Nature Search

HSD17B4 deficiency causes dysregulation of primary cilia and is alleviated by acetyl-CoA

HSD17B4 deficiency disrupts peroxisomal metabolism and causes ciliopathy-like phenotypes. Here the authors show that acetyl-CoA restores primary cilia and improves cerebellar defects in Hsd17B4-deficient models, suggesting a potential therapeutic strategy.

Ji-Eun Bae
Soyoung Jang
Dong-Hyung Cho
ResearchOpen Access18 Mar 2025
Nature Communications

Volume: 16, P: 1-13
A mouse model for Zellweger syndrome

Myriam Baes
Pierre Gressens
Guy P. Mannaerts
Research01 Sept 1997
Nature Genetics

Volume: 17, P: 49-57
Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

A Janssen
M Baes
P P Van Veldhoven
Research01 Jan 2000
Laboratory Investigation

Volume: 80, P: 31-35
Spatiotemporal contact between peroxisomes and lipid droplets regulates fasting-induced lipolysis via PEX5

Lipid droplets are organelles that regulate lipid metabolism but if organellar contacts play a role during lipolysis is unclear. Here, the authors show that peroxisomes and peroxisomal protein PEX5 play pivotal roles in the spatial and temporal regulation of fasting-induced lipolysis by translocating ATGL onto lipid droplets

Jinuk Kong
Yul Ji
Jae Bum Kim
ResearchOpen Access29 Jan 2020
Nature Communications

Volume: 11, P: 1-16
Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation

Peter Carmeliet
Lieve Moons
Désiré Collen
Research01 Dec 1997
Nature Genetics

Volume: 17, P: 439-444
Oligodendroglial fatty acid metabolism as a central nervous system energy reserve

Brain functions require a constant supply of glucose. However, the brain energy stores are unclear. Here, the authors show that oligodendroglial fatty acid metabolism can be an energy reserve for white matter axons, supporting their function.

Ebrahim Asadollahi
Andrea Trevisiol
Klaus-Armin Nave
ResearchOpen Access09 Sept 2024
Nature Neuroscience

Volume: 27, P: 1934-1944
Correction: Corrigendum: Fatty acid carbon is essential for dNTP synthesis in endothelial cells

Sandra Schoors
Ulrike Bruning
Peter Carmeliet
Amendments and Corrections05 Aug 2015
Nature

Volume: 526, P: 144
Author Correction: Oligodendroglial fatty acid metabolism as a central nervous system energy reserve

Ebrahim Asadollahi
Andrea Trevisiol
Klaus-Armin Nave
Amendments and CorrectionsOpen Access17 Sept 2024
Nature Neuroscience

Volume: 27, P: 2046
Fatty acid carbon is essential for dNTP synthesis in endothelial cells

This study identifies a crucial role for fatty acid oxidation (FAO) in endothelial cells during angiogenesis, and reveals that fatty-acid-derived carbons are used for the de novo synthesis of nucleotides, and hence FAO stimulates vessel sprouting by increasing endothelial cell proliferation.

Sandra Schoors
Ulrike Bruning
Peter Carmeliet
Research01 Apr 2015
Nature

Volume: 520, P: 192-197
Axonal loss and neuroinflammation caused by peroxisome-deficient oligodendrocytes

Celia M Kassmann
Corinna Lappe-Siefke
Klaus-Armin Nave
Research22 Jul 2007
Nature Genetics

Volume: 39, P: 969-976
Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism

Julián Aragonés
Martin Schneider
Peter Carmeliet
Research06 Jan 2008
Nature Genetics

Volume: 40, P: 170-180
Constitutive IP₃ signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP₃ receptor disruptor BIRD-2

Mart Bittremieux
Rita M. La Rovere
Geert Bultynck
ResearchOpen Access13 Jun 2018
Cell Death & Differentiation

Volume: 26, P: 531-547
Immunogenic cell death and DAMPs in cancer therapy

In recent years a new concept of immunogenic cell death (ICD) has emerged. In this Review, the authors discuss the role of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) in regulating the immunogenicity of dying cancer cells and how this might relate to therapeutic intervention.

Dmitri V. Krysko
Abhishek D. Garg
Peter Vandenabeele
Reviews15 Nov 2012
Nature Reviews Cancer

Volume: 12, P: 860-875

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HSD17B4 deficiency causes dysregulation of primary cilia and is alleviated by acetyl-CoA

A mouse model for Zellweger syndrome

Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

Spatiotemporal contact between peroxisomes and lipid droplets regulates fasting-induced lipolysis via PEX5

Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation

Oligodendroglial fatty acid metabolism as a central nervous system energy reserve

Correction: Corrigendum: Fatty acid carbon is essential for dNTP synthesis in endothelial cells

Author Correction: Oligodendroglial fatty acid metabolism as a central nervous system energy reserve

Fatty acid carbon is essential for dNTP synthesis in endothelial cells

Axonal loss and neuroinflammation caused by peroxisome-deficient oligodendrocytes

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism

Constitutive IP₃ signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP₃ receptor disruptor BIRD-2

Immunogenic cell death and DAMPs in cancer therapy

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