Evidence map›Paper›PMID 17989364›Full record

ArticleMolecular biology of the cell2008

The SPARC-related factor SMOC-2 promotes growth factor-induced cyclin D1 expression and DNA synthesis via integrin-linked kinase.

Peijun Liu, Jining Lu, Wellington V Cardoso, Cyrus Vaziri

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Fibroblastic SMOC2 Suppresses Mechanical Nociception by Inhibiting Coupled Activation of Primary Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  9. Suppression of SMOC2 alleviates myocardial fibrosisFrontiers in cardiovascular medicine · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The SPARC-related modular calcium binding protein 2 (Clinical ophthalmology (Auckland, N.Z.) · 2017
    Article
  18. Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Peijun LiuThe Department of Genetics and Genomics and The Pulmonary Center, Boston University School of Medicine, Boston, MA 02118, USA.
Jining Lu
Wellington V Cardoso
Cyrus Vaziri
Boston University · USInstitut thématique Génétique, génomique et bioinformatique · FR

Funding

T1alpha in type I cell formation, regulation &functionP01HL047049 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LU, JINING · 1992 to 2012
$27.6M
A Novel Carcinogen-Induced Cell Cycle CheckpointR01ES009558 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI VAZIRI, CYRUS · 2002 to 2016
$4.8M
NOVEL CARCINOGEN INDUCED CELL CYCLE CHECKPOINTR29ES009558 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAZIRI, CYRUS · 1998 to 2001
$221k
NHLBI NIH HHS P01 HL047049NHLBI NIH HHS P01 HL47049NIEHS NIH HHS ES09558NIEHS NIH HHS R01 ES009558NIEHS NIH HHS R29 ES009558
6 · The paper itself

Abstract

Secreted modular calcium-binding protein-2 (SMOC-2) is a recently-identified SPARC-related protein of unknown function. In mRNA profiling experiments we, found that SMOC-2 expression was elevated in quiescent (G0) mouse fibroblasts and repressed after mitogenic stimulation with serum. The G0-specific expression of SMOC-2 was similar to that of platelet-derived growth factor-beta receptor (PDGFbetaR), a major mitogenic receptor. Therefore, we tested a possible role for SMOC-2 in growth factor-induced cell cycle progression. SMOC-2 overexpression augmented DNA synthesis induced by serum and fibroblast mitogens (including PDGF-BB and basic fibroblast growth factor). Conversely, SMOC-2 ablation by using small interfering RNA attenuated DNA synthesis in response to PDGF-BB and other growth factors. Mitogen-induced expression of cyclin D1 was attenuated in SMOC-2-ablated cells, and cyclin D1-overexpressing cells were resistant to inhibition of mitogenesis after SMOC-2 ablation. Therefore, cyclin D1 is limiting for G1 progression in SMOC-2-deficient cells. SMOC-2 ablation did not inhibit PDGF-induced PDGFbetaR autophosphorylation or PDGF-BB-dependent activation of mitogen-activated protein kinase and Akt kinases, suggesting that SMOC-2 is dispensable for growth factor receptor activation. However, integrin-linked kinase (ILK) activity was reduced in SMOC-2-ablated cells. Ectopic expression of hyperactive ILK corrected the defective mitogenic response of SMOC-2-deficient cells. Therefore, SMOC-2 contributes to cell cycle progression by maintaining ILK activity during G1. These results identify a novel role for SMOC-2 in cell cycle control.

Indexed as

AnimalsCalcium-Binding ProteinsCell LineCyclin D1DNAEmbryo, MammalianEnzyme ActivationGene Expression Regulation, DevelopmentalHumansIntercellular Signaling Peptides and ProteinsMiceModels, BiologicalPlatelet-Derived Growth FactorProtein Serine-Threonine KinasesRatsReceptor, Platelet-Derived Growth Factor betaCalcium-Binding ProteinsCyclin D1DNAIntercellular Signaling Peptides and ProteinsPlatelet-Derived Growth FactorProtein Serine-Threonine KinasesReceptor, Platelet-Derived Growth Factor betaRNA, MessengerScaffold Protein ILKSMOC-2 protein, mouse

Identifiers

PMID17989364
PMCPMC2174189
OpenAlexW2016671423

What OpenQuestion holds

Textmetadata
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.