Evidence map›Paper›PMID 18728388›Full record

ReviewCell cycle (Georgetown, Tex.)2008

Expanding role of cyclin dependent kinases in cytokine inducible gene expression.

Allan R Brasier

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. CTIP2 is a negative regulator of P-TEFb.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

1 author at 1 institution in 1 country.

Allan R BrasierDepartment of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77555-1060, USA. arbrasie@utmb.edu
The University of Texas Medical Branch at Galveston · US

Funding

Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
The Training CoreP50HL083794 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2006 to 2010
$11.3M
VASCULAR INFLAMMATION, IL-6 &RENIN ANGIOTENSIN SYSTEMR01HL070925 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BRASIER, ALLAN R. · 2002 to 2011
$2.6M
NHLBI PROTEOMICS INITIATIVE-N01HV28184N01HV028184 · HV · UNIV OF TEXAS MEDICAL BRANCH · PI KUROSKY, ALEXANDER NONE · 2002 to 2006
–
NHLBI NIH HHS 1 P50 HL083794NHLBI NIH HHS N01 HV028184NHLBI NIH HHS P50 HL083794NHLBI NIH HHS R01 HL070925NHLBI NIH HHS R01 HL70925NIEHS NIH HHS P30 ES006676NIEHS NIH HHS P30 ES06676
6 · The paper itself

Abstract

The Positive Transcriptional Elongation Factor b (P-TEFb), a heterodimer of CDK9 and Cyclin T1, is widely implicated in control of basal gene expression. Here, P-TEFb is involved in transitioning paused RNA polymerase II to enter productive transcriptional elongation mode by phosphorylating negative elongation factors and Ser(2) of the heptad repeat in the RNA Pol II COOH terminal domain (CTD). This perspective will examine recent work in two unrelated inducible signaling pathways that illustrate the central role of P-TEFb in mediating cytokine inducible transcription networks. Specifically, P-TEFb has been recently discovered to play a key role in TNF-inducible NFkappaB activation and IL-6-inducible STAT3 signaling. In these signaling cascades, P-TEFb forms protein complexes with the activated nuclear RelA and STAT3 transcription factor in the cellular nucleoplasm, an association important for P-TEFb's promoter targeting. Studies using siRNA-mediated knockdown and/or selective CDK inhibitors show that P-TEFb plays a functional role in activation of a subset of NFkappaB-dependent targets and all STAT3-dependent genes studied to date. Interestingly, cytokine inducible genes that are sensitive to P-TEFb inhibition share an induction mechanism requiring inducible RNA Pol II recruitment. Chromatin immunoprecipitation studies have preliminarily indicated that this recruitment is dependent on CDK enzymatic activity. The potential of inhibiting P-TEFb as an anti-inflammatory therapy in innate immunity and systemic inflammation will be discussed.

Indexed as

AnimalsCyclin-Dependent KinasesCytokinesGene Expression RegulationHumansNF-kappa BPositive Transcriptional Elongation Factor BTranscription, GeneticCyclin-Dependent KinasesCytokinesNF-kappa BPositive Transcriptional Elongation Factor B

Identifiers

PMID18728388
PMCPMC3019574
OpenAlexW2053002159

What OpenQuestion holds

Textmetadata
LicenceTDM
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.