Evidence map›Paper›PMID 18574673›Full record

ArticleMolecular and cellular biochemistry2008

Impact of protein kinase CK2 on inhibitor of apoptosis proteins in prostate cancer cells.

Guixia Wang, Kashif A Ahmad, Nathan H Harris, Khalil Ahmed

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Protein Kinase CK2, a Potential Therapeutic Target in Carcinoma ManagementAsian Pacific journal of cancer prevention : APJCP · 2019
    Review
  6. Review
  7. Review
  8. Article
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  10. Article
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  12. Article
  13. Article
  14. Article
  15. Inhibition of CK2α down-regulates Notch1 signalling in lung cancer cells.Journal of cellular and molecular medicine · 2013
    Article
  16. Article
  17. [Protein kinase CK2 and human malignant tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2012
    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

4 authors at 2 institutions in 1 country.

Guixia WangCellular and Molecular Biochemistry Research Laboratory (151), Minneapolis Veterans Affairs Medical Center, University of Minnesota, One Veterans Drive, Minneapolis, MN 55417, USA.
Kashif A Ahmad
Nathan H Harris
Khalil Ahmed
University of Minnesota · USUniversity of Minnesota Medical Center · US

Funding

Studies of Normal and Neoplastic ProstateU01CA015062 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI AHMED, KHALIL · 2004 to 2008
$1.1M
STUDIES OF NORMAL AND NEOPLASTIC PROSTATER01CA015062 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI AHMED, KHALIL · 1985 to 2002
$578k
STUDIES OF NORMAL AND NEOPLASTIC PROSTATER37CA015062 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI AHMED, KHALIL · 1986 to 1993
–
NCI NIH HHS CA-15062
6 · The paper itself

Abstract

We have previously demonstrated that protein kinase CK2 is a potent suppressor of apoptosis in cells subjected to diverse mediators of apoptosis. The process of apoptosis involves a complex series of molecules localized in various cellular compartments. Among the various proteins that modulate apoptotic activity are inhibitors of apoptosis proteins (IAPs) which are elevated in cancers and have been proposed to block caspase activity. We have examined the impact of CK2 signal on these proteins in prostate cancer cells. Cellular IAPs demonstrate distinct localization and responsiveness to altered CK2 expression or activity in the cytoplasmic and nuclear matrix fractions. Modulation of cellular CK2 by various approaches impacts on cellular IAPs such that inhibition or downregulation of CK2 results in reduction in these proteins. Further, IAPs are also reduced when cells are treated with sub-optimal concentrations of chemical inhibitors of CK2 combined with low or sub-optimal levels of apoptosis-inducing agents (such as etoposide) suggesting that downregulation of CK2 sensitizes cells to induction of apoptosis which may be related to attenuation of IAPs. Decreased IAP protein levels in response to apoptotic agents such as TNFalpha or TRAIL were potently blocked upon forced overexpression of CK2 in cells. Together, our results suggest that one of the modes of CK2-mediated modulation of apoptotic activity is via its impact on cellular IAPs.

Indexed as

ApigeninApoptosisApoptosis Regulatory ProteinsCasein Kinase IICaspasesCell Line, TumorHumansMaleProstatic NeoplasmsProtein Kinase InhibitorsSubcellular FractionsTriazoles4,5,6,7-tetrabromobenzotriazoleApigeninApoptosis Regulatory ProteinsCasein Kinase IICaspasesProtein Kinase InhibitorsTriazoles

Identifiers

PMID18574673
OpenAlexW2093023696

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.