Evidence map›Paper›PMID 20087894›Full record

ReviewBioFactors (Oxford, England)

Functional role of KLF10 in multiple disease processes.

Malayannan Subramaniam, John R Hawse, Nalini M Rajamannan, James N Ingle, Thomas C Spelsberg

Open access · greenAbstract readReview
In one paragraph

Review in BioFactors (Oxford, England). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Probing transcription factor subsets in gene regulatory networks.Algorithms for molecular biology : AMB · 2026
    Article
  3. Article
  4. Article
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  8. Contact Lens Wear Alters Transcriptional Responses tobioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. New Insights into the Role of KLF10 in Tissue Fibrosis.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Bone mesenchymal stem cell-derived extracellular vesicles containing NORAD promote osteosarcoma by miR-30c-5p.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  20. Article

16 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Malayannan SubramaniamDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA. subramaniam.malayannan@mayo.edu
John R Hawse
Nalini M Rajamannan
James N Ingle
Thomas C Spelsberg
Mayo Clinic in Arizona · USIn-Q-Tel · USNorthwestern University · US

Funding

Role of a TGF-? Regulated Gene in Human and Mouse Osteoblasts and SkeletonR01DE014036 · NIDCR · MAYO CLINIC ROCHESTER · PI HAWSE, JOHN R., SUBRAMANIAM, MALAYANNAN · 2001 to 2016
$4.7M
Role of Lrp5/Beta-Catenin in Aortic Valve CalcificationR01HL085591 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI RAJAMANNAN, NALINI M · 2007 to 2011
$2.1M
ROLE OF TGF-B INDUCIBLE EARLY GENE IN OSTEOCLASTOGENESISR01AR052004 · NIAMS · MAYO CLINIC ROCHESTER · PI OURSLER, MERRY JO · 2006 to 2010
$1.6M
NHLBI NIH HHS R01 HL085591NIAMS NIH HHS AR52004NIAMS NIH HHS R01 AR052004NIDCR NIH HHS R01 DE014036NIDCR NIH HHS R01 DE-14036
6 · The paper itself

Abstract

Since the discovery by this laboratory of the zinc finger transcription factor, KLF10, a member of the Krüppel-like family of transcription factors, there have been multiple publications regarding its functions and its immediate family members, in numerous cell types. KLF10 has been shown to be rapidly induced by TGFbeta1, 2, 3, E(2), epidermal growth factor, and bone morphogenetic protein-2. TGFbeta inducible early gene-1 activates the TGFbeta-Smad signaling pathway via repression of Smad 7 expression and activation of Smad 2 expression and activity. Overall, KLF10 has been implicated in cell differentiation, as a target gene for a variety of signaling pathways, and in serving as a potential marker for human diseases such as breast cancer, cardiac hypertrophy, and osteoporosis. Like other KLF members, KLF10 is expressed in specific cell types in numerous tissues and is known to be involved in repressing cell proliferation and inflammation as well as inducing apoptosis similar to that of TGFbeta. KLF10 binds to Sp-1-GC rich DNA sequences and can activate or repress the transcription of a number of genes. Overall, KLF10 has been shown to play a major role in the TGFbeta inhibition of cell proliferation and inflammation and induction of apoptosis, and its overexpression in human osteoblasts and pancreatic carcinoma cells mimics the actions of TGFbeta.

Indexed as

AnimalsApoptosisBone and BonesBone Diseases, MetabolicBone RemodelingBreast NeoplasmsCardiomegalyCell DifferentiationCell ProliferationConnective Tissue DiseasesEarly Growth Response Transcription FactorsFemaleHumansKruppel-Like Transcription FactorsMaleMiceEarly Growth Response Transcription FactorsKLF10 protein, humanKruppel-Like Transcription FactorsSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID20087894
PMCPMC3104724
OpenAlexW2025209024

What OpenQuestion holds

Textmetadata
LicenceTDM
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.