ArticleEndocrine pathology2015
Latent Pathways Identification by Microarray Expression Profiles in Thyroid-Associated Ophthalmopathy Patients.
Article in Endocrine pathology, 2015. 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, 12 citations in OpenAlex.
- Graph-based deep learning for integrating single-cell and bulk transcriptomic data to identify clinical cancer subtypes.Briefings in bioinformatics · 2025Article
- Article
- Comprehensive analysis of key genes and pathways for biological and clinical implications in thyroid-associated ophthalmopathy.BMC genomics · 2022Article
- Integrative metabolic analysis of orbital adipose/connective tissue in patients with thyroid-associated ophthalmopathy.Frontiers in endocrinology · 2022Article
- Differential expression and alternative splicing of transcripts in orbital adipose/connective tissue of thyroid-associated ophthalmopathy.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Noncanonical Functions and Cellular Dynamics of the Mammalian Signal Recognition Particle Components.Frontiers in molecular biosciences · 2021Review
- Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model.Scientific reports · 2017Article
- Proteomics of Tear in Inactive Thyroid-Associated Ophthalmopathy.Acta endocrinologica (Bucharest, Romania : 2005)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to screen potential genes related to thyroid-associated ophthalmopathy (TAO) and get a further understanding about the pathogenesis of this disease. GSE9340 was downloaded from Gene Expression Omnibus, including eight thyroid tissue samples from hyperthyroid patients without TAO and ten ones from hyperthyroid patients with TAO. The differentially expressed genes (DEGs) were identified by the linear models for microarray data package. And their potential functions were predicted by Gene Ontology (GO) and pathway enrichment analyses. Furthermore, protein-protein interaction (PPI) was obtained from the Search Tool for the Retrieval of Interacting Genes database, and the PPI network was visualized with Cytoscape. Then, module analysis was performed by the Molecular Complex Detection analysis. Additionally, the potential pathway interactions were identified by Latent Pathway Identification Analysis. Totally, 511 upregulated and 507 downregulated DEGs in TAO were screened. Some DEGs (e.g., UBE2C) were related to cell cycle, and DEGs encoding proteasome (e.g., PSMA1, PSMC5, PSMC4, and PSMD1) were related to negative regulation of ubiquitin-protein ligase activity. Several upregulated DEGs encoding signal recognition particle (e.g., SRP14, SRP54, and SRP9) were found to be enriched in protein export pathway. Furthermore, some pathways (e.g., ribosome and protein export) had interactions. The DEGs related to cell cycle (e.g., UBE2C), DEGs encoding proteasome (e.g., PSMA1, PSMC5, PSMC4, and PSMD1) and signal recognition particle (e.g., SRP14, SRP54, and SRP9), as well as pathways of ribosome, protein export and retinol metabolism, might play key roles in the development of TAO.
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.