Evidence map›Paper›PMID 21262846›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Casein kinase-2 mediates cell survival through phosphorylation and degradation of inositol hexakisphosphate kinase-2.

Anutosh Chakraborty, J Kent Werner, Michael A Koldobskiy, Asif K Mustafa, Krishna R Juluri, Joseph Pietropaoli, Adele M Snowman, Solomon H Snyder

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Inositol hexakisphosphate kinase-2 non-catalytically regulates mitophagy by attenuating PINK1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Whole BodyInternational journal of molecular sciences · 2022
    Article
  11. 5-IPNature metabolism · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Inositol Hexakisphosphate Kinase-2 in Cerebellar Granule Cells Regulates Purkinje Cells and Motor Coordination via Protein 4.1N.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  16. Article
  17. The inositol pyrophosphate pathway in health and diseases.Biological reviews of the Cambridge Philosophical Society · 2018
    Review
  18. Article
  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

8 authors at 2 institutions in 1 country.

Anutosh ChakrabortyThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
J Kent Werner
Michael A Koldobskiy
Asif K Mustafa
Krishna R Juluri
Joseph Pietropaoli
Adele M Snowman
Solomon H Snyder
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

UNDERSTANDING NO SIGNALING RESULTING IN NEUROPROTECTION.P50DA000266 · NIDA · JOHNS HOPKINS UNIVERSITY · PI WORLEY, PAUL F · 1985 to 2017
$45.2M
NEUROTRANSMITTER RECEPTORSK05DA000074 · NIDA · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2009
$1.3M
NIDA NIH HHS DA-000266NIDA NIH HHS DA00074NIDA NIH HHS K05 DA000074NIDA NIH HHS P50 DA000266
6 · The paper itself

Abstract

The inositol pyrophosphate, diphosphoinositol pentakisphosphate, regulates p53 and protein kinase Akt signaling, and its aberrant increase in cells has been implicated in apoptosis and insulin resistance. Inositol hexakisphosphate kinase-2 (IP6K2), one of the major inositol pyrophosphate synthesizing enzymes, mediates p53-linked apoptotic cell death. Casein kinase-2 (CK2) promotes cell survival and is upregulated in tumors. We show that CK2 mediated cell survival involves IP6K2 destabilization. CK2 physiologically phosphorylates IP6K2 at amino acid residues S347 and S356 contained within a PEST sequence, a consensus site for ubiquitination. HCT116 cells depleted of IP6K2 are resistant to cell death elicited by CK2 inhibitors. CK2 phosphorylation at the degradation motif of IP6K2 enhances its ubiquitination and subsequent degradation. IP6K2 mutants at the CK2 sites that are resistant to CK2 phosphorylation are metabolically stable.

Indexed as

ApoptosisGene Expression Regulation, EnzymologicSignal TransductionUp-RegulationAmino Acid MotifsCasein Kinase IICell SurvivalEnzyme StabilityGene Expression Regulation, NeoplasticHEK293 CellsHeLa CellsHumansInsulin ResistanceNeoplasmsPhosphorylationPhosphotransferases (Phosphate Group Acceptor)Casein Kinase IIinositol hexakisphosphate kinasePhosphotransferases (Phosphate Group Acceptor)Proto-Oncogene Proteins c-aktTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID21262846
PMCPMC3038742
OpenAlexW2014863678

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.