Willnow T E, Armstrong S A, Hammer R E, Herz J
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235, USA.
Proc Natl Acad Sci U S A. 1995 May 9;92(10):4537-41. doi: 10.1073/pnas.92.10.4537.
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.
39 kDa受体相关蛋白(RAP)与多功能低密度脂蛋白(LDL)受体相关蛋白(LRP)结合,从而阻止包括α2-巨球蛋白和乳糜微粒残粒在内的所有已知配体的结合。RAP主要定位于内质网,这增加了其在LRP的生物合成或细胞内运输中作为伴侣蛋白或护送蛋白发挥作用的可能性。在此,我们利用基因靶向技术表明RAP在体内促进功能性LRP的表达。在RAP缺陷小鼠的肝脏和大脑中,成熟的、经过加工的LRP数量减少。结果,α2-巨球蛋白的肝脏清除受损,并且在同样缺乏功能性LDL受体的RAP缺陷小鼠的血浆中残留脂蛋白积聚。这些结果与RAP在分泌途径中稳定LRP的假说一致。它们还提示了一种在体内调节内吞受体活性的进一步机制。