and Differentiation of Cultured Neuroblastoma Cells

Hirayama

Bujo

Yamazaki

et al. 2000

Biochemical and Biophysical Research Communications

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cDNA Cloning of a New Low-Density Lipoprotein Receptor-Related Protein and Mapping of Its Gene (LRP3) to Chromosome Bands 19q12–q13.2

Cited by 42 publications

References 11 publications

Evidence for a QTL on chromosome 19 influencing LDL cholesterol levels in the general population

Evidence for a QTL on chromosome 19 influencing LDL cholesterol levels in the general population

Multifarious effects of 17-β-estradiol on apolipoprotein E receptors gene expression during osteoblast differentiation <i>in vitro </i>

Differential Expression of LR11 during Proliferation and Differentiation of Cultured Neuroblastoma Cells

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