Biosynthesis and processing of normal and mutant receptors for low density lipoprotein

W. J. Schneider; H. Tolleshaug; M. S. Brown; J. L. Goldstein

Biosynthesis and processing of normal and mutant receptors for low density lipoprotein

W. J. Schneider, H. Tolleshaug, M. S. Brown, J. L. Goldstein

Research output: Contribution to journal › Article › peer-review

Abstract

In familial hypercholesterolemia, mutations in the structural gene for the LDL receptor disrupt normal synthesis, transport, and processing of this cell surface glycoprotein. As a consequence, mutant LDL receptors do not carry out effectively their physiological function, i.e., to remove LDL-cholesterol from the plasma. The resulting overaccumulation of cholesterol in the plasma leads to premature atherosclerosis.

Original language	English (US)
Pages (from-to)	10-12
Number of pages	3
Journal	Arztliche Laboratorium
Volume	34
Issue number	1
State	Published - Jan 1 1988

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

Cite this

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title = "Biosynthesis and processing of normal and mutant receptors for low density lipoprotein",

abstract = "In familial hypercholesterolemia, mutations in the structural gene for the LDL receptor disrupt normal synthesis, transport, and processing of this cell surface glycoprotein. As a consequence, mutant LDL receptors do not carry out effectively their physiological function, i.e., to remove LDL-cholesterol from the plasma. The resulting overaccumulation of cholesterol in the plasma leads to premature atherosclerosis.",

author = "Schneider, {W. J.} and H. Tolleshaug and Brown, {M. S.} and Goldstein, {J. L.}",

year = "1988",

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AU - Schneider, W. J.

AU - Tolleshaug, H.

AU - Brown, M. S.

AU - Goldstein, J. L.

PY - 1988/1/1

Y1 - 1988/1/1

N2 - In familial hypercholesterolemia, mutations in the structural gene for the LDL receptor disrupt normal synthesis, transport, and processing of this cell surface glycoprotein. As a consequence, mutant LDL receptors do not carry out effectively their physiological function, i.e., to remove LDL-cholesterol from the plasma. The resulting overaccumulation of cholesterol in the plasma leads to premature atherosclerosis.

AB - In familial hypercholesterolemia, mutations in the structural gene for the LDL receptor disrupt normal synthesis, transport, and processing of this cell surface glycoprotein. As a consequence, mutant LDL receptors do not carry out effectively their physiological function, i.e., to remove LDL-cholesterol from the plasma. The resulting overaccumulation of cholesterol in the plasma leads to premature atherosclerosis.

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SN - 1433-6510

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Biosynthesis and processing of normal and mutant receptors for low density lipoprotein

Abstract

ASJC Scopus subject areas

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