Evidence map›Paper›PMID 16641271›Full record

ArticleJournal of virology2006

Tax interacts with P-TEFb in a novel manner to stimulate human T-lymphotropic virus type 1 transcription.

Meisheng Zhou, Hanxin Lu, Hyeon Park, Jaime Wilson-Chiru, Rebecca Linton, John N Brady

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Latency Reversing Agents: Kick and Kill of HTLV-1?International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. P-TEFb goes viral.Inside the cell · 2016
    Review
  14. Article
  15. Article
  16. Review
  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

6 authors at 2 institutions in 1 country.

Meisheng ZhouVirus Tumor Biology Section, Laboratory of Cellular Oncology, Center for Cancer Research, NCI/NIH, , Bethesda, MD 20892, USA.
Hanxin Lu
Hyeon Park
Jaime Wilson-Chiru
Rebecca Linton
John N Brady
Center for Cancer Research · USNational Institutes of Health · US

Funding

REGULATION OF VIRAL AND CELLULAR GENE EXPRESSONZ01BC005254 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 1996 to 2008
$1.1M
HIV Tat Transcriptional Activation Z01BC005753 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 1996 to 2008
$714k
Regulation of HTLV-I TranscriptionZIABC005254 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 2009 to 2009
$532k
HIV Tat Transcriptional ActivationZIABC005753 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 2009 to 2009
$355k
6 · The paper itself

Abstract

Human T-lymphotropic virus type 1 (HTLV-1) encodes a transcriptional activator, Tax, whose function is essential for viral transcription and replication. Tax transactivates the viral long-terminal repeat through a series of protein-protein interactions which facilitate CREB and CBP/p300 binding. In addition, Tax dissociates transcription repressor histone deacetylase 1 interaction with the CREB response element. The subsequent events through which Tax interacts and communicates with RNA polymerase II and cyclin-dependent kinases (CDKs) are not clearly understood. Here we present evidence that Tax recruits positive transcription elongation factor b (P-TEFb) (CDK9/cyclin T1) to the viral promoter. This recruitment likely involves protein-protein interactions since Tax associates with P-TEFb in vitro as demonstrated by glutathione S-transferase fusion protein pull-down assays and in vivo as shown by co-immunoprecipitation assays. Functionally, small interfering RNA directed toward CDK9 inhibited Tax transactivation in transient assays. Consistent with these findings, the depletion of CDK9 from nuclear extracts inhibited Tax transactivation in vitro. Reconstitution of the reaction with wild-type P-TEFb, but not a kinase-dead mutant, recovered HTLV-1 transcription. Moreover, the addition of the CDK9 inhibitor flavopiridol blocked Tax transactivation in vitro and in vivo. Interestingly, we found that Tax regulates CDK9 kinase activity through a novel autophosphorylation pathway.

Indexed as

Cell LineCyclin-Dependent Kinase 9Gene Products, taxHeLa CellsHumansHuman T-lymphotropic virus 1PhosphorylationPositive Transcriptional Elongation Factor BRNA, ViralThreonineTranscriptional ActivationCDK9 protein, humanCyclin-Dependent Kinase 9Gene Products, taxPositive Transcriptional Elongation Factor BRNA, ViralThreonine

Identifiers

PMID16641271
PMCPMC1472077
OpenAlexW2116992772

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.