Evidence map›Paper›PMID 21928348›Full record

ArticleJournal of cellular biochemistry2012

Nemo-like kinase inhibits osteoblastogenesis by suppressing bone morphogenetic protein and WNT canonical signaling.

Stefano Zanotti, Ernesto Canalis

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. [Gene silencing of Nemo-like kinase promotes neuralized tissue engineered bone regeneration].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. TCF-1 participates in the occurrence of dedifferentiated chondrosarcoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. Article
  9. Article
  10. Prognostic significance of nemo-like kinase (NLK) expression in patients with gallbladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  11. 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

2 authors at 2 institutions in 1 country.

Stefano ZanottiDepartment of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105-1299, USA.
Ernesto Canalis
Saint Francis Hospital & Medical Center · USSaint Francis University · US

Funding

Growth Factors; Effect on Aspects of Bone FormationR01AR021707 · NIAMS · ST. FRANCIS HOSPITAL AND MEDICAL CENTER · PI CANALIS, ERNESTO · 1986 to 2012
$2.5M
GROWTH FACTORS EFFECT ON ASPECTS OF BONE FORMATIONR37AR021707 · NIAMS · ST. FRANCIS HOSPITAL AND MEDICAL CENTER · PI CANALIS, ERNESTO · 1992 to 2001
$624k
NIAMS NIH HHS AR021707NIAMS NIH HHS R01 AR021707NIAMS NIH HHS R37 AR021707
6 · The paper itself

Abstract

The bone morphogenetic protein/Signaling mothers against decapentaplegic (BMP/Smad) and the WNT signaling pathways regulate the commitment of mesenchymal cells to the osteoblastic lineage. Nemo-like kinase (Nlk) is an evolutionary conserved kinase that suppresses Smad transactivation and WNT canonical signaling. However, it is not clear whether these effects of Nlk have any consequence on the differentiation of mammalian cells. To study the function of Nlk during the commitment of ST-2 bone marrow stromal cells to the osteoblastic fate, Nlk was downregulated by RNA interference (RNAi), following transfection of a specific small interfering (si)RNA. Nlk downregulation increased alkaline phosphatase and osteocalcin expression and sensitized ST-2 cells to the effects of BMP2 and WNT3 on alkaline phosphatase mRNA expression and activity. Accordingly, Nlk downregulation enhanced the effect of BMP2 on the transactivation of the BMP/Smad reporter construct 12xSBE-Oc-pGL3, and on the levels of phosphorylated Smad1/5/8, whereas it did not affect the transactivation of the transforming growth factor-β/Smad reporter pSBE-Luc. Nlk downregulation sensitized ST-2 cells to the effects of WNT3 on the transactivation of the WNT/T-cell factor (Tcf) reporter construct 16xTCF-Luc, whereas it did not affect cytosolic β-catenin levels. To understand the function of Nlk in cells committed to the osteoblastic lineage, Nlk was suppressed by RNAi in primary calvarial osteoblasts. Downregulation of Nlk increased alkaline phosphatase and osteocalcin transcripts and sensitized osteoblasts to the effects of BMP2 on alkaline phosphatase activity and Smad1/5/8 transactivation and phosphorylation. In conclusion, Nlk suppresses osteoblastogenesis by opposing BMP/Smad and WNT canonical signaling.

Indexed as

Cell DifferentiationAnimalsBone Morphogenetic Protein 2Cells, CulturedGene Expression RegulationGene Knockdown TechniquesMiceMitogen-Activated Protein KinasesOsteoblastsProtein Serine-Threonine KinasesSmad ProteinsTransforming Growth Factor betaWnt3A ProteinWnt Signaling PathwayBmp2 protein, mouseBone Morphogenetic Protein 2Mitogen-Activated Protein KinasesNlk protein, mouseProtein Serine-Threonine KinasesSmad ProteinsTransforming Growth Factor betaWnt3A ProteinWnt3a protein, mouse

Identifiers

PMID21928348
PMCPMC3253257
OpenAlexW2115617775

What OpenQuestion holds

Textmetadata
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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.