ArticleBiochemical and biophysical research communications2008
Genetic determination of the role of PU.1 in macrophage gene expression.
Article in Biochemical and biophysical research communications, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Hyperglycemia-induced P300/CBP acetyltransferase drives ZEB2-mediated proinflammatory macrophages and delays wound healing.JCI insight · 2026Article
- Epigallocatechin gallate regulates the myeloid-specific transcription factor PU.1 in macrophages.PloS one · 2024Article
- The role of a key transcription factor PU.1 in autoimmune diseases.Frontiers in immunology · 2022Review
- Article
- Lipopolysaccharide-dependent interaction between PU.1 and c-Jun determines production of lipocalin-type prostaglandin D synthase and prostaglandin D2 in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
PU.1, an Ets family transcription factor, mediates macrophage effector function in inflammation by regulating gene expression. But, the extent and nature of PU.1 function in gene expression has not been genetically determined because ablation of PU.1 gene abolishes macrophage development. Here, we epigenetically suppressed PU.1 by stably expressing PU.1 specific siRNA in macrophages, and determined the effect of PU.1 deficiency on expressions of key inflammatory genes: Toll-like receptor 4 (TLR4), cyclooxygenase-2 (COX-2), and macrophage inflammatory protein-1alpha (MIP-1alpha). PU.1-silenced cell lines expressed lower TLR4 mRNA and COX-2 protein, but higher MIP-1alpha protein, than controls. Over-expression of PU.1 suppressed lipopolysaccharide-induced MIP-1alpha production. PU.1 occupied proximal and distal cognate sites in the endogenous MIP-1alpha promoter, but dissociated only from the distal sites in response to lipopolysaccharide, suggesting a novel negative regulatory mechanism by PU.1. Together, our results defined PU.1 function in differentially regulating expressions of TLR4, COX-2, and MIP-1alpha.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.