Evidence map›Paper›PMID 17431504›Full record

ArticleThe Journal of clinical investigation2007

CaMKII regulates retinoic acid receptor transcriptional activity and the differentiation of myeloid leukemia cells.

Jutong Si, LeMoyne Mueller, Steven J Collins

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  5. Put in a "CaCells · 2022
    Review
  6. CaJournal of cellular immunology · 2021
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  19. Retinoid receptors trigger neuritogenesis in retinal degenerations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    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

3 authors at 1 institution in 1 country.

Jutong SiHuman Biology Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N., Seattle, WA 98109, USA.
LeMoyne Mueller
Steven J Collins
Fred Hutch Cancer Center · US

Funding

TRANSDUCTION OF BABOON HEMATOPOIETIC STEM CELLSP50HL054881 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BERNSTEIN, IRWIN · 1995 to 2004
$11.0M
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 CA 118971NCI NIH HHS R01 CA118971NHLBI NIH HHS HL 54881NHLBI NIH HHS P50 HL054881
6 · The paper itself

Abstract

Retinoic acid receptors (RARs) are members of the nuclear hormone receptor family and regulate the proliferation and differentiation of multiple different cell types, including promyelocytic leukemia cells. Here we describe a biochemical/functional interaction between the Ca(2+)/calmodulin-dependent protein kinases (CaMKs) and RARs that modulates the differentiation of myeloid leukemia cells. We observe that CaMKIIgamma is the CaMK that is predominantly expressed in myeloid cells. CaMKII inhibits RAR transcriptional activity, and this enzyme directly interacts with RAR through a CaMKII LxxLL binding motif. CaMKIIgamma phosphorylates RARalpha both in vitro and in vivo, and this phosphorylation inhibits RARalpha activity by enhancing its interaction with transcriptional corepressors. In myeloid cell lines, CaMKIIgamma localizes to RAR target sites within myeloid gene promoters but dissociates from the promoter upon retinoic acid-induced myeloid cell differentiation. KN62, a pharmacological inhibitor of the CaMKs, enhances the terminal differentiation of myeloid leukemia cell lines, and this is associated with a reduction in activated (autophosphorylated) CaMKII in the terminally differentiating cells. These observations reveal a significant cross-talk between Ca(2+) and retinoic acid signaling pathways that regulates the differentiation of myeloid leukemia cells, and they suggest that CaMKIIgamma may provide a new therapeutic target for the treatment of certain human myeloid leukemias.

Indexed as

Calcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationEnzyme ActivationGene Expression Regulation, NeoplasticHL-60 CellsHumansLeukemia, Promyelocytic, AcutePromoter Regions, GeneticReceptors, Retinoic AcidSignal TransductionTretinoinCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Receptors, Retinoic AcidTretinoin

Identifiers

PMID17431504
PMCPMC1847537
OpenAlexW1978479780

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.