ArticleProtein and peptide letters2025
Exploring the Regulatory Interaction of Differentially Expressed Proteins in Cleft Palate Induced by Retinoic Acid.
Article in Protein and peptide letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Senescent epithelial cells remodel the tumor microenvironment and drive early LUAD progression: a multiomics risk model and single-cell analysis.Cellular and molecular life sciences : CMLS · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
objectiveThis study aimed to identify novel proteins involved in retinoic acid (RA)-induced embryonic cleft palate development.
methodsThe palate tissues of the control and RA-treated E14.5 were dissected and subjected to iTRAQ-based proteomic analysis.
resultsDifferential expression analysis identified 196 significantly upregulated and 149 downregulated considerably proteins in RA-induced palate tissues. Comprehensive Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed the significant involvement of cytoplasmic translation, ribosome biogenesis, glycolysis/gluconeogenesis, and glutathione metabolism pathways in cleft palate pathogenesis triggered by RA. In particular, ribosome-related pathways were highly enriched, while glycolysis was disrupted. Protein-protein interaction analysis, facilitated by the STRING database, revealed a tightly interconnected network of differentially expressed proteins. Further analysis using the cytoHubba plugin in Cytoscape identified ten hub proteins, including Eif4a1, Gapdh, Eno1, Imp3, Rps20, Rps27a, Eef2, Hsp90ab1, Rpl19, and Rps16, indicating their potential roles in RA-induced cleft palate development, and thus positioning them as potential biomarkers for cleft palate.
conclusionThese findings provide valuable insights into the proteomic changes associated with RA-induced cleft palate and shed light on key pathways and proteins that can contribute significantly to the pathogenesis of this congenital condition.
Indexed as
Identifiers
39473103What 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.