PEX16

Last update 08 May 2025

Basic Info

Synonyms

Peroxin-16, peroxisomal biogenesis factor 16, Peroxisomal membrane protein PEX16

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Introduction

Required for peroxisome membrane biogenesis. May play a role in early stages of peroxisome assembly. Can recruit other peroxisomal proteins, such as PEX3 and PMP34, to de novo peroxisomes derived from the endoplasmic reticulum (ER). May function as receptor for PEX3.

100 Clinical Results associated with PEX16

100 Translational Medicine associated with PEX16

0 Patents (Medical) associated with PEX16

Literatures (Medical) associated with PEX16

01 Nov 2023·Free Radical Biology and Medicine

Under peroxisome proliferation acyl-CoA oxidase coordinates with catalase to enhance ethanol metabolism

Article

Author: Lu, Yongke ; Lawrence, Logan M ; Chen, Xue ; Wang, Xiaodong ; Denning, Krista L ; Mazur, Anna

In peroxisomes, acyl-CoA oxidase (ACOX) oxidizes fatty acids and produces H₂O₂, and the latter is decomposed by catalase. If ethanol is present, ethanol will be oxidized by catalase coupling with decomposition of H₂O₂. Peroxisome proliferator-activated receptor α (PPARα) agonist WY-14,643 escalated ethanol clearance, which was not observed in catalase knockout (Cat^-/-) mice or partially blocked by an ACOX1 inhibitor. WY-14,643 induced peroxisome proliferation via peroxin 16 (PEX16). PEX16 liver-specific knockout (Pex16^Alb-Cre) mice lack intact peroxisomes in liver, but catalase and ACOX1 were upregulated. Due to lacking intact peroxisomes, the upregulated catalase and ACOX1 in the Pex16^Alb-Cre mice were mislocated in cytosol and microsomes, and the escalated ethanol clearance was not observed in the Pex16^Alb-Cre mice, implicating that the intact functional peroxisomes are essential for ACOX1/catalase to metabolize ethanol. Alcohol-associated liver disease (ALD) is a spectrum of liver disorders ranging from alcoholic steatosis to steatohepatitis. WY-14,643 ameliorated alcoholic steatosis but tended to enhance alcoholic steatohepatitis. In mice lacking nuclear factor erythroid 2-related factor 2 (Nrf2^-/-), WY-14,643 still induced PEX16, ACOX1 and catalase to escalate ethanol clearance and blunt alcoholic steatosis, which was not observed in the PPARα-absent Nrf2^-/- mice (Pparα^-/-/Nrf2^-/-) mice, suggesting that WY-14,643 escalates ethanol clearance through PPARα but not through Nrf2.

20 Jun 2023·Cellular and molecular life sciences : CMLS

Loss of functional peroxisomes leads to increased mitochondrial biogenesis and reduced autophagy that preserve mitochondrial function.

Article

Author: Leung, Sharon ; Vissa, Miluska ; Chi, Lijun ; Lee, Dorothy ; Brumell, John H ; Bandsma, Robert H J ; Kim, Peter K ; Li, Ren ; Hu, Guanlan ; Delgado-Olguin, Paul ; Wen, Bijun

Peroxisomes are essential for mitochondrial health, as the absence of peroxisomes leads to altered mitochondria. However, it is unclear whether the changes in mitochondria are a function of preserving cellular function or a response to cellular damage caused by the absence of peroxisomes. To address this, we developed conditional hepatocyte-specific Pex16 deficient (Pex16 KO) mice that develop peroxisome loss and subjected them to a low-protein diet to induce metabolic stress. Loss of PEX16 in hepatocytes led to increased biogenesis of small mitochondria and reduced autophagy flux but with preserved capacity for respiration and ATP capacity. Metabolic stress induced by low protein feeding led to mitochondrial dysfunction in Pex16 KO mice and impaired biogenesis. Activation of PPARα partially corrected these mitochondrial disturbances, despite the absence of peroxisomes. The findings of this study demonstrate that the absence of peroxisomes in hepatocytes results in a concerted effort to preserve mitochondrial function, including increased mitochondrial biogenesis, altered morphology, and modified autophagy activity. Our study underscores the relationship between peroxisomes and mitochondria in regulating the hepatic metabolic responses to nutritional stressors.

24 Jan 2023·Proceedings of the National Academy of SciencesQ1 · CROSS-FIELD

The ASH1–PEX16 regulatory pathway controls peroxisome biogenesis for appressorium-mediated insect infection by a fungal pathogen

Q1 · CROSS-FIELD

Article

Author: Cao, Xuan ; Wang, Sibao ; Zheng, Yitong ; Lai, Yiling ; Li, Fang ; Wang, Lili ; Zheng, Weilu ; Wei, Gang ; Chen, Jingjing ; Dong, Ling

Entomopathogenic fungi infect insects by penetrating through the cuticle into the host body. To breach the host cuticle, some fungal pathogens produce specialized infection cells called appressoria, which develop enormous turgor pressure to allow cuticle penetration. However, regulatory mechanisms underlying appressorium turgor generation are poorly understood. Here, we show that the histone lysine methyltransferase ASH1 in the insecticidal fungus Metarhizium robertsii , which is strongly induced during infection of the mosquito cuticle, regulates appressorium turgor generation and cuticle penetration by activating the peroxin gene Mrpex16 via H3K36 dimethylation. MrPEX16 is required for the biogenesis of peroxisomes that participate in lipid catabolism and further promotes the hydrolysis of triacylglycerols stored in lipid droplets to produce glycerol for turgor generation, facilitating appressorium-mediated insect infection. Together, the ASH1–PEX16 pathway plays a pivotal role in regulating peroxisome biogenesis to promote lipolysis for appressorium turgor generation, providing insights into the molecular mechanisms underlying fungal pathogenesis.

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PEX16

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