Ask about this productRelated genes to: PEX11G antibody
- Gene:
- PEX11G NIH gene
- Name:
- peroxisomal biogenesis factor 11 gamma
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-14
- Date modifiied:
- 2014-11-19
Related products to: PEX11G antibody
Related articles to: PEX11G antibody
- Colorectal cancer (CRC) is a significant global health burden, with current treatment strategies often limited by the TNM classification system's inability to fully capture tumor heterogeneity. This study aims to explore the biological functions and prognostic value of differentially expressed ferroptosis-related long non-coding RNAs (DEFRlncRNAs) in CRC. - Source: PubMed
Publication date: 2025/04/29
Ge XiaoxuXu JiashengHe JinjieWang JianQian Yucheng - The high-protein diet (HPD) has emerged as a potent dietary approach to curb obesity. Peroxisome, a highly malleable organelle, adapts to nutritional changes to maintain homeostasis by remodeling its structure, composition, and quantity. However, the impact of HPD on peroxisomes and the underlying mechanism remains elusive. Using Drosophila melanogaster as a model system, we discovered that HPD specifically increases peroxisome levels within the adipose tissues. This HPD-induced peroxisome elevation is attributed to cysteine and methionine by triggering the expression of CG33474, a fly homolog of mammalian PEX11G. Both the overexpression of Drosophila CG33474 and human PEX11G result in increased peroxisome size. In addition, cysteine and methionine diets both reduce lipid contents, a process that depends on the presence of CG33474. Furthermore, CG33474 stimulates the breakdown of neutral lipids in a cell-autonomous manner. Moreover, the expression of CG33474 triggered by cysteine and methionine requires TOR signaling. Finally, we found that CG33474 promotes inter-organelle contacts between peroxisomes and lipid droplets (LDs), which might be a potential mechanism for CG33474-induced fat loss. In summary, our findings demonstrate that CG33474/PEX11G may serve as an essential molecular bridge linking HPD to peroxisome dynamics and lipid metabolism. - Source: PubMed
Publication date: 2024/04/22
Liu MengHe Li - Obesity is an established risk factor for hypertension, but the mechanisms are only partially understood. We examined whether body mass index (BMI)-related DNA methylation (DNAm) variation would mediate the association of BMI with blood pressure (BP). We first conducted a genomewide DNA methylation analysis in monozygotic twin pairs to detect BMI-related DNAm variation and then evaluated the mediating effect of DNAm on the relationship between BMI and BP levels using the causal inference test (CIT) method and mediation analysis. Ontology enrichment analysis was performed for CpGs using the GREAT tool. A total of 60 twin pairs for BMI and systolic blood pressure (SBP) and 58 twin pairs for BMI and diastolic blood pressure (DBP) were included. BMI was positively associated with SBP (β = 1.86, = .0004). The association between BMI and DNAm of 85 CpGs reached < 1×10 level. Eleven BMI-related differentially methylated regions (DMRs) within , , , , , , , , , and were found. Of the 85 CpGs, 9 mapped to , , , , , and were significantly associated with SBP levels. Of the 9 CpGs, 2 within negatively mediated the association between BMI and SBP, with a mediating effect of -0.24 (95% CI [-0.65, -0.01]). BMI was also positively associated with DBP (β = 0.60, = .0495). The association between BMI and DNAm of 193 CpGs reached < 1×10 level. Twenty-five BMI-related DMRs within , , , , , , and were found. Of the 193 CpGs, 33 mapped to , , , , , , and were significantly associated with DBP levels. Of the 33 CpGs, 12 within , , , , , , and negatively mediated the association between BMI and DBP, with a total mediation effect of -0.66 (95% CI [-1.07, -0.30]). Interestingly, BMI might also negatively mediate the association between the DNAm of most CpG mediators mentioned above and BP. The mediating effect of DNAm was also found when stratified by sex. In conclusion, DNAm variation may partially negatively mediate the association of BMI with BP. Our findings may provide new clues to further elucidate the pathogenesis of obesity to hypertension and identify new diagnostic biomarkers and therapeutic targets for hypertension. - Source: PubMed
Publication date: 2024/01/31
Yao JieNing FengWang WeijingZhang Dongfeng - Mevalonate kinase deficiency (MKD) is an autosomal recessive auto‑inflammatory disease, caused by impairment of the mevalonate pathway. Although the molecular mechanism remains to be elucidated, there is clinical evidence suggesting that other regulatory genes may be involved in determining the phenotype. The identification of novel target genes may explain non‑homogeneous genotype‑phenotype correlations, and provide evidence in support of the hypothesis that novel regulatory genes predispose or amplify deregulation of the mevalonate pathway in this orphan disease. In the present study, DNA samples were obtained from five patients with MKD, which were then analyzed using whole exome sequencing. A missense variation in the PEX11γ gene was observed in homozygosis in P2, possibly correlating with visual blurring. The UNG rare gene variant was detected in homozygosis in P5, without correlating with a specific clinical phenotype. A number of other variants were found in the five analyzed DNA samples from the MKD patients, however no correlation with the phenotype was established. The results of the presents study suggested that further analysis, using next generation sequencing approaches, is required on a larger sample size of patients with MKD, who share the same MVK mutations and exhibit 'extreme' clinical phenotypes. As MVK mutations may be associated with MKD, the identification of specific modifier genes may assist in providing an earlier diagnosis. - Source: PubMed
Publication date: 2016/02/22
Marcuzzi AnnalisaVozzi DiegoGirardelli MartinaTricarico Paola MauraKnowles AlessandraCrovella SergioVuch JosefTommasini AlbertoPiscianz ElisaBianco Anna Monica - Insulin receptors have been demonstrated to be involved in embryogenesis, food intake regulation and glucose metabolism in several fish, while more researchis needed for further understanding. In this study, the complete coding sequence (CDS) of insulin receptor a (insra) gene and insulin receptor b (insrb) gene in grass carp were obtained, the CDS were 4068 bp and 4514 bp in length, encoding 1355 aa protein and 1351 aa protein. Both of insra and insrb in grass carp showed high amino acid identities with other fish. Insra and insrb genes were widely expressed in all tested tissues with an overlapping but distinct expressions. The high levels of insra mRNA were distributed in hindgut and heart tissues. The insrb gene showed the highest expression levels in liver and hindgut. We also proved that two forms of grass carp insulin receptors participate in the regulation of blood glucose and might act differently. Phylogenetic analysis confirmed that different isoforms of fish insulin receptors are derived from two distinct genes, which was inconsistent with the generation of mammalian insulin receptors. Synteny analyses of insulin receptor genes showed that genes surrounding the insulin receptor genes were conserved in fish. Arhgef18, PEX11G, humanC19orf45 genes were highly conserved among mammal species. However, no conserved synteny was observed among fish, mammals, avians and amphibians. - Source: PubMed
Publication date: 2016/01/06
Cai WenjingLiang Xu-fangYuan XiaochenLi AixuanHe YuhuiHe Shan