Evidence map›Paper›PMID 21308735›Full record

ArticleJournal of cellular biochemistry2011

Creatine kinase brain overexpression protects colorectal cells from various metabolic and non-metabolic stresses.

Steven M Mooney, Krithika Rajagopalan, Brenten H Williams, Yu Zeng, Christhunesa S Christudass, Youqiang Li, Bo Yin, Prakash Kulkarni, Robert H Getzenberg

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Energy Metabolism Profiling of Human Colorectal Tumours.Journal of cellular and molecular medicine · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Creatine maintains intestinal homeostasis and protects against colitis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Creatine kinase in ischemic and inflammatory disorders.Clinical and translational medicine · 2016
    Review
  18. Review
  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

9 authors at 2 institutions in 1 country.

Steven M MooneyDepartment of Urology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Krithika Rajagopalan
Brenten H Williams
Yu Zeng
Christhunesa S Christudass
Youqiang Li
Bo Yin
Prakash Kulkarni
Robert H Getzenberg
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
Refinement and Discovery of Nuclear Matrix Protein Markers for Colorectal CancerU01CA152753 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KINZLER, KENNETH W., SCHOEN, ROBERT E. · 2010 to 2021
$6.8M
Pilot and Feasibility ProgramP50DK082998 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ISAACS, WILLIAM B · 2009 to 2011
$3.3M
Urology Research Training GrantT32DK007552 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI COFFEY, DONALD STRALEY · 1987 to 2012
$2.9M
NCI NIH HHS P50 CA058236NCI NIH HHS U01 CA152753NIDDK NIH HHS P50 DK082998NIDDK NIH HHS T32 DK007552
6 · The paper itself

Abstract

Creatine kinase brain (CKB) is one of three cytosolic isoforms of creatine kinase that is predominantly expressed in the brain. The enzyme is overexpressed in a wide variety of cancers, with the exception of colon cancer, where it is downregulated. The significance of this downregulation remains poorly understood. Here, we demonstrate that overexpression of CKB-C283S, a dominant-negative construct that lacks the kinase function but retains its ability to dimerize, causes remarkable changes in cell shape, adhesion, and invasion. Furthermore, it results in increased expression of stromal cell markers such as PAGE4 and SNAIL, suggesting an epithelial-to-mesenchymal transition (EMT) in these cells. In cells transfected with a CKB-expressing construct, CKB localizes not only to the cytosol but also to the nucleus, indicating a structural or kinase role unrelated to ATP storage. Furthermore, overexpression of CFP-tagged wild-type (WT) CKB in Caco-2 colon cancer cells dramatically increased the number of cells in G2/M but had little effect on cell proliferation. Taken together, these data demonstrate that the downregulation of CKB may play an important role in colon cancer progression by promoting EMT.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAntigens, Neoplasmbeta CateninCaco-2 CellsCell CycleCell MovementCell NucleusCell SurvivalColorectal NeoplasmsCreatine Kinase, BB FormCytoplasmEpithelial-Mesenchymal TransitionHCT116 CellsHumansImmunoblottingAntigens, Neoplasmbeta CateninCreatine Kinase, BB FormLuminescent ProteinsPAGE4 protein, humanSnail Family Transcription FactorsTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID21308735
PMCPMC4380256
OpenAlexW2137712935

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.