Evidence map›Paper›PMID 20139419›Full record

ArticleNucleic acids research2010

Modifications in host cell cytoskeleton structure and function mediated by intracellular HIV-1 Tat protein are greatly dependent on the second coding exon.

M R López-Huertas, S Callejas, D Abia, E Mateos, A Dopazo, J Alcamí, M Coiras

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019
    Review
  16. Article
  17. Review
  18. Review
  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

7 authors at 5 institutions in 2 countries.

M R López-HuertasAIDS Immunopathology Unit, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.
S Callejas
D Abia
E Mateos
A Dopazo
J Alcamí
M Coiras
Centro de Biología Molecular Severo Ochoa · ESInstituto de Salud Carlos III · ESCentro Nacional de Investigaciones Científicas · CUCentro Nacional de Microbiologia · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human immunodeficiency virus type 1 (HIV-1) regulator Tat is essential for viral replication because it achieves complete elongation of viral transcripts. Tat can be released to the extracellular space and taken up by adjacent cells, exerting profound cytoskeleton rearrangements that lead to apoptosis. In contrast, intracellular Tat has been described as protector from apoptosis. Tat gene is composed by two coding exons that yield a protein of 101 amino acids (aa). First exon (1-72aa) is sufficient for viral transcript elongation and second exon (73-101 aa) appears to contribute to non-transcriptional functions. We observed that Jurkat cells stably expressing intracellular Tat101 showed gene expression deregulation 4-fold higher than cells expressing Tat72. Functional experiments were performed to evaluate the effect of this deregulation. First, NF-kappaB-, NF-AT- and Sp1-dependent transcriptional activities were greatly enhanced in Jurkat-Tat101, whereas Tat72 induced milder but efficient activation. Second, cytoskeleton-related functions as cell morphology, proliferation, chemotaxis, polarization and actin polymerization were deeply altered in Jurkat-Tat101, but not in Jurkat-Tat72. Finally, expression of several cell surface receptors was dramatically impaired by intracellular Tat101 but not by Tat72. Consequently, these modifications were greatly dependent on Tat second exon and they could be related to the anergy observed in HIV-1-infected T cells.

Indexed as

HIV-1Cell ProliferationChemotaxisComputational BiologyCytoskeletonExonsGene Expression ProfilingHumansJurkat CellsModels, MolecularReceptors, Cell Surfacetat Gene Products, Human Immunodeficiency VirusTranscriptional ActivationReceptors, Cell Surfacetat Gene Products, Human Immunodeficiency Virustat peptide (1-72), Human immunodeficiency virus 1

Identifiers

PMID20139419
PMCPMC2879518
OpenAlexW2165911674

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.