Evidence map›Paper›PMID 11526477›Full record

ArticleOncogene2001

Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1.

A Ikeguchi, H Y Yang, G Gao, S P Goff

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 2 institutions in 1 country.

A IkeguchiDepartment of Medicine, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
H Y Yang
G Gao
S P Goff
Columbia University · USHoward Hughes Medical Institute · US

Funding

THE DETERMINANTS OF MUTATIONP01CA023767 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI AXEL, RICHARD · 1985 to 2008
$8.3M
NCI NIH HHS P01 CA 23767
6 · The paper itself

Abstract

The abi-1 gene encodes a protein that binds and is phosphorylated by the Abelson protein tyrosine kinase. Constructs expressing a full-length abi-1 cDNA, and a smaller cDNA arising from an alternatively spliced form, were generated and tested for their effect on transformation of NIH3T3 cells by the Abelson murine leukemia virus. Overexpression of both forms of the protein strongly inhibited transformation by the wild-type P160 strain of the virus, but not by the non-interacting mutant P90A strain. The inhibition required the SH3 domain of Abi-1, suggesting that a direct interaction was required for the effect. Rare breakthrough P160 transformants of the Abi-1 overexpressing lines were found to have downregulated Abi-1 protein levels by a post-transcriptional mechanism.

Indexed as

Adaptor Proteins, Signal TransducingCell Transformation, ViralCytoskeletal Proteins3T3 CellsAlternative SplicingAmino Acid SequenceAnimalsCarrier ProteinsHomeodomain ProteinsMiceMolecular Sequence DataOncogene Proteins v-ablRNA, Messengersrc Homology DomainsTransfectionAbi1 protein, mouseAdaptor Proteins, Signal TransducingCarrier ProteinsCytoskeletal ProteinsHomeodomain ProteinsOncogene Proteins v-ablRNA, Messenger

Identifiers

PMID11526477
OpenAlexW2332087904

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.