Evidence map›Paper›PMID 22522110›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012

Salt-inducible kinase 1 regulates E-cadherin expression and intercellular junction stability.

Kristina Eneling, Laura Brion, Vanda Pinto, Maria J Pinho, Jacob I Sznajder, Naoki Mochizuki, Kazuo Emoto, Patricio Soares-da-Silva, Alejandro M Bertorello

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  8. Review
  9. Article
  10. Acute salt loading induces sympathetic nervous system overdrive in mice lacking salt-inducible kinase 1 (SIK1).Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Pathological implications of cadherin zonation in mouse liver.Cellular and molecular life sciences : CMLS · 2015
    Article
  18. Article
  19. Inositol pyrophosphates promote tumor growth and metastasis by antagonizing liver kinase B1.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

9 authors at 6 institutions in 4 countries.

Kristina EnelingMembrane Signaling Networks, Atherosclerosis Research Unit, Department of Medicine, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital-Solna, Stockholm, Sweden.
Laura Brion
Vanda Pinto
Maria J Pinho
Jacob I Sznajder
Naoki Mochizuki
Kazuo Emoto
Patricio Soares-da-Silva
Alejandro M Bertorello
Universidade do Porto · PTKarolinska Institutet · SEKarolinska University Hospital · SENational Cerebral and Cardiovascular Center · JPNorthwestern University · USOsaka Science Museum · JP

Funding

Role and Regulation of Sodium, Potasium ATPase in LungR37HL048129 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SZNAJDER, JACOB I · 2008 to 2017
$4.0M
ROLE AND REGULATION OF SODIUM, POTASSIUM ATPASE IN LUNGR01HL048129 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SZNAJDER, JACOB I · 1996 to 2007
$2.7M
NHLBI NIH HHS HL-48129NHLBI NIH HHS R01 HL048129NHLBI NIH HHS R37 HL048129
6 · The paper itself

Abstract

The protein kinase liver kinase B1 (LKB1) regulates cell polarity and intercellular junction stability. Also, LKB1 controls the activity of salt-inducible kinase 1 (SIK1). The role and relevance of SIK1 and its downstream effectors in linking the LKB1 signals within these processes are partially understood. We hypothesize that SIK1 may link LKB1 signals to the maintenance of epithelial junction stability by regulating E-cadherin expression. Results from our studies using a mouse lung alveolar epithelial (MLE-12) cell line or human renal proximal tubule (HK2) cell line transiently or stably lacking the expression of SIK1 (using SIK1 siRNAs or shRNAs), or with its expression abrogated (sik1(+/+) vs. sik1(-/-) mice), indicate that suppression of SIK1 (∼40%) increases the expression of the transcriptional repressors Snail2 (∼12-fold), Zeb1 (∼100%), Zeb2 (∼50%), and TWIST (∼20-fold) by activating cAMP-response element binding protein. The lack of SIK1 and activation of transcriptional repressors decreases the availability of E-cadherin (mRNA and protein expression by ∼100 and 80%, respectively) and the stability of intercellular junctions in epithelia (decreases in transepithelial resistance). Furthermore, LKB1-mediated increases in E-cadherin expression are impaired in cells where SIK1 has been disabled. We conclude that SIK1 is a key regulator of E-cadherin expression, and thereby contributes to the stability of intercellular junctions.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsCadherinsCell LineCyclic AMP Response Element-Binding ProteinHumansIntercellular JunctionsKidney Tubules, ProximalMiceProtein Serine-Threonine KinasesSnail Family Transcription FactorsTranscription FactorsAMP-Activated Protein Kinase KinasesCadherinsCREB1 protein, humanCyclic AMP Response Element-Binding ProteinProtein Serine-Threonine KinasesSIK1 protein, humanSik1 protein, mouseSNAI1 protein, humanSnai1 protein, mouseSnail Family Transcription FactorsSTK11 protein, humanTranscription Factors

Identifiers

PMID22522110
PMCPMC3405263
OpenAlexW2127991850

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.