Evidence map›Paper›PMID 15956585›Full record

ArticleJournal of virology2005

Mobilization and mechanism of transcription of integrated self-inactivating lentiviral vectors.

Hideki Hanawa, Derek A Persons, Arthur W Nienhuis

Abstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. HIV-based lentiviral vectors: origin and sequence differences.Molecular therapy. Methods & clinical development · 2021
    Article
  8. Article
  9. Production of Lentiviral Vectors Using Suspension Cells Grown in Serum-free Media.Molecular therapy. Methods & clinical development · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Production of lentiviral vectors.Molecular therapy. Methods & clinical development · 2016
    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

3 authors at 1 institution in 1 country.

Hideki HanawaDivision of Experimental Hematology, Department of Hematology/Oncology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Mail Stop #272, Memphis, Tennessee 38105, USA.
Derek A Persons
Arthur W Nienhuis
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
VIROSOME/PROTEOLIPOSOME MEDIATED GENE TRANSFERP01HL053749 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 1994 to 2022
$43.6M
NCI NIH HHS P30 CA021765NCI NIH HHS P30 CA 21765NHLBI NIH HHS P01 HL053749NHLBI NIH HHS P01 HL 53749
6 · The paper itself

Abstract

Permanent genetic modification of replicating primitive hematopoietic cells by an integrated vector has many potential therapeutic applications. Both oncoretroviral and lentiviral vectors have a predilection for integration into transcriptionally active genes, creating the potential for promoter activation or gene disruption. The use of self-inactivating (SIN) vectors in which a deletion of the enhancer and promoter sequences from the 3' long terminal repeat (LTR) is copied over into the 5' LTR during vector integration is designed to improve safety by reducing the risk of mobilization of the vector genome and the influence of the LTR on nearby cellular promoters. Our results indicate that SIN vectors are mobilized in cells expressing lentiviral proteins, with the frequency of mobilization influenced by features of the vector design. The mechanism of transcription of integrated vector genomes was evaluated using a promoter trap design with a vector encoding tat but lacking an upstream promoter in a cell line in which drug resistance depended on tat expression. In six clones studied, all transcripts originated from cryptic promoters either upstream or within the vector genome. We estimate that approximately 1 in 3,000 integrated vector genomes is transcribed, leading to the inference that activation of cryptic promoters must depend on local features of chromatin structure and the constellation of nearby regulatory elements as well as the nature of the regulatory elements within the vector.

Indexed as

Terminal Repeat SequencesAnimalsBase SequenceDNA PrimersEnhancer Elements, GeneticGenes, ReporterGreen Fluorescent ProteinsLentivirusPlasmidsPromoter Regions, GeneticRNA, ViralSequence DeletionTranscription, GeneticVirus IntegrationDNA PrimersGreen Fluorescent ProteinsRNA, Viral

Identifiers

PMID15956585
PMCPMC1143763
OpenAlexW2122552050

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.