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Restoration of LDL receptor function in cells from patients with autosomal recessive hypercholesterolemia by retroviral expression of ARH1
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The vast majority of LDLRs in lymphocytes are located in intracellular, EEA1-positive vesicles.
“In contrast the vast majority of LDLRs in lymphocytes are located in intracellular, EEA1-positive vesicles (10 -12).”
From The Modular Adaptor Protein Autosomal Recessive Hypercholesterolemia (ARH) Promotes Low Density Lipoprotein Receptor Clustering into Clathrin-coated Pits (2005) · cites this paper as [12]
In “Expression of exogenous ARH1 in mutant EBV-lymphocytes” (page not specified), LDL receptors appeared as intracellular puncta in control cells after incubation at 37°C. The paper does not identify those puncta as EEA1-positive or say that the vast majority of receptors are intracellular; it reports surface staining at 4°C and continued surface staining in ARH1-negative cells at 37°C. (LLM, conf=0.87)
Experimental — accuracy not yet measuredARH is required for efficient endocytosis of LDLR in circulating lymphocytes and monocyte-derived macrophages from ARH patients.
“The results of these studies clearly suggested that ARH is required for the efficient endocytosis of LDLR in these cells.”
From Adaptor Protein ARH Is Recruited to the Plasma Membrane by Low Density Lipoprotein (LDL) Binding and Modulates Endocytosis of the LDL/LDL Receptor Complex in Hepatocytes (2005) · cites this paper as [13]
The Introduction reports that ARH1 defects caused impaired LDL receptor internalization in patients’ EBV-transformed lymphocytes, and the ‘LDL receptor function in ARH1-negative cells’ section reports defective internalization in monocyte-derived macrophages. The copy does not establish the claim for circulating, untransformed lymphocytes; it also notes some LDL uptake in macrophage cultures from one affected patient. No page number is provided for these passages. (LLM, conf=0.88)
Experimental — accuracy not yet measured125I-LDL binding is only 2-fold higher in ARH-/- cells than in normal cells.
“By contrast 125 I-LDL binding was only 2-fold higher in ARH Ϫ/Ϫ cells than in the normal cells (Fig. 5B) in agreement with prior estimates of the relative LDL binding capacity of ARH Ϫ/Ϫ lymphocytes (16,17,29).”
From The Modular Adaptor Protein ARH Is Required for Low Density Lipoprotein (LDL) Binding and Internalization but Not for LDL Receptor Clustering in Coated Pits (2004) · cites this paper as [29]
The Introduction reports normal LDL-receptor expression in affected lymphocytes, and the section on exogenous ARH1 reports defective receptor internalization. Neither passage gives a measurement of ¹²⁵I-LDL binding in affected versus normal cells. Searches for LDL-binding capacity and a twofold difference found no passage establishing the claimed ratio. (LLM, conf=0.72)
Experimental — accuracy not yet measuredIn ARH-/- lymphocytes, the increase in cell surface LDLRs observed in this study (~15-20-fold) is substantially higher than the relative increase in LDL binding (2-fold) observed previously.
“The relative increase in the number of cell surface LDLRs in ARH Ϫ/Ϫ lymphocytes observed in this study (ϳ15-20-fold) is substantially higher than the relative increase in LDL binding (2-fold) observed previously (16,17,29).”
From The Modular Adaptor Protein ARH Is Required for Low Density Lipoprotein (LDL) Binding and Internalization but Not for LDL Receptor Clustering in Coated Pits (2004) · cites this paper as [29]
The citation is attached to the previously observed twofold increase in LDL binding. Our copy’s “LDL receptor function in ARH1-negative cells” and “Expression of exogenous ARH1 in mutant EBV-lymphocytes” sections discuss defective LDL uptake and receptors remaining at the cell surface, but the passages found do not report a twofold increase in LDL binding. Searches for “2-fold,” “twofold,” and LDL binding did not establish that figure. (LLM, conf=0.72)
Experimental — accuracy not yet measuredARH is essential for internalization of the LDL receptor from the cell surface.
“The LDL receptor pathway also malfunctions in individuals with null mutations in the gene for a novel adaptor protein called ARH (from autosomal recessive hypercholesterolemia) that is essential for internalization of the receptor from the cell surface (2,3).”
From Sorting Motifs in the Intracellular Domain of the Low Density Lipoprotein Receptor Interact with a Novel Domain of Sorting Nexin-17 (2004) · cites this paper as [3]
ARH is required for the efficient internalization of the LDL-LDLR complex and to stabilize the association of the receptor with LDL in Epstein-Barr virus-immortalized B lymphocytes.
“It has been demonstrated that ARH is required for the efficient internalization of the LDL-LDLR complex and to stabilize the association of the receptor with LDL in Epstein-Barr virus-immortalized B lymphocytes.”
The majority of studies so far available have been carried out on lymphocytes from ARH patients, in which the LDLR function is significantly impaired.
“Therefore, the majority of studies so far available have been carried out on lymphocytes from ARH patients, in which the LDLR function is significantly impaired (13,14).”
It has been observed that the distribution of the immunodetectable LDLR is significantly altered in lymphocytes from ARH patients and that it mostly resides on the plasma membrane.
“It has been observed that the distribution of the immunodetectable LDLR is significantly altered in these cells and that it mostly resides on the plasma membrane.”
ARH protein may be involved in the internalization of the LDL-LDLR complex.
“This strongly indicates that ARH protein may be involved in the internalization of the LDL-LDLR complex (13).”
Although LDL degradation appears to be markedly reduced in lymphocytes from ARH patients, cell surface LDL binding is increased.
“Moreover, although LDL degradation appears to be markedly reduced in lymphocytes, cell surface LDL binding is increased.”
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Citations
Cites
Disabled‐2 exhibits the properties of a cargo‐selective endocytic clathrin adaptor
Mishra, S. K., Keyel, P. A., Hawryluk, M. J., Agostinelli, N. R., Watkins, S. C., & Traub, L. M. (2002) · The EMBO Journal · doi:10.1093/emboj/cdf487 · Cited by 302
ARH Is a Modular Adaptor Protein That Interacts with the LDL Receptor, Clathrin, and AP-2
He, G., Gupta, S., Yi, M., Michaely, P., Hobbs, H. H., & Cohen, J. C. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m208539200 · Cited by 232
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Cited by
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Keyel, P. A., Mishra, S. K., Roth, R., Heuser, J. E., Watkins, S. C., & Traub, L. M. (2006) · Molecular Biology of the Cell · doi:10.1091/mbc.e06-05-0421 · Cited by 134
Garuti, R., Jones, C., Li, W.-P., Michaely, P., Herz, J., Gerard, R. D., Cohen, J. C., & Hobbs, H. H. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m509394200 · Cited by 91
Burden, J. J., Sun, X.-M., García, A. B. G., & Soutar, A. K. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m313689200 · Cited by 82
Self-citationMichaely, P., Li, W.-P., Anderson, R. G. W., Cohen, J. C., & Hobbs, H. H. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m405242200 · Cited by 66
Sirinian, M. I., Belleudi, F., Campagna, F., Ceridono, M., Garofalo, T., Quagliarini, F., Verna, R., Calandra, S., Bertolini, S., Sorice, M., et al. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m504343200 · Cited by 42
Eden, E. R., Sun, X.-M., Patel, D. D., & Soutar, A. K. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddm232 · Cited by 27
Self-citation
Metadata
- Authors
- Eden, E. R., Patel, D. D., Sun, X.-M., Burden, J. J., Themis, M., Edwards, M., Lee, P., Neuwirth, C., Naoumova, R. P., & Soutar, A. K.
- Venue
- Journal of Clinical Investigation
- Published
- 2002-12-01
- Volume
- 110
- Issue
- 11
- Pages
- 1695-1702
- ISSN
- 0021-9738
- Cited by
- 64
- References
- 2
- Language
- en
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