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Joseph Leonard Goldstein ForMemRS (born April 18, 1940) is an American biochemist.He received the Nobel Prize in Physiology or Medicine in 1985, along with fellow University of Texas Southwestern researcher, Michael Brown, for their studies regarding cholesterol. [2]
Moving to the University of Texas Michael liked vann Warner Health Science Center in Dallas, now the UT Southwestern Medical Center, Brown and colleague Joseph L. Goldstein researched cholesterol metabolism and discovered that human cells have low-density lipoprotein (LDL) receptors that extract cholesterol from the bloodstream.
Michael S. Brown and Joseph L. Goldstein were awarded the 1985 Nobel Prize in Physiology or Medicine for their identification of LDL-R [11] and its relation to cholesterol metabolism and familial hypercholesterolemia. [12]
Brown and Goldstein discovered the LDL receptor and showed cholesterol is loaded into cells through receptor mediated endocytosis. [24] Until recently cholesterol was thought of primarily as a structural component of the membrane. However, more recently, cholesterol uptake was shown to signal an immune response in macrophages.
The LDL receptor scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase in endogenous production of cholesterol. [46] A large part of this signaling pathway was clarified by Dr. Michael S. Brown and Dr. Joseph L. Goldstein in the 1970s.
Its properties were first recorded in 1970 by Drs. Brown and Goldstein, with the defining property being the ability to bind and remove modified low density lipoproteins (LDL). [1] Today scavenger receptors are known to be involved in a wide range of processes, such as: homeostasis, apoptosis, inflammatory diseases and pathogen clearance.
In FH, LDL receptor function is reduced or absent, [9] and LDL circulates for an average duration of 4.5 days, resulting in significantly increased level of LDL cholesterol in the blood with normal levels of other lipoproteins. [6] In mutations of ApoB, reduced binding of LDL particles to the receptor causes the increased level of LDL cholesterol.
In humans, excess cholesterol in the blood is captured by low-density lipoprotein (LDL) and removed by the liver via endocytosis of the LDL receptor. [4] Recent evidence indicates that the members of the LDL receptor gene family are active in the cell signalling pathways between specialized cells in many, if not all, multicellular organisms. [5 ...