Evidence map›Paper›PMID 22147607›Full record

ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2011

TNIP1, a retinoic acid receptor corepressor and A20-binding inhibitor of NF-κB, distributes to both nuclear and cytoplasmic locations.

Igor Gurevich, Carmen Zhang, Nidhish Francis, Brian J Aneskievich

Open access · bronzeAbstract read
In one paragraph

Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  7. Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022
    Article
  8. Review
  9. Observational
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. TNIP1 RegulatesFrontiers in immunology · 2018
    Article
  16. Relationship between theOncotarget · 2017
    Article
  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

4 authors at 1 institution in 1 country.

Igor GurevichGraduate Program in Pharmacology & Toxicology, Department of Pharmaceutical Sciences, University of Connecticut, Storrs, Connecticut 06269-3092, USA.
Carmen Zhang
Nidhish Francis
Brian J Aneskievich
University of Connecticut · US

Funding

Keratinocyte Nuclear Receptor CoactivatorsR01AR048660 · NIAMS · UNIVERSITY OF CONNECTICUT STORRS · PI ANESKIEVICH, BRIAN J · 2005 to 2009
$1.4M
NIAMS NIH HHS AR048660NIAMS NIH HHS R01 AR048660
6 · The paper itself

Abstract

An increasingly wide range of functions, from repression of NF-κB signaling to protection from apoptosis, is being recognized for tumor necrosis factor α-induced protein 3-interacting protein 1 (TNIP1). The authors recently demonstrated TNIP1 interaction with and repression of liganded retinoic acid receptors, distinguishing it from the more typical NCoR and SMRT corepressors, which function only in the absence of ligand. To improve their understanding of TNIP1's roles in physiologic and pathologic events, the authors examined its distribution in normal and malignant human tissues and cultured cells. They found cytoplasmic and nuclear TNIP1 in normal skin keratinocytes as it colocalized with retinoic acid receptor α, one of the nuclear receptors it corepresses. Nuclear and cytoplasmic TNIP1 was also found in the malignant keratinocytes of squamous cell carcinomas. Compared to adjacent normal tissues of other organs, TNIP1 staining and distribution varied with increased levels in esophageal cancer and marked decreases in prostate cancer. The varying levels and distribution of TNIP1 in normal and disease state tissues could be expected to affect processes in which TNIP1 is involved, such as NF-κB and nuclear receptor signaling, possibly contributing to the disease course or response to therapies targeting these key players of cell growth and differentiation.

Indexed as

Cell NucleusCells, CulturedCo-Repressor ProteinsCytoplasmDNA-Binding ProteinsEpidermal CellsEpidermisHumansInfant, NewbornIntracellular Signaling Peptides and ProteinsKeratinocytesMaleNeoplasmsNF-kappa BNuclear ProteinsOrgan SpecificityCo-Repressor ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNF-kappa BNuclear ProteinsRARA protein, humanReceptors, Retinoic AcidRecombinant ProteinsRetinoic Acid Receptor alphaTNFAIP3 protein, humanTNIP1 protein, humanTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID22147607
PMCPMC3283085
OpenAlexW1994799948

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.