Ask about this productRelated genes to: PEX11A antibody
- Gene:
- PEX11A NIH gene
- Name:
- peroxisomal biogenesis factor 11 alpha
- Previous symbol:
- -
- Synonyms:
- PEX11-ALPHA, MGC119947, MGC138534
- Chromosome:
- 15q26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-11
- Date modifiied:
- 2015-03-11
Related products to: PEX11A antibody
Related articles to: PEX11A antibody
- Peroxisomes are eukaryotic organelles that compartmentalize crucial metabolic reactions. Peroxisome size, shape, and number are governed by the peroxisomal membrane protein PEX11. PEX11 is encoded in multiple isoforms across diverse eukaryotes, including five in Arabidopsis, but the functional distinctions among these isoforms are largely uncharacterized. Here we report null pex11 mutants in plants expressing reporters that mark peroxisome membranes and lumen to illuminate distinct functions for PEX11 isoforms. We find that PEX11C/D/E promotes the formation of peroxisomal intralumenal vesicles, limits peroxisome size throughout development, and is required for efficient fatty acid β-oxidation in germinating seedlings. Unlike the pervasive roles of PEX11C/D/E, we find that PEX11A/B promotes the formation of peroxisomal intralumenal vesicles and limits peroxisome enlargement specifically during seedling lipid mobilization. Complete loss of the PEX11 family confers seedling lethality, even though peroxisomes remain abundant. Our findings reveal that Arabidopsis PEX11 isoforms shape internal peroxisome membranes and have distinct functions in cellular physiology that are essential for plant development. These results extend the roles of PEX11 beyond its canonical function in peroxisome division. - Source: PubMed
Publication date: 2026/04/21
Tharp Nathan EAn ChelseaHwang JamesShad Nayeli SWright Zachary JBartel Bonnie - Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c), a 16-amino acid mitochondrial-derived peptide, regulates cellular metabolism through AMPK and mTOR signaling and exerts protective effects across multiple endocrine tissues. However, its role in adrenal physiology remains unexplored. We hypothesized that MOTS-c establishes "steroidogenic readiness" by priming metabolic pathways rather than directly activating hormone synthesis. - Source: PubMed
Publication date: 2026/03/11
Blatkiewicz MalgorzataKaminski KacperSobalska-Kwapis MartaSzyszka MartaOlechnowicz AnnaJopek KarolRucinski Marcin - Peroxisomal biogenesis defects frequently trigger processes of remodeling, increased oxidative stress and metabolic dysregulations that cause cellular dysfunction. Despite extensive research into cardiomyocyte ultrastructure and metabolism, knowledge on peroxisomal function in these cells is scarce. The objective of this study was therefore to investigate the impact of the purportedly asymptomatic (mild) deficiency of the peroxisomal biogenesis protein PEX11a on cardiomyocyte structure and cardiac function in mice. Langendorff-reperfusion experiments revealed diminished post-ischemic recovery following knockout suggesting compromised cardiac response to ischemic stress. The suboptimal recovery might be attributable to increased ischemia-induced tissue deterioration consequent to morphological and metabolic abnormalities of the cardiomyocytes. Indeed, several alterations were observed in these cells in knockout mice: (i) augmented size and number of peroxisomes and lipid droplets; (ii) increased sarcomere length; (iii) altered gene expression of peroxisome proliferator-activated receptors, organellar fission machinery proteins and cardiac markers; and (iv) a lipid composition shift. We hypothesized that peroxisomes contribute to the preservation of cardiomyocyte structure and functionality under conditions of ischemia-reperfusion. We further proposed that even "mild", undiagnosed peroxisomal defects can significantly impact cardiac performance following ischemia. This poses novel challenges for the risk assessment of cardiac pathologies. - Source: PubMed
Publication date: 2025/12/20
Colasante ClaudiaChen JiangpingGarikapati VannuruswamySpengler BernhardSchlüter Klaus-DieterBaumgart-Vogt Eveline - Male infertility is a growing global health concern increasingly linked to environmental exposure to endocrine-disrupting chemicals (EDCs). However, the specific molecular mechanisms by which EDCs contribute to impaired reproductive function remain unclear. In this study, we systematically identified EDC-related genes using curated chemical-gene interaction databases and assessed their causal roles in male infertility through Mendelian randomization (MR) and colocalization analyses, utilizing large-scale cis-eQTL and GWAS datasets. A total of six genes, RHEB, PARP1, SLTM, PLIN1, PEX11A, and SDCBP, showed strong evidence of causal relationships and shared genetic variants associated with both gene expression and infertility traits. Single-cell RNA sequencing of human testicular tissue revealed that these genes are predominantly expressed in germ cells and are significantly dysregulated in non-obstructive azoospermia (NOA) samples, supporting their functional relevance. Additionally, environmental mapping indicated that several widely encountered EDCs, including bisphenol A (BPA) and its analogs, triphenyl phosphate (TPP), and sodium arsenite, interact with multiple candidate genes. These findings provide mechanistic insight into how chemical exposures can dysregulate gene expression in testicular cells and contribute to male infertility, highlighting the need for targeted environmental risk assessments and regulatory strategies. - Source: PubMed
Publication date: 2025/07/22
Hong YanggangWang YirongLi JiajunShu WanyiChen HaolinChen Congde - Highland barley (HB) consumption offers numerous health benefits; however, its impact on glycolipid metabolism abnormalities induced by a high-fat diet remains unclear. Consequently, this study aimed to investigate the therapeutic effects and underlying molecular mechanisms of HB in the context of obesity; Rats were fed either a high-fat diet (HFD) to induce obesity or a standard diet (SD) for six weeks. The rats in the HFD group were randomly assigned into five groups: HFD+HFD, HFD+SD, and low (30%), medium (45%), and high (60%) doses of the HB diet for an additional ten weeks. Analyses of serum lipid profiles, liver histology, transcriptomes, and untargeted metabolomes were conducted; HB intake resulted in decreased weight gain, reduced feed intake, lower serum triglyceride and cholesterol levels, and diminished hepatic lipid accumulation. It also improved insulin and fasting blood glucose levels, and antioxidant capacity in the HFD-fed rats. Transcriptome analysis revealed that HB supplementation significantly suppressed the HFD-induced increase in the expression of Angptl8, Apof, CYP7A1, GDF15, Marveld1, and Nr0b2. Furthermore, HB supplementation reversed the HFD-induced decrease in Pex11a expression. Untargeted metabolome analysis indicated that HB primarily influenced the pentose phosphate pathway, the Warburg effect, and tryptophan metabolism. Additionally, integrated transcriptome and metabolome analyses demonstrated that the treatments affected the expression of genes associated with glycolipid metabolism, specifically ABCG8, CYP2C12, CYP2C24, CYP7A1, and IRS2. Western blotting confirmed that HB supplementation impacted the IRS2/PI3K/AKT signaling pathway; HB alleviates HFD-induced obesity and liver injury in an obese rat model possibly through the IRS2/PI3K/Akt signaling pathway. - Source: PubMed
Publication date: 2024/10/17
Shi XiaodongSong WeiJiang BoyueMa JieLi WanyangSun MingyaoCui HongyuanChen Wei