Evidence map›Paper›PMID 29745857›Full record

ArticleBMC systems biology2018

Identification of novel drug targets for diamond-blackfan anemia based on RPS19 gene mutation using protein-protein interaction network.

Abbas Khan, Arif Ali, Muhammad Junaid, Chang Liu, Aman Chandra Kaushik, William C S Cho, Dong-Qing Wei

Open access · diamondAbstract read
In one paragraph

Article in BMC systems biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. How I manage children with Diamond-Blackfan anaemia.British journal of haematology · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Abbas KhanDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Arif AliDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Muhammad JunaidDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Chang LiuDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Aman Chandra KaushikDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
William C S ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong.
Dong-Qing WeiDepartment of Bioinformatics and Biostatistics, College of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China. dqwei@sjtu.edu.cn.
Shanghai Jiao Tong University · CNQueen Elizabeth Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiamond-Blackfan anemia (DBA) is a congenital erythroid aplasia that usually presents in infancy. In order to explore the molecular mechanisms of wild and mutated samples from DBA patients were exposed to bioinformatics investigation. Biological network of differentially expressed genes was constructed. This study aimed to identify novel therapeutic signatures in DBA and uncovered their mechanisms. The gene expression dataset of GSE14335 was used, which consists of 6 normal and 4 diseased cases. The gene ontology (GO), as well as Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, and then protein-protein interaction (PPI) network of the identified differentially expressed genes (DEGs) was constructed by Cytoscape software.

resultsA total of 607 DEGs were identified in DBA, including 433 upregulated genes and 174 downregulated genes. GO analysis results showed that upregulated DEGs were significantly enriched in biological processes, negative regulation of transcription from RNA polymerase II promoter, chemotaxis, inflammatory response, immune response, positive regulation of cell proliferation, negative regulation of cell proliferation, response to mechanical stimulus, positive regulation of cell migration, response to lipopolysaccharide, and defence response. KEGG pathway analysis revealed the TNF signalling pathway, Osteoclast differentiation, Chemokine signalling pathway, Cytokine -cytokine receptor interaction, Rheumatoid arthritis, Biosynthesis of amino acids, Biosynthesis of antibiotics and Glycine, serine and threonine metabolism. The top 10 hub genes, AKT1, IL6, NFKB1, STAT3, STAT1, RAC1, EGR1, IL8, RELA, RAC3, mTOR and CCR2 were identified from the PPI network and sub-networks.

conclusionThe present study flagged that the identified DEGs and hub genes enrich our understanding of the molecular mechanisms underlying the development of DBA, and might shine some lights on identifying molecular targets and diagnostic biomarkers for DBA.

Indexed as

Computational BiologyMolecular Targeted TherapyMutationProtein Interaction MapsAnemia, Diamond-BlackfanDown-RegulationGene OntologyHumansRibosomal ProteinsUp-RegulationRibosomal Proteinsribosomal protein S19Diamond-Blackfan anemia (DBA)Differentially expressed geneGene expression omnibusKEGG pathwaysMicroarray

Identifiers

PMID29745857
PMCPMC5998885
OpenAlexW2802028619

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.