Evidence map›Paper›PMID 12069692›Full record

ArticleBMC biochemistry2002

Gene expression profile of HIV-1 Tat expressing cells: a close interplay between proliferative and differentiation signals.

Cynthia de la Fuente, Francisco Santiago, Longwen Deng, Carolyne Eadie, Irene Zilberman, Kylene Kehn, Anil Maddukuri, Shanese Baylor, Kaili Wu, Chee Gun Lee and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in BMC biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  4. HIV Tat Impairs Neurogenesis through Functioning As a Notch Ligand and Activation of Notch Signaling Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  5. Functional roles of HIV-1 Tat protein in the nucleus.Cellular and molecular life sciences : CMLS · 2016
    Review
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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

12 authors at 2 institutions in 1 country.

Cynthia de la FuenteDepartment of Biochemistry and Molecular Biology George Washington University School of Medicine Washington DC 20037, USA. bcmfxk@gwumc.edu
Francisco Santiago
Longwen Deng
Carolyne Eadie
Irene Zilberman
Kylene Kehn
Anil Maddukuri
Shanese Baylor
Kaili Wu
Chee Gun Lee
Anne Pumfery
Fatah Kashanchi
George Washington University · USRutgers, The State University of New Jersey · US

Funding

HIV1 INHIBITION USING TAT PEPTIDE DERIVATIVESR01AI043894 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KASHANCHI, FATAH · 1999 to 2015
$4.4M
CELL CYCLE REGULATED TRANSCRIPTION BY HIV1 TRANSACT TATR29AI044357 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KASHANCHI, FATAH · 1998 to 2002
$322k
NIAID NIH HHS AI43894NIAID NIH HHS AI44357NIAID NIH HHS R01 AI043894NIAID NIH HHS R29 AI044357PHS HHS 13969
6 · The paper itself

Abstract

backgroundExpression profiling holds great promise for rapid host genome functional analysis. It is plausible that host expression profiling in an infection could serve as a universal phenotype in virally infected cells. Here, we describe the effect of one of the most critical viral activators, Tat, in HIV-1 infected and Tat expressing cells. We utilized microarray analysis from uninfected, latently HIV-1 infected cells, as well as cells that express Tat, to decipher some of the cellular changes associated with this viral activator.

resultsUtilizing uninfected, HIV-1 latently infected cells, and Tat expressing cells, we observed that most of the cellular host genes in Tat expressing cells were down-regulated. The down-regulation in Tat expressing cells is most apparent on cellular receptors that have intrinsic receptor tyrosine kinase (RTK) activity and signal transduction members that mediate RTK function, including Ras-Raf-MEK pathway. Co-activators of transcription, such as p300/CBP and SRC-1, which mediate gene expression related to hormone receptor genes, were also found to be down-regulated. Down-regulation of receptors may allow latent HIV-1 infected cells to either hide from the immune system or avoid extracellular differentiation signals. Some of the genes that were up-regulated included co-receptors for HIV-1 entry, translation machinery, and cell cycle regulatory proteins.

conclusionsWe have demonstrated, through a microarray approach, that HIV-1 Tat is able to regulate many cellular genes that are involved in cell signaling, translation and ultimately control the host proliferative and differentiation signals.

Indexed as

Cell CycleCell DifferentiationCell DivisionChromatinGene Expression ProfilingGene Expression RegulationGene Products, tatHeLa CellsHIV-1HumansProtein BiosynthesisSignal Transductiontat Gene Products, Human Immunodeficiency VirusThymosinTranscription FactorsTranscription, GeneticChromatinGene Products, tattat Gene Products, Human Immunodeficiency VirusThymosinTranscription Factors

Identifiers

PMID12069692
PMCPMC116586
OpenAlexW2140351115

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.