Evidence map›Paper›PMID 15254183›Full record

ArticleJournal of virology2004

Human immunodeficiency virus type 1 infection induces cyclin T1 expression in macrophages.

Li-Ying Liou, Christine H Herrmann, Andrew P Rice

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-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

20 citing papers in PubMed, 44 citations in OpenAlex.

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  15. Calpain and proteasomal regulation of antiretroviral zinc finger protein OTK18 in human macrophages: visualization in live cells by intramolecular FRET.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009
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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

3 authors at 1 institution in 1 country.

Li-Ying LiouDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA.
Christine H Herrmann
Andrew P Rice
Baylor College of Medicine · US

Funding

REGULATION OF MRNA FOR TAK SUBUNITS IN T LYMPHOCYTESR01AI045374 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI RICE, ANDREW P · 1999 to 2008
$1.9M
Function and localization of HIV cofactor TAK/P-TEFbR01AI042558 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI HERRMANN, CHRISTINE · 2002 to 2005
$1.1M
Regulation of Tak/P-TEFbR21AI045374 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI RICE, ANDREW P · 2003 to 2003
$263k
REGULATION OF THE TAT ASSOCIATED KINASE, TAKR29AI042558 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI HERRMANN, CHRISTINE · 1998 to 2002
$251k
NIAID NIH HHS AI42558NIAID NIH HHS AI45374NIAID NIH HHS R01 AI042558NIAID NIH HHS R01 AI045374NIAID NIH HHS R21 AI045374NIAID NIH HHS R29 AI042558
6 · The paper itself

Abstract

The Tat protein of human immunodeficiency virus type 1 (HIV-1) is essential for viral replication and activates RNA polymerase II transcriptional elongation through the association with a cellular protein kinase composed of Cdk9 and cyclin T1. Tat binds to this kinase complex through a direct protein-protein interaction with cyclin T1. Monocytes/macrophages are important targets of HIV-1 infection, and previous work has shown that cyclin T1 but not Cdk9 protein expression is low in monocytes isolated from blood. While Cdk9 expression is expressed at a high level during monocyte differentiation to macrophages in vitro, cyclin T1 expression is induced during the first few days of differentiation and is shut off after 1 to 2 weeks. We show here that the shutoff of cyclin T1 expression in late-differentiated macrophages involves proteasome-mediated proteolysis. We also show that cyclin T1 can be reinduced by a number of pathogen-associated molecular patterns that activate macrophages, indicating that up-regulation of cyclin T1 is part of an innate immune response. Furthermore, we found that HIV-1 infection early in macrophage differentiation results in sustained cyclin T1 expression, while infection at late times in differentiation results in the reinduction of cyclin T1. Expression of the viral Nef protein from an adenovirus vector suggests that Nef contributes to the HIV-1 induction of cyclin T1. These findings suggest that HIV-1 infection hijacks a component of the innate immune response in macrophages that results in enhancement rather than inhibition of viral replication.

Indexed as

AdenoviridaeCyclinsCyclin TCysteine EndopeptidasesGene Products, nefHIV-1HumansImmunity, InnateMacrophagesMultienzyme Complexesnef Gene Products, Human Immunodeficiency VirusProteasome Endopeptidase ComplexCCNT1 protein, humanCyclinsCyclin TCysteine EndopeptidasesGene Products, nefMultienzyme Complexesnef Gene Products, Human Immunodeficiency VirusProteasome Endopeptidase Complex

Identifiers

PMID15254183
PMCPMC446126
OpenAlexW2020434640

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.