The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Functional expression of low density lipoprotein receptor-related protein is controlled by receptor-associated protein in vivo.
Abstract
The 39-kDa receptor-associated protein (RAP) associates with the multifunctional low density lipoprotein (LDL) receptor-related protein (LRP) and thereby prevents the binding of all known ligands, including alpha 2-macroglobulin and chylomicron remnants. RAP is predominantly localized in the endoplasmic reticulum, raising the possibility that it functions as a chaperone or escort protein in the biosynthesis or intracellular transport of LRP. Here we have used gene targeting to show that RAP promotes the expression of functional LRP in vivo. The amount of mature, processed LRP is reduced in liver and brain of RAP-deficient mice. As a result, hepatic clearance of alpha 2-macroglobulin is impaired and remnant lipoproteins accumulate in the plasma of RAP-deficient mice that also lack functional LDL receptors. These results are consistent with the hypothesis that RAP stabilizes LRP within the secretory pathway. They also suggest a further mechanism by which the activity of an endocytic receptor may be modulated in vivo.
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RAP-/- mice do not exhibit any gross alterations.
“although R APϪ/Ϫ mice do not exhibit any gross alterations (Willnow et al., 1995;Umans et al., 1999;Van Uden et al., 1999a)”
From Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein (2002) · cites this paper as Willnow et al., 1995
Mice deficient in RAP are viable and have normal lifespans because the maturation of LRP is only partially dependent upon RAP.
“Unlike LRP, mice deficient in RAP are viable and have normal lifespans because the maturation of LRP is only partially dependent upon RAP; neurons of RAP KO mice show 75% reductions in the levels of endoproteolytically processed, mature, LRP [26].”
From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [26]
Neurons of RAP KO mice show 75% reductions in the levels of endoproteolytically processed, mature LRP.
“Unlike LRP, mice deficient in RAP are viable and have normal lifespans because the maturation of LRP is only partially dependent upon RAP; neurons of RAP KO mice show 75% reductions in the levels of endoproteolytically processed, mature, LRP [26].”
From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [26]
The homozygous LRP knock-out model is lethal.
“because the homozygous LRP knock-out model is lethal (Willnow et al., 1995).”
From Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein (2002) · cites this paper as Willnow et al., 1995
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Cites
Carbohydrate-Specific Receptors of the Liver
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Sorted by citations
Mahley, R. W., & Ji, Z.-S. (1999) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)33334-4 · Cited by 693
Hepatic uptake of chylomicron remnants
Cooper, A. D. (1997) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)34932-4 · Cited by 499
Rohlmann, A., Gotthardt, M., Hammer, R. E., & Herz, J. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1240 · Cited by 455
Self-citationLipoprotein receptors in the nervous system
Herz, J., & Bock, H. H. (2002) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.71.110601.135342 · Cited by 457
Self-citationShinohara, M., Tachibana, M., Kanekiyo, T., & Bu, G. (2017) · Journal of Lipid Research · doi:10.1194/jlr.r075796 · Cited by 297
Willnow, T. E., Rohlmann, A., Horton, J., Otani, H., Braun, J. R., Hammer, R. E., & Herz, J. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00623.x · Cited by 276
Self-citationTamaki, C., Ohtsuki, S., Iwatsubo, T., Hashimoto, T., Yamada, K., Yabuki, C., & Terasaki, T. (2006) · Pharmaceutical Research · doi:10.1007/s11095-006-0208-7 · Cited by 119
Van Uden, E., Mallory, M., Veinbergs, I., Alford, M., Rockenstein, E., & Masliah, E. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-21-09298.2002 · Cited by 91
The generation and function of soluble apoE receptors in the CNS
Rebeck, G. W., LaDu, M. J., Estus, S., Bu, G., & Weeber, E. J. (2006) · Molecular Neurodegeneration · doi:10.1186/1750-1326-1-15 · Cited by 66
Ionita-Laza, I., Makarov, V., & Buxbaum, J. D. (2012) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2012.04.010 · Cited by 57
Xu, G., Karch, C., Li, N., Lin, N., Fromholt, D., Gonzales, V., & Borchelt, D. R. (2008) · PLoS ONE · doi:10.1371/journal.pone.0003159 · Cited by 14
Metadata
- Authors
- Willnow, T. E., Armstrong, S. A., Hammer, R. E., & Herz, J.
- Affiliations
- Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235, USA.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1995-05-09
- Volume
- 92
- Issue
- 10
- Pages
- 4537-4541
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 228
- References
- 1
- Language
- en
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