Evidence map›Paper›PMID 11827176›Full record

ArticleMolecular and cellular biochemistry2001

Consequences of CK2 signaling to the nuclear matrix.

S Yu, H Wang, A Davis, K Ahmed

Abstract read
PubMed
In one paragraph

Article in Molecular and cellular biochemistry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Protein kinase CK2--a key suppressor of apoptosis.Advances in enzyme regulation · 2008
    Review
  12. Article
  13. Regulation of DeltaFosB stability by phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  14. Article
  15. Modulation of death receptor-mediated apoptosis by CK2.Molecular and cellular biochemistry · 2005
    Article
  16. Article
  17. Review
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 3 institutions in 1 country.

S YuDepartment of Laboratory Medicine and Pathology and University of Minnesota Cancer Center, University of Minnesota, Minneapolis, USA.
H Wang
A Davis
K Ahmed
Masonic Cancer CenterUniversity 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

Protein kinase CK2 is recognized as one of the key cellular signals for cell growth and proliferation. Its nuclear targeting appears to be critical to its role in these functions. In the nucleus, nuclear matrix (NM) which plays a major role in growth-related activities is a primary locus for CK2 signaling. A variety of growth stimuli evoke a rapid translocation of the CK2 to the NM whereas removal of these factors has the opposite effect. These studies, employing various experimental models of cell growth (involving different growth-stimulatory factors), have suggested that rapid shuttling of CK2 to the NM is a key feature of early growth control. By contrast, removal of growth-stimulatory factors leading to the loss of cell viability is associated with early loss of CK2 from the NM (and chromatin). This indicates that absence of CK2 from the nuclear compartment is contributory to induction of cell death via apoptosis, implying a protective role for CK2 against cell death. Here, we review the evidence that suggests that CK2 signaling in the NM is not only involved in cell growth but also in cell survival.

Indexed as

Active Transport, Cell NucleusAmino Acid SequenceAnimalsApoptosisCasein Kinase IICell DeathCell DivisionCell NucleusCell SurvivalHumansMaleMolecular Sequence DataProtein Serine-Threonine KinasesRatsRats, Sprague-DawleySignal TransductionCasein Kinase IIProtein Serine-Threonine Kinases

Identifiers

PMID11827176
OpenAlexW1558129207

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.