Evidence map›Paper›PMID 15601829›Full record

ArticleMolecular and cellular biology2005

Molecular mechanism of hTid-1, the human homolog of Drosophila tumor suppressor l(2)Tid, in the regulation of NF-kappaB activity and suppression of tumor growth.

Hua Cheng, Carlo Cenciarelli, Gina Nelkin, Rachel Tsan, Dominic Fan, Cecilia Cheng-Mayer, Isaiah J Fidler

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. DNAJA: emerging targets for anti-tumor therapy.Future oncology (London, England) · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. The one thousand and one chaperones of the NF-κB pathway.Cellular and molecular life sciences : CMLS · 2020
    Review
  7. Role of Mycoplasma Chaperone DnaK in Cellular Transformation.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. Targeting Heat Shock Proteins in Cancer: A Promising Therapeutic Approach.International journal of molecular sciences · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  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 3 institutions in 2 countries.

Hua ChengDepartment of Cancer Biology, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Carlo Cenciarelli
Gina Nelkin
Rachel Tsan
Dominic Fan
Cecilia Cheng-Mayer
Isaiah J Fidler
Università Cattolica del Sacro Cuore · ITAaron Diamond AIDS Research Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS CA 16672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

hTid-1, a human homolog of the Drosophila tumor suppressor l(2)Tid and a novel DnaJ protein, regulates the activity of nuclear factor kappaB (NF-kappaB), but its mechanism is not established. We report here that hTid-1 strongly associated with the cytoplasmic protein complex of NF-kappaB-IkappaB through direct interaction with IkappaBalpha/beta and the IKKalpha/beta subunits of the IkappaB kinase complex. These interactions resulted in suppression of the IKK activity in a J-domain-dependent fashion and led to the cytoplasmic retention and enhanced stability of IkappaB. Overexpression of hTid-1 by using recombinant baculovirus or adenovirus led to inhibition of cell proliferation and induction of apoptosis of human osteosarcoma cells regardless of the p53 expression status. Adherent cultured cells transduced with Ad.hTid-1 detached from the dish surface. Morphological changes consistent with apoptosis and cell death were evident 48 h after Ad.EGFP-hTid-1 transduction. In contrast, cells transduced with Ad.EGFP or Ad.EGFP-hTd-1DeltaN100, a mutant that has the N-terminal J domain deletion and that lost suppressive activity on IKK, continued to proliferate. Similar data were obtained with A375 human melanoma cells. Ad.EGFP or Ad.EGFP-hTd-1DeltaN100 ex vivo-transduced A375 cells injected subcutaneously into nude mice produced growing tumors, whereas Ad.EGFP-hTid-1-transduced cells did not. Collectively, the data suggest that hTid-1 represses the activity of NF-kappaB through physical and functional interactions with the IKK complex and IkappaB and, in doing so, it modulates cell growth and death.

Indexed as

AdenoviridaeAgarAnimalsApoptosisBaculoviridaeCell DeathCell LineCell Line, TumorCell ProliferationCytoplasmDrosophilaGene DeletionGene Expression RegulationGenes, ReporterGlutathione TransferaseGreen Fluorescent ProteinsAgarDNAJA3 protein, humanGlutathione TransferaseGreen Fluorescent ProteinsHeat-Shock ProteinsHSP40 Heat-Shock ProteinsI-kappa B ProteinsNF-kappa BRecombinant Fusion ProteinsTetrazolium SaltsThiazolesthiazolyl blueTumor Suppressor Protein p53

Identifiers

PMID15601829
PMCPMC538758
OpenAlexW2159302760

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.