ArticleCurrent genomics2024
Effect of Calebin-A on Critical Genes Related to NAFLD: A Protein-Protein Interaction Network and Molecular Docking Study.
Article in Current genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- The METTL3/TRIM37 axis contributes to the progression of non-alcoholic fatty liver disease by promoting CAV1 degradation.Molecular and cellular biochemistry · 2026Article
- MCD biomarkers Egfr, Hmox1, Lgmn identified in NAFLD.BMC endocrine disorders · 2026Article
- Exploring the Potential of Calebin-A in Targeting Obesity-Related Genes and Pathways.Journal of cellular and molecular medicine · 2026Article
- Bioinformatics and experimental validation of druggable targets in non-alcoholic fatty liver disease.Scientific reports · 2026Article
- METTL16 promotes MASLD progression through the regulation of lipid synthesis and immune response.Biology direct · 2026Article
- Multi-Target Anti-Steatotic Effects of Andrographolide in MAFLD: Insights from Network Pharmacology and in vitro Study.Journal of experimental pharmacology · 2026Article
- Computational prioritization of candidate TCDD-associated targets in retinoblastoma using network toxicology and transcriptomic analysis.Frontiers in genetics · 2026Article
- LIG1 overexpression enhances DNA repair and immune escape leading to poor prognosis in osteosarcoma.European journal of medical research · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Calebin-A is a minor phytoconstituent of turmeric known for its activity against inflammation, oxidative stress, cancerous, and metabolic disorders like Non-alcoholic fatty liver disease(NAFLD). Based on bioinformatic tools. Subsequently, the details of the interaction of critical proteins with Calebin-A were investigated using the molecular docking technique. Methods: We first probed the intersection of genes/ proteins between NAFLD and Calebin-A through online databases. Besides, we performed an enrichment analysis using the ClueGO plugin to investigate signaling pathways and gene ontology. Next, we evaluate the possible interaction of Calebin-A with significant hub proteins involved in NAFLD through a molecular docking study. Results: We identified 87 intersection genes Calebin-A targets associated with NAFLD. PPI network analysis introduced 10 hub genes (TP53, TNF, STAT3, HSP90AA1, PTGS2, HDAC6, ABCB1, CCT2, NR1I2, and GUSB). In KEGG enrichment, most were associated with Sphingolipid, vascular endothelial growth factor A (VEGFA), C-type lectin receptor, and mitogen-activated protein kinase (MAPK) signaling pathways. The biological processes described in 87 intersection genes are mostly concerned with regulating the apoptotic process, cytokine production, and intracellular signal transduction. Molecular docking results also directed that Calebin-A had a high affinity to bind hub proteins linked to NAFLD. Conclusion: Here, we showed that Calebin-A, through its effect on several critical genes/ proteins and pathways, might repress the progression of NAFLD.
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