Evidence map›Paper›PMID 16044163›Full record

ArticleOncogene2005

ARK5 is transcriptionally regulated by the Large-MAF family and mediates IGF-1-induced cell invasion in multiple myeloma: ARK5 as a new molecular determinant of malignant multiple myeloma.

Atsushi Suzuki, Shinsuke Iida, Miyuki Kato-Uranishi, Emi Tajima, Fenghuang Zhan, Ichiro Hanamura, Yongsheng Huang, Tsutomu Ogura, Satoru Takahashi, Ryuzo Ueda and 3 more

Abstract read
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In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Review
  3. NUAK: never underestimate a kinase.Essays in biochemistry · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Role of ARK5 in cancer and other diseases (Review).Experimental and therapeutic medicine · 2021
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

13 authors at 4 institutions in 2 countries.

Atsushi SuzukiCancer Physiology Project, National Cancer Center Research Institute East, 6-5-1 Kashiwanoha, Kashiwa, Chiba 277-8577, Japan.
Shinsuke Iida
Miyuki Kato-Uranishi
Emi Tajima
Fenghuang Zhan
Ichiro Hanamura
Yongsheng Huang
Tsutomu Ogura
Satoru Takahashi
Ryuzo Ueda
Bart Barlogie
John Shaughnessy
Hiroyasu Esumi
University of Arkansas for Medical Sciences · USNagoya City University · JPNational Cancer Center Hospital East · JPUniversity of Tsukuba · JP

Funding

Tumor Cell-Microenvironment Interactions in the Molecular Pathogenesis of MultiplP01CA055819 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI YACCOBY, SHMUEL · 1993 to 2013
$49.7M
Molecular Diagnosis and Prognosis of Multiple MyelomaR33CA097513 · NCI · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI SHAUGHNESSY, JOHN DAMIAN · 2002 to 2004
$1.4M
NCI NIH HHS CA55819NCI NIH HHS CA97513
6 · The paper itself

Abstract

ARK5, AMP-activated protein kinase (AMPK)-related protein kinase mediating Akt signals, is closely involved in tumor progression, and its stage-associated expression was observed in colorectal cancer. In this study, we found ARK5 expression in multiple myeloma cell lines expressing c-MAF and MAFB. In addition, gene expression profiling of 351 clinical specimens revealed ARK5 expression in primary myelomas expressing c-MAF and MAFB, suggesting that ARK5 may be a transcriptional target of the Large-MAF family. Sequence analysis of the ARK5 gene promoter revealed that it contains two putative MAF-recognition element (MARE) sequences. In support of this hypothesis, ARK5 was induced when an MAFB or c-MAF expression vector was introduced into non-ARK5-expressing colon cancer cells. Furthermore, ARK5 promoter activity was dramatically decreased by mutation or deletion of MARE sequences. Chromatin immunoprecipitation assays revealed an interaction between the Large-MAF family proteins and MARE sequences in the ARK5 promoter. Moreover, in ARK5 mRNA-expressing multiple myeloma lines, but not in ARK5-negative lines, insulin-like growth factor (IGF)-1 increased invasion activity. IGF-1-induced invasion was reproduced when ARK5 was overexpressed in Burkitt's lymphoma and plasmacytoma lines. Based on results, we conclude that ARK5 is a transcriptional target of the Large-MAF family through MARE sequence and that ARK5 may in part mediate the aggressive phenotype associated with c-MAF- and MAFB-expressing myelomas.

Indexed as

Base SequenceCell Line, TumorDNA PrimersGene Expression Regulation, NeoplasticHumansMaf Transcription Factors, LargeMultiple MyelomaProtein KinasesRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionTranscription, GeneticDNA PrimersMaf Transcription Factors, LargeNUAK1 protein, humanProtein KinasesRepressor Proteins

Identifiers

PMID16044163
OpenAlexW2151492223

What OpenQuestion holds

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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.