Evidence map›Paper›PMID 20838382›Full record

ArticleOncogene2010

Molecular determinants of PDLIM2 in suppressing HTLV-I Tax-mediated tumorigenesis.

J Fu, P Yan, S Li, Z Qu, G Xiao

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

37 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025
    Article
  5. PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The unexpected versatility of ALP/Enigma family proteins.Frontiers in cell and developmental biology · 2022
    Review
  11. PDLIM2: Signaling pathways and functions in cancer suppression and host immunity.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  12. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Prognostic value of the PDLIM family in acute myeloid leukemia.American journal of translational research · 2019
    Article
  18. IMiD compounds affect CD34Blood advances · 2018
    Article
  19. Review
  20. Exome and transcriptome sequencing identifies loss ofCancer management and research · 2017
    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

5 authors at 2 institutions in 1 country.

J FuUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
P Yan
S Li
Z Qu
G Xiao
UPMC Hillman Cancer Center · USUniversity of Pittsburgh · US

Funding

PDLIM2 as a cancer and chemosensitizing targetR01CA172090 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2017
$1.6M
HTLV deregulation of NF-kappaB2 p100 processing in tumorR01CA116616 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2006 to 2010
$1.1M
NCI NIH HHS R01 CA116616NCI NIH HHS R01 CA172090
6 · The paper itself

Abstract

Human T-cell leukemia virus type I (HTLV-I) encodes a Tax oncoprotein that has crucial roles in both virus replication and cell transformation. Our recent studies suggest that the counterbalance between HTLV-I/Tax and PDZ-LIM domain-containing protein PDLIM2 may determine the outcome of HTLV-I infection. Although HTLV-I represses PDLIM2 epigenetically and specifically in transformed cells, PDLIM2 shuttles Tax into the nuclear matrix for ubiquitination-mediated proteasomal degradation, thereby suppressing the transforming ability of HTLV-I. Here, we have further shown that PDLIM2 binds to Tax directly, which was mediated by a putative α-helix motif of PDLIM2 at amino acids 236-254. Consistently, selective disruption of this short-helix crippled PDLIM2 in shutting Tax to the nuclear matrix for ubiquitination-mediated degradation, therefore, PDLIM2 lost the ability in tumor suppression. Although the C-terminal LIM domain of PDLIM2 was not required for Tax binding, it was important for PDLIM2 to interact with the nuclear matrix. Accordingly, the LIM domain was essential for PDLIM2-mediated Tax repression. On the contrary, the N-terminal PDZ domain of PDLIM2 was dispensable for all these events, although the PDZ domain was involved in PDLIM2 binding to cytoskeleton. These studies dissect functional sequences within PDLIM2 and their distinct roles in Tax regulation.

Indexed as

Cell Transformation, ViralAmino Acid MotifsCells, CulturedGene Products, taxHTLV-I InfectionsHumansHuman T-lymphotropic virus 1LIM Domain ProteinsMicrofilament ProteinsProtein Interaction Domains and MotifsT-LymphocytesGene Products, taxLIM Domain ProteinsMicrofilament ProteinsPDLIM2 protein, humantax protein, Human T-lymphotrophic virus 1

Identifiers

PMID20838382
PMCPMC3013277
OpenAlexW2049734724

What OpenQuestion holds

Textmetadata
LicenceTDM
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.