Evidence map›Paper›PMID 35318430›Full record

ArticleCommunications biology2022

β-cell-specific deletion of PFKFB3 restores cell fitness competition and physiological replication under diabetogenic stress.

Jie Min, Feiyang Ma, Berfin Seyran, Matteo Pellegrini, Oppel Greeff, Salvador Moncada, Slavica Tudzarova

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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 4 countries.

Jie MinHillblom Islet Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Feiyang MaMolecular Cell and Developmental Biology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-6260-0787
Berfin SeyranHillblom Islet Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Matteo PellegriniMolecular Cell and Developmental Biology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA, USA.
Oppel GreeffDepartment of Pharmacology, University of Pretoria, Pretoria, South Africa.
Salvador MoncadaUniversity of Manchester, Manchester, UK.
Slavica TudzarovaHillblom Islet Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. STudzarova@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-9617-3779
University of California, Los Angeles · USUniversity of Manchester · GBUniversity of Pretoria · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIF1α and PFKFB3 play a critical role in the survival of damaged β-cells in type-2 diabetes while rendering β-cells non-responsive to glucose stimulation. To discriminate the role of PFKFB3 from HIF1α in vivo, we generated mice with conditional β-cell specific disruption of the Pfkfb3 gene on a human islet pancreatic polypeptide (hIAPP

Indexed as

Diabetes Mellitus, Type 2Glucose IntoleranceInsulin-Secreting CellsAnimalsInsulinMicePhosphofructokinase-2InsulinPhosphofructokinase-2

Identifiers

PMID35318430
PMCPMC8941137
OpenAlexW4221006296

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.