ArticleCells2021
CEBPD Potentiates the Macrophage Inflammatory Response but CEBPD Knock-Out Macrophages Fail to Identify CEBPD-Dependent Pro-Inflammatory Transcriptional Programs.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Pooled it
- Enteric-colonizedGut microbes · 2026Article
- Exploratory single-nucleus multiomics analysis of myeloid cell states associated with neoadjuvant chemotherapy response in pancreatic ductal adenocarcinoma.Clinical and translational medicine · 2026Article
- Hepatic responses as potential biomarkers of idiosyncratic drug reaction risk.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- CEBPD-MMP8 Axis Contributes to Cardiomyocyte Injury in Septic Shock.Applied biochemistry and biotechnology · 2026Article
- Article
- MARCO+ Tumor-Associated Macrophages Impede CD8+ T Cell Immunity to Facilitate Immunotherapy Resistance in Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CEBPD regulates CD47 and MAP4K4 via chromatin accessibility in canine mammary tumor monocytes.Scientific reports · 2025Article
- miRNA let-7-5p present in the extracellular vesicles of Trichinella spiralis newborn larvae inhibits the function of M1-type RAW264.7 macrophages by targeting C/EBPδ.Parasites & vectors · 2025Article
- Protein interactions, network pharmacology, and machine learning work together to predict genes linked to mitochondrial dysfunction in hypertrophic cardiomyopathy.Scientific reports · 2025Article
- Testosterone/androgen receptor antagonizes immobility-induced muscle atrophy through Inhibition of myostatin transcription and inflammation in mice.Scientific reports · 2025Article
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- The feasibility of targeting macrophage for disease treatment: roles of CEBPD.Frontiers in immunology · 2025Review
- Is the endotoxin-complement cascade the major driver in lipedema?Trends in endocrinology and metabolism: TEM · 2024Review
- A Cell Cycle-Aware Network for Data Integration and Label Transferring of Single-Cell RNA-Seq and ATAC-Seq.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Identification of key biomarkers for predicting CAD progression in inflammatory bowel disease via machine-learning and bioinformatics strategies.Journal of cellular and molecular medicine · 2024Article
- Article
- The Multifunction of TRIM26: From Immune Regulation to Oncology.Protein and peptide letters · 2024Review
- Tripartite motif containing 26 prevents steatohepatitis progression by suppressing C/EBPδ signalling activation.Nature communications · 2023Article
- CAGE sequencing reveals CFTR-dependent dysregulation of type I IFN signaling in activated cystic fibrosis macrophages.Science advances · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
CCAAT/enhancer-binding protein delta (C/EBPδ) is a member of the C/EBP family of transcription factors. According to the current paradigm, C/EBPδ potentiates cytokine production and modulates macrophage function thereby enhancing the inflammatory response. Remarkably, however, C/EBPδ deficiency does not consistently lead to a reduction in Lipopolysaccharide (LPS)-induced cytokine production by macrophages. Here, we address this apparent discrepancy and show that the effect of C/EBPδ on cytokine production and macrophage function depends on both the macrophage subtype and the LPS concentration used. Using CRISPR-Cas generated macrophages in which the transactivation domain of C/EBPδ was deleted from the endogenous locus (ΔTAD macrophages), we next show that the context-dependent role of C/EBPδ in macrophage biology relies on compensatory transcriptional activity in the absence of C/EBPδ. We extend these findings by revealing a large discrepancy between transcriptional programs in C/EBPδ knock-out and C/EBPδ transactivation dead (ΔTAD) macrophages implying that compensatory mechanisms do not specifically modify C/EBPδ-dependent inflammatory responses but affect overall macrophage biology. Overall, these data imply that knock-out approaches are not suited for identifying the genuine transcriptional program regulated by C/EBPδ, and we suggest that this phenomenon applies for transcription factor families in general.
Indexed as
Identifiers
What OpenQuestion holds
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.