Evidence map›Paper›PMID 24710090›Full record

ArticleGenes2010

Role of Cell Division Autoantigen 1 (CDA1) in Cell Proliferation and Fibrosis.

Ban-Hock Toh, Yugang Tu, Zemin Cao, Mark E Cooper, Zhonglin Chai

Open access · goldAbstract read
In one paragraph

Article in Genes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Pathogenesis of diabetic nephropathy.Journal of diabetes investigation · 2011
    Review
  10. 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

5 authors at 2 institutions in 1 country.

Ban-Hock TohAutoimmunity Laboratory, Centre for Inflammatory Diseases, Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria 3168, Australia. ban-hock.toh@monash.edu.
Yugang TuDiabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. yugang.tu@bakeridi.edu.au.
Zemin CaoDiabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. zemin.cao@bakeridi.edu.au.
Mark E CooperDiabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. mark.cooper@bakeridi.edu.au.
Zhonglin ChaiDiabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, Victoria 3004, Australia. zhonglin.chai@bakeridi.edu.au.
Baker Heart and Diabetes Institute · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell Division Autoantigen 1 (CDA1) was discovered following screening a human expression library with serum from a patient with Discoid Lupus Erythematosus. CDA1, encoded by TSPYL2 on the X chromosome, shares anti-proliferative and pro‑fibrotic properties with TGF-b. It inhibits cell growth through p53, pERK1/2 and p21‑mediated pathways and is implicated in tumorigenesis and the DNA damage response. Its pro-fibrotic property is mediated through cross-talk with TGF-b that results in upregulation of extracellular matrix proteins. The latter properties have identified a key role for CDA1 in diabetes associated atherosclerosis. These dual properties place CDA1 as an attractive molecular target for treating tumors and vascular fibrosis including atherosclerosis and other vascular disorders associated with enhanced TGF-β action and tissue scarring.

Identifiers

PMID24710090
PMCPMC3966230
OpenAlexW1977626768

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.