Regulation of LDL receptor mRNA levels in human lymphocytes by functional demand and ambient sterols.

J. A. Cuthbert, P. E. Lipsky

Research output: Contribution to journalArticle

Abstract

Mitogenic stimulation increases lymphocyte LDL receptor gene expression. Increases are dependent on protein synthesis, not explained by altered mRNA stability and subject to negative feedback regulation. Furthermore, transcription occurs for at least 24 hr and requires ongoing protein synthesis. Depletion of putative endogenous pools of cholesterol that regulate cellular sterol metabolism cannot account for the increase in LDL receptor gene expression caused by mitogenic stimulation. Mitogen-stimulated cells always contain substantially higher levels of LDL receptor messenger RNA than corresponding resting cells. Mitogenic stimulation thus provides a signal that increases LDL receptor gene expression over and above that predicted from the concentration of exogenous sterols. These studies, therefore, indicate that LDL receptor transcription is modulated by signals transduced during cellular activation as well as by negative feedback from regulatory sterols.

Original languageEnglish (US)
Pages (from-to)68-77
Number of pages10
JournalTransactions of the Association of American Physicians
Volume102
StatePublished - 1989

Fingerprint

LDL Receptors
Sterols
Lymphocytes
Messenger RNA
Gene Expression
RNA Stability
Lymphocyte Activation
Mitogens
Proteins
Cholesterol

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{3b6c09347fb04ec1a8ff3b2b456c3c37,
title = "Regulation of LDL receptor mRNA levels in human lymphocytes by functional demand and ambient sterols.",
abstract = "Mitogenic stimulation increases lymphocyte LDL receptor gene expression. Increases are dependent on protein synthesis, not explained by altered mRNA stability and subject to negative feedback regulation. Furthermore, transcription occurs for at least 24 hr and requires ongoing protein synthesis. Depletion of putative endogenous pools of cholesterol that regulate cellular sterol metabolism cannot account for the increase in LDL receptor gene expression caused by mitogenic stimulation. Mitogen-stimulated cells always contain substantially higher levels of LDL receptor messenger RNA than corresponding resting cells. Mitogenic stimulation thus provides a signal that increases LDL receptor gene expression over and above that predicted from the concentration of exogenous sterols. These studies, therefore, indicate that LDL receptor transcription is modulated by signals transduced during cellular activation as well as by negative feedback from regulatory sterols.",
author = "Cuthbert, {J. A.} and Lipsky, {P. E.}",
year = "1989",
language = "English (US)",
volume = "102",
pages = "68--77",
journal = "Transactions of the Association of American Physicians",
issn = "0066-9458",

}

TY - JOUR

T1 - Regulation of LDL receptor mRNA levels in human lymphocytes by functional demand and ambient sterols.

AU - Cuthbert, J. A.

AU - Lipsky, P. E.

PY - 1989

Y1 - 1989

N2 - Mitogenic stimulation increases lymphocyte LDL receptor gene expression. Increases are dependent on protein synthesis, not explained by altered mRNA stability and subject to negative feedback regulation. Furthermore, transcription occurs for at least 24 hr and requires ongoing protein synthesis. Depletion of putative endogenous pools of cholesterol that regulate cellular sterol metabolism cannot account for the increase in LDL receptor gene expression caused by mitogenic stimulation. Mitogen-stimulated cells always contain substantially higher levels of LDL receptor messenger RNA than corresponding resting cells. Mitogenic stimulation thus provides a signal that increases LDL receptor gene expression over and above that predicted from the concentration of exogenous sterols. These studies, therefore, indicate that LDL receptor transcription is modulated by signals transduced during cellular activation as well as by negative feedback from regulatory sterols.

AB - Mitogenic stimulation increases lymphocyte LDL receptor gene expression. Increases are dependent on protein synthesis, not explained by altered mRNA stability and subject to negative feedback regulation. Furthermore, transcription occurs for at least 24 hr and requires ongoing protein synthesis. Depletion of putative endogenous pools of cholesterol that regulate cellular sterol metabolism cannot account for the increase in LDL receptor gene expression caused by mitogenic stimulation. Mitogen-stimulated cells always contain substantially higher levels of LDL receptor messenger RNA than corresponding resting cells. Mitogenic stimulation thus provides a signal that increases LDL receptor gene expression over and above that predicted from the concentration of exogenous sterols. These studies, therefore, indicate that LDL receptor transcription is modulated by signals transduced during cellular activation as well as by negative feedback from regulatory sterols.

UR - http://www.scopus.com/inward/record.url?scp=0024841451&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024841451&partnerID=8YFLogxK

M3 - Article

C2 - 2638531

AN - SCOPUS:0024841451

VL - 102

SP - 68

EP - 77

JO - Transactions of the Association of American Physicians

JF - Transactions of the Association of American Physicians

SN - 0066-9458

ER -