ArticleFEBS open bio2020
Notch signaling increases PPARγ protein stability and enhances lipid uptake through AKT in IL-4-stimulated THP-1 and primary human macrophages.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 35 citations in OpenAlex.
- Research progress on targeted regulatory proteins in the prevention and treatment of atherosclerosis.Frontiers in immunology · 2026Review
- Identification of Notch pathway-related biomarkers in patients with idiopathic pulmonary fibrosis.PloS one · 2026Article
- BMPR2 Loss Activates AKT by Disrupting DLL4/NOTCH1 and PPARγ Signaling in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024Article
- Article
- Article
- Transcriptomic and functional analysis of ANGPTL4 overexpression in pancreatic cancer nominates targets that reverse chemoresistance.BMC cancer · 2023Article
- Integrated Whole-Exome and Transcriptome Sequencing Indicated Dysregulation of Cholesterol Metabolism in Eyelid Sebaceous Gland Carcinoma.Translational vision science & technology · 2023Article
- Transcriptomic and functional analysis of ANGPTL4 overexpression in pancreatic cancer nominates targets that reverse chemoresistance.Research square · 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Notch signaling and nuclear receptor PPARγ are involved in macrophage polarization, but cross talk between them has not been reported in macrophages. In this study, the effect of Notch signaling on PPARγ in IL-4-stimulated human macrophages (M(IL-4)) was investigated using THP-1-derived macrophages and human monocyte-derived macrophages as models. Human M(IL-4) increased the expression of JAGGED1 and activated Notch signaling. Overexpression of Notch1 intracellular domain (NIC1) increased PPARγ expression, while inhibiting Notch signaling decreased PPARγ levels in M(IL-4). NIC1 overexpression in THP-1-derived macrophages increased PPARγ protein stability by delaying its proteasome-mediated degradation, but did not affect its mRNA. Phosphorylation of AKT was enhanced in NIC1-overexpressing cells, and a specific AKT inhibitor reduced the level of PPARγ. NIC1-overexpressing THP-1 cells exhibited increased CD36 levels via activation of PPARγ, resulting in enhanced intracellular lipid accumulation. In summary, this study provides evidence linking Notch signaling and PPARγ via AKT in M(IL-4).
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.