Ask about this productRelated genes to: PEX10 antibody
- Gene:
- PEX10 NIH gene
- Name:
- peroxisomal biogenesis factor 10
- Previous symbol:
- -
- Synonyms:
- RNF69
- Chromosome:
- 1p36.32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-05
- Date modifiied:
- 2015-08-25
Related products to: PEX10 antibody
Related articles to: PEX10 antibody
- Objectives Myocardial ischemia-reperfusion (I / R) injury is a major clinical challenge, largely caused by oxidative stress-induced cardiomyocyte death. Ferroptosis, an iron-dependent form of regulated cell death, plays a key role in this process, but its upstream modulators remain unclear. This study aimed to investigate the role of PEX10, a peroxisomal biogenesis factor, in ferroptosis during myocardial I / R injury.Material and methods Peroxisome biogenesis factor 10 (PEX10) expression was analyzed in the GSE4105 dataset and validated in H9c2 cells subjected to oxygen-glucose deprivation / reoxygenation (OGD / R). PEX10 was silenced using siRNA, and cell viability, oxidative stress, iron accumulation, and ferroptosis-related markers were measured. Glutathione peroxidase 4 (GPX4) transcriptional regulation was examined, and rescue experiments were conducted using the GPX4 inhibitor RSL3. Ferrostatin-1 was used to pharmacologically inhibit ferroptosis.Results PEX10 was significantly upregulated in I / R-injured myocardium and OGD / R-treated cardiomyocytes. PEX10 knockdown improved cell viability and reduced oxidative stress, iron accumulation, and ferroptosis markers. Mechanistically, PEX10 suppressed GPX4 transcription, and the protective effects of its silencing were partially reversed by RSL3 (RAS-selective lethal). Ferrostatin-1 mimicked the protective effects of PEX10 knockdown.Conclusion PEX10 acts as a previously unrecognized mediator of ferroptosis by repressing GPX4 transcription. Targeting the PEX10-GPX4 axis may provide a promising therapeutic strategy for mitigating myocardial I / R injury. - Source: PubMed
Publication date: 2026/04/02
Li JingMa Xiaofeng - Heimler syndrome is an ultra-rare autosomal recessive disorder belonging to the spectrum of peroxisomal disorders. Heimler syndrome is characterized by sensorineural hearing loss, retinal dystrophy and dental anomalies. It is caused by hypomorphic mutations in peroxisomal biogenesis genes, namely PEX1, PEX6, PEX26, and PEX10. Fewer than 30 cases have been reported to date.We report the case of a male infant born at 36 weeks of gestation with congenital bilateral sensorineural hearing loss, confirmed by abnormal auditory brainstem responses and managed with early bilateral cochlear implantation. Poor visual behavior led to ophthalmologic evaluation, which revealed a "salt-and-pepper" appearance of the peripheral retina and markedly attenuated retinal vessels. Full-field electroretinogram (ffERG) responses were severely reduced and optical coherence tomography revealed abnormal retinal layering. Whole-exome sequencing in trio identified two novel compound heterozygous variants in PEX26.This case broadens the phenotypic and genotypic spectrum of peroxisome biogenesis disorder linked with PEX26, manifesting as Heimler syndrome. The discovery of two novel PEX26 variants contributes to the mutational landscape of peroxisomal biogenesis disorders and underscores the diagnostic value of early ophthalmologic and genetic screening in children with congenital hearing loss. - Source: PubMed
Publication date: 2026/03/29
Aziz AuroreBernard-Cuisinier TristanDenis DanieleDavid ThierryDefoort-Dhellemes SabineMeunier IsabelleGrunewald OlivierSmirnov Vasily - Peroxisomes import all matrix proteins post-translationally from the cytosol, a process that requires recycling of cargo receptors across the peroxisomal membrane. The membrane-embedded ubiquitin ligase, composed of Pex2, Pex10, and Pex12, is central to this process, but its mechanism remains unclear. Here we determined cryo-electron microscopy structures of the Pex2-10-12 complex in closed and open states bound to Pex8, an essential factor of previously undefined function. The structures reveal how Pex2-10-12 gates its retro-translocation pore to control receptor entry and how the closed-to-open transition repositions the Pex10 RING domain to enable receptor mono-ubiquitination. Pex8 docks onto Pex2-10-12 from the matrix and guides receptors into the pore. Functional analyses show that the receptor's N-terminal segment downstream of its mono-ubiquitination site initiates a loop insertion into the pore. These findings establish how Pex2-10-12 coordinates receptor recognition, retro-translocation, and ubiquitination, providing the molecular basis for receptor recycling in peroxisomal protein import. - Source: PubMed
Publication date: 2026/03/20
Dempsey Nathaniel W MWang LaurieGao NingjianZhao KangtingCope JessicaPark Eunyong - - Source: PubMed
Publication date: 2026/02/07
Onder HalilKablan AhmetErdem Haktan Bagis - MYB transcription factors play a crucial regulatory role in plant growth and stress response. The gene , obtained from , a dominant lichen in the Tengger Desert, was transferred to creeping bentgrass to explore its effects on plant growth and response to abiotic stress. - Source: PubMed
Publication date: 2025/12/29
Ai YeLiu JielinChen YinglongQian XuChen JiabaoLi JiaxingXu LixinSun XinboRan FuHan LiebaoChao Yuehui