Evidence map›Paper›PMID 24896358›Full record

ReviewFrontiers in bioscience (Landmark edition)2014

Id transcriptional regulators in adipogenesis and adipose tissue metabolism.

Mallikarjun Patil, Bal Krishan Sharma, Ande Satyanarayana

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Diverse repertoire of human adipocyte subtypes develops from transcriptionally distinct mesenchymal progenitor cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
  9. 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

3 authors at 1 institution in 1 country.

Mallikarjun Patil
Bal Krishan Sharma
Ande Satyanarayana
Molecular Oncology (United States) · US

Funding

Role of Id1 in adiposity, energy balance and obesity associated liver tumorigenesK22CA168828 · NCI · AUGUSTA UNIVERSITY · PI ANDE, SATYANARAYANA · 2013 to 2015
$382k
NCI NIH HHS K22 CA168828NCI NIH HHS K22CA168828
6 · The paper itself

Abstract

Id proteins (Id1-Id4) are helix-loop-helix (HLH) transcriptional regulators that lack a basic DNA binding domain. They act as negative regulators of basic helix-loop-helix (bHLH) transcription factors by forming heterodimers and inhibit their DNA binding and transcriptional activity. Id proteins are implicated in the regulation of various cellular mechanisms such as cell proliferation, cellular differentiation, cell fate determination, angiogenesis and tumorigenesis. A handful of recent studies also disclosed that Id proteins have critical functions in adipocyte differentiation and adipose tissue metabolism. Here, we reviewed the progress made thus far in understanding the specific functions of Id proteins in adipose tissue differentiation and metabolism. In addition to reviewing the known mechanisms of action, we also discuss possible additional mechanisms in which Id proteins might participate in regulating adipogenic and metabolic pathways.

Indexed as

Gene Expression RegulationAdipogenesisAdipose TissueAnimalsBasic Helix-Loop-Helix ProteinsHumansInhibitor of Differentiation ProteinsModels, GeneticProtein IsoformsSignal TransductionBasic Helix-Loop-Helix ProteinsInhibitor of Differentiation ProteinsProtein Isoforms

Identifiers

PMID24896358
PMCPMC4117208
OpenAlexW1968334319

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.