ArticleMolecular biology of the cell2007
Adipocyte enhancer-binding protein-1 promotes macrophage inflammatory responsiveness by up-regulating NF-kappaB via IkappaBalpha negative regulation.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- FAM-related prognostic molecular subtype screening identified epithelial-derivedFrontiers in cell and developmental biology · 2026Article
- Targeting Adipocyte Enhancer-Binding Protein 1 to Induce Microglial Phenotype Shift for Immunotherapy in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- AEBP1-GLI1 pathway attenuates the FACT complex dependency of bladder cancer cell survival.Biochemistry and biophysics reports · 2025Article
- Identification of foam cell like M2 macrophages, AEBP1 biomarkers, and resveratrol as potential therapeutic in MASLD using Ecotyper and WGCNA.Scientific reports · 2025Article
- Crosstalk between lipid metabolism and macrophages in atherosclerosis: therapeutic potential of natural products.Frontiers in cardiovascular medicine · 2025Review
- AEBP1 is a negative regulator of skeletal muscle cell differentiation in oral squamous cell carcinoma.Scientific reports · 2024Article
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- Adipocyte enhancer binding protein 1 knockdown alleviates osteoarthritis through inhibiting NF-κB signaling pathway-mediated inflammation and extracellular matrix degradation.Journal of cell communication and signaling · 2024Article
- Dysregulated AEBP1 and COLEC12 Genes in Late-Onset Alzheimer's Disease: Insights from Brain Cortex and Peripheral Blood Analysis.Journal of molecular neuroscience : MN · 2024Article
- Inactive metallopeptidase homologs: the secret lives of pseudopeptidases.Frontiers in molecular biosciences · 2024Review
- ACLP Activates Cancer-Associated Fibroblasts and Inhibits CD8+ T-Cell Infiltration in Oral Squamous Cell Carcinoma.Cancers · 2023Article
- Impact of Lipid Metabolism on Macrophage Polarization: Implications for Inflammation and Tumor Immunity.International journal of molecular sciences · 2023Review
- Transcriptomic analysis of glutamate-induced HT22 neurotoxicity as a model for screening anti-Alzheimer's drugs.Scientific reports · 2023Article
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- Whole-genome profiling of nasopharyngeal carcinoma reveals viral-host co-operation in inflammatory NF-κB activation and immune escape.Nature communications · 2021Article
- Weighted Gene Co-expression Network Analysis Identifies a Cancer-Associated Fibroblast Signature for Predicting Prognosis and Therapeutic Responses in Gastric Cancer.Frontiers in molecular biosciences · 2021Article
- Developing the novel bioinformatics algorithms to systematically investigate the connections among survival time, key genes and proteins for Glioblastoma multiforme.BMC bioinformatics · 2020Article
- Glycomics: Immunoglobulin GOmics : a journal of integrative biology · 2020Article
- Prenatal exposure to bisphenol A alters the transcriptome-interactome profiles of genes associated with Alzheimer's disease in the offspring hippocampus.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor kappaB (NF-kappaB) subunits comprise a family of eukaryotic transcription factors that are critically involved in cell proliferation, inflammation, and apoptosis. Under basal conditions, NF-kappaB subunits are kept under inhibitory regulation by physical interaction with NF-kappaB inhibitors (IkappaB subunits) in the cytosol. Upon stimulation, IkappaB subunits become phosphorylated, ubiquitinated, and subsequently degraded, allowing NF-kappaB subunits to translocate to the nucleus and bind as dimers to kappaB responsive elements of target genes. Previously, we have shown that AEBP1 enhances macrophage inflammatory responsiveness by inducing the expression of various proinflammatory mediators. Herein, we provide evidence suggesting that AEBP1 manifests its proinflammatory function by up-regulating NF-kappaB activity via hampering IkappaBalpha, but not IkappaBbeta, inhibitory function through protein-protein interaction mediated by the discoidin-like domain (DLD) of AEBP1. Such interaction renders IkappaBalpha susceptible to enhanced phosphorylation and degradation, subsequently leading to augmented NF-kappaB activity. Collectively, we propose a novel molecular mechanism whereby NF-kappaB activity is modulated by means of protein-protein interaction involving AEBP1 and IkappaBalpha. Moreover, our study provides a plausible mechanism explaining the differential regulatory functions exhibited by IkappaBalpha and IkappaBbeta in various cell types. We speculate that AEBP1 may serve as a potential therapeutic target for the treatment of various chronic inflammatory diseases and cancer.
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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.