Evidence map›Paper›PMID 32733884›Full record

ArticleFrontiers in cell and developmental biology2020

Peroxisome-Deficiency and HIF-2α Signaling Are Negative Regulators of Ketohexokinase Expression.

Tanja Eberhart, Miriam J Schönenberger, Katharina M Walter, Khanichi N Charles, Phyllis L Faust, Werner J Kovacs

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Pharmacophore-based virtual screening andFrontiers in pharmacology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Impacts and mechanisms of alternative mRNA splicing in cancer metabolism, immune response, and therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  10. 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

6 authors at 3 institutions in 2 countries.

Tanja EberhartInstitute of Molecular Health Sciences, ETH Zürich, Zurich, Switzerland.
Miriam J SchönenbergerInstitute of Molecular Health Sciences, ETH Zürich, Zurich, Switzerland.
Katharina M WalterInstitute of Molecular Health Sciences, ETH Zürich, Zurich, Switzerland.
Khanichi N CharlesDepartment of Biology, San Diego State University, San Diego, CA, United States.
Phyllis L FaustDepartment of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, United States.
Werner J KovacsInstitute of Molecular Health Sciences, ETH Zürich, Zurich, Switzerland.
ETH Zurich · CHColumbia University · USSan Diego State University · US

Funding

Promoting wellness and resiliencyT34GM008303 · NIGMS · SAN DIEGO STATE UNIVERSITY · PI ATKINS, CATHERINE J · 1989 to 2022
$6.4M
NOVEL GENES OF THE MEVALONATE PATHWAYR01DK058040 · NIDDK · SAN DIEGO STATE UNIVERSITY · PI KRISANS, SKAIDRITE K · 2000 to 2004
$1.8M
Mouse Model for Zellwege SyndromeR01DK058238 · NIDDK · SAN DIEGO STATE UNIVERSITY · PI KRISANS, SKAIDRITE K · 2001 to 2004
$1.1M
NIDDK NIH HHS R01 DK058040NIDDK NIH HHS R01 DK058238NIGMS NIH HHS T34 GM008303
6 · The paper itself

Abstract

Ketohexokinase (KHK) is the first and rate-limiting enzyme of fructose metabolism. Expression of the two alternatively spliced KHK isoforms, KHK-A and KHK-C, is tissue-specific and KHK-C is predominantly expressed in liver, kidney and intestine and responsible for the fructose-catabolizing function. While KHK isoform choice has been linked to the development of disorders such as obesity, diabetes, cardiovascular disease and cancer, little is known about the regulation of total KHK expression. In the present study, we investigated how hypoxic signaling influences fructose metabolism in the liver. Hypoxia or von Hippel-Lindau (VHL) tumor suppressor loss leads to the stabilization of hypoxia-inducible factors alpha (HIF-1α and HIF-2α) and the activation of their signaling to mediate adaptive responses. By studying liver-specific

Indexed as

EPAS1fructoseHIF-2αketohexokinaseperoxisomesPex2VHLZellweger syndrome

Identifiers

PMID32733884
PMCPMC7360681
OpenAlexW3040675549

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.