Evidence map›Paper›PMID 28425845›Full record

ArticleAdipocyte2017

Nck2, an unexpected regulator of adipogenesis.

N Haider, J Dusseault, A Rudich, L Larose

Open access · goldAbstract read
In one paragraph

Article in Adipocyte, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. CaJournal of cell science · 2019
    Article
  4. 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 3 institutions in 2 countries.

N Haidera Department of Medicine , McGill University , Montreal , Quebec , Canada.
J Dusseaulta Department of Medicine , McGill University , Montreal , Quebec , Canada.
A Rudichc Department of Clinical Biochemistry and Pharmacology , Ben-Gurion University of the Negev , Beer-Sheva , Israel.
L Larosea Department of Medicine , McGill University , Montreal , Quebec , Canada.
McGill University Health Centre · CABen-Gurion University of the Negev · ILMcGill University · CA

Funding

CIHR MOP-115045
6 · The paper itself

Abstract

The regulation of adipose tissue expansion by adipocyte hypertrophy and/or hyperplasia is the topic of extensive investigations given the potential differential contribution of the 2 processes to the development of numerous chronic diseases associated with obesity. We recently discovered that the loss-of-function of the Src homology domain-containing protein Nck2 in mice promotes adiposity accompanied with adipocyte hypertrophy and impaired function, and enhanced adipocyte differentiation in vitro. Moreover, in severely-obese human's adipose tissue, we found that Nck2 expression is markedly downregulated. In this commentary, our goal is to expand upon additional findings providing further evidence for a unique Nck2-dependent mechanism regulating adipogenesis. We propose that Nck2 should be further investigated as a regulator of the reliance of white adipose tissue on hyperplasia versus hypertrophy during adipose tissue expansion, and hence, as a potential novel molecular target in obesity.

Indexed as

3T3-L1 CellsAdaptor Proteins, Signal TransducingAdipocytesAdipogenesisAdipose TissueAdipose Tissue, WhiteAdiposityAnimalsDown-RegulationHypertrophyMiceObesityOncogene ProteinsAdaptor Proteins, Signal TransducingNck2 protein, mouseOncogene Proteins3T3-L1 and SGBS preadipocytesadipocyte differentiationAdipogenesisPERK activation and signalingPPARγ regulationSrc homology adaptor protein Nck2

Identifiers

PMID28425845
PMCPMC5477721
OpenAlexW2587310367

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.