Evidence map›Paper›PMID 18483256›Full record

ArticleCancer research2008

Activated Ca2+/calmodulin-dependent protein kinase IIgamma is a critical regulator of myeloid leukemia cell proliferation.

Jutong Si, Steven J Collins

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
1.8field-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

52 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  3. pSTAT3 activation ofProceedings of the National Academy of Sciences of the United States of America · 2024
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  16. Sex determination without sex chromosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021
    Review
  17. Review
  18. Review
  19. CaJournal of cellular immunology · 2021
    Article
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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 1 institution in 1 country.

Jutong SiHuman Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Steven J Collins
Fred Hutch Cancer Center · US

Funding

Targeting the CaM Kinases in Treating Myeloid LeukemiaR01CA118971 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI COLLINS, STEVEN COLLINS · 2006 to 2009
$1.1M
NCI NIH HHS R01 CA118971
6 · The paper itself

Abstract

Ca(2+) signaling is an important component of signal transduction pathways regulating B and T lymphocyte proliferation, but the functional role of Ca(2+) signaling in regulating myeloid leukemia cell proliferation has been largely unexplored. We observe that the activated (autophosphorylated) Ca(2+)/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma) is invariably present in myeloid leukemia cell lines as well as in the majority of primary acute myelogenous leukemia patient samples. In contrast, myeloid leukemia cells induced to terminally differentiate or undergo growth arrest display a marked reduction in this CaMKIIgamma autophosphorylation. In cells harboring the bcr-abl oncogene, the activation (autophosphorylation) of CaMKIIgamma is regulated by this oncogene. Moreover, inhibition of CaMKIIgamma activity with pharmacologic agents, dominant-negative constructs, or short hairpin RNAs inhibits the proliferation of myeloid leukemia cells, and this is associated with the inactivation/down-regulation of multiple critical signal transduction networks involving the mitogen-activated protein kinase, Janus-activated kinase/signal transducers and activators of transcription (Jak/Stat), and glycogen synthase kinase (GSK3beta)/beta-catenin pathways. In myeloid leukemia cells, CaMKIIgamma directly phosphorylates Stat3 and enhances its transcriptional activity. Thus, CaMKIIgamma is a critical regulator of multiple signaling networks regulating the proliferation of myeloid leukemia cells. Inhibiting CaMKIIgamma may represent a novel approach in the targeted therapy of myeloid leukemia.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, LeukemicAntigens, CD34ApoptosisCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationCell Line, TumorCell ProliferationEnzyme ActivationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansK562 CellsLeukemia, MyeloidPhosphorylationSignal TransductionAntigens, CD34Calcium-Calmodulin-Dependent Protein Kinase Type 2CAMK2G protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, human

Identifiers

PMID18483256
PMCPMC2443690
OpenAlexW2172245356

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.