Evidence map›Paper›PMID 16232120›Full record

ArticleThe Biochemical journal2006

Post-translational and transcriptional regulation of DMT1 during P19 embryonic carcinoma cell differentiation by retinoic acid.

Prasad N Paradkar, Jerome A Roth

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Hyperglycemia promotes microvillus membrane expression of DMT1 in intestinal epithelial cells in a PKCα-dependent manner.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Manganese homeostasis and transport.Metal ions in life sciences · 2013
    Article
  12. Isoform specific regulation of divalent metal (ion) transporter (DMT1) by proteasomal degradation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2012
    Article
  13. Article
  14. Human iron transporters.Genes & nutrition · 2011
    Article
  15. Review
  16. Review
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

2 authors at 1 institution in 1 country.

Prasad N ParadkarDepartment of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14214, USA.
Jerome A Roth
University at Buffalo, State University of New York · US

Funding

NIEHS NIH HHS R01 ES1112
6 · The paper itself

Abstract

Studies were performed to determine the regulation of DMT1 (divalent metal transporter 1) during RA (retinoic acid)-induced differentiation of P19 embryonic carcinoma cells. Protein and mRNA expression for the +/-IRE (iron response element) forms of DMT1, but not the 1A isoform, were down-regulated within the first few hours upon removal of RA, at which time the cells began to differentiate. The turnover of the +/-IRE isoforms of DMT1 protein during this period was found to be dependent on both the proteasomal and lysosomal pathways. Changes in mRNA levels were shown to be regulated by nitric oxide produced by the induction of neuronal nitric oxide synthase after removal of RA. Nitric oxide functions by inhibiting NF-kappaB (nuclear factor kappaB) nuclear translocation and the subsequent binding to the putative NF-kappaB response element (at -19 to -23) within the 1B promoter. Gel-shift analysis and chromatin immunoprecipitation assay indicated that nuclear NF-kappaB is capable of binding to this response element and that binding decreases during early stages of differentiation. Luciferase reporter gene assay demonstrated that a mutation in this binding domain leads to decreased activity. These results demonstrate that during neuronal differentiation of P19 cells, there is a decrease in specific isoforms of DMT1 via both post-translational and transcriptional mechanisms.

Indexed as

CarcinomaCation Transport ProteinsCell DifferentiationCell LineHumansImmunoglobulinsIron-Binding ProteinsNF-kappa BPromoter Regions, GeneticProtein BindingProtein IsoformsProtein Processing, Post-TranslationalRNA, MessengerSolute Carrier Family 11, Member 2Time FactorsTranscription, GeneticCation Transport ProteinsImmunoglobulinsIron-Binding ProteinsNF-kappa BProtein IsoformsRNA, MessengerSolute Carrier Family 11, Member 2SP1 antigenTretinoin

Identifiers

PMID16232120
PMCPMC1386015
OpenAlexW1963783971

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.