pubmed-article:2919164 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0034821 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0063164 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0815047 | lld:lifeskim |
pubmed-article:2919164 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:2919164 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:2919164 | pubmed:dateCreated | 1989-3-27 | lld:pubmed |
pubmed-article:2919164 | pubmed:abstractText | Transcription of the low density lipoprotein receptor (LDL-R) and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase genes was rapidly and transiently induced (8.5- and 2.3-fold, respectively) early during phorbol 12-myristate 13-acetate (PMA)-induced macrophage differentiation of the human monocytic leukemia cell line THP-1. The levels of mRNA coding for LDL-R and HMG-CoA reductase increased soon after induction, reached a maximum (12- and 7-fold increase, respectively) in 2-3 hr, and then rapidly returned to the low constitutive levels observed before induction. The stability of LDL-R mRNA did not change significantly during differentiation, whereas that of HMG-CoA reductase mRNA decreased by about 5-fold 6 hr after the addition of PMA. Transcriptional induction of both LDL-R and HMG-CoA reductase genes (5.6- and 2-fold, respectively) was also observed when undifferentiated cells were treated with cycloheximide (CHX), resulting in a transient increase in steady-state mRNA (7- and 3-fold, respectively). These results suggest that expression of the two genes is maintained at low constitutive levels in uninduced THP-1 cells by a protein with a short half-life. Superinduction of both genes occurred when PMA and CHX were added simultaneously. The induction of LDL-R and HMG-CoA reductase mRNAs during early macrophage differentiation is mediated by protein kinase C. It is hypothesized that protein kinase C acts directly or indirectly to inactivate the labile negative regulatory protein. Induction of LDL-R mRNA was also observed when the human hepatocarcinoma cell line Hep G2 was treated with PMA and CHX, suggesting that this mechanism of regulation may exist in several cell types. | lld:pubmed |
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pubmed-article:2919164 | pubmed:language | eng | lld:pubmed |
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pubmed-article:2919164 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:2919164 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2919164 | pubmed:month | Feb | lld:pubmed |
pubmed-article:2919164 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:2919164 | pubmed:author | pubmed-author:ChaixMM | lld:pubmed |
pubmed-article:2919164 | pubmed:author | pubmed-author:DeanS CSC | lld:pubmed |
pubmed-article:2919164 | pubmed:author | pubmed-author:AuwerxJ HJH | lld:pubmed |
pubmed-article:2919164 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2919164 | pubmed:volume | 86 | lld:pubmed |
pubmed-article:2919164 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2919164 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2919164 | pubmed:pagination | 1133-7 | lld:pubmed |
pubmed-article:2919164 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:2919164 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2919164 | pubmed:articleTitle | Regulation of the low density lipoprotein receptor and hydroxymethylglutaryl coenzyme A reductase genes by protein kinase C and a putative negative regulatory protein. | lld:pubmed |
pubmed-article:2919164 | pubmed:affiliation | Department of Medicine, University of Washington, Seattle 98195. | lld:pubmed |
pubmed-article:2919164 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2919164 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2919164 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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