Ask about this productRelated genes to: PEX16 antibody
- Gene:
- PEX16 NIH gene
- Name:
- peroxisomal biogenesis factor 16
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-07
- Date modifiied:
- 2015-03-11
Related products to: PEX16 antibody
Related articles to: PEX16 antibody
- Pigmented diseases can significantly impact people's quality of life, with melanogenesis playing a key role. In this study, we first analysed the relationship between peroxisomes, peroxisomal biogenesis factor 16 (PEX16), and melanin synthesis using omics data and clinical samples. Our results showed that peroxisome function and PEX16 expression were negatively associated with melanogenesis. Overexpression of PEX16 in the melanin-producing MNT1 cell line resulted in an increase in peroxisome production and the inhibition of key genes related to melanogenesis, such as microphthalmia-associated transcription factor (MITF), tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1), and dopachrome tautomerase (DCT). Consistently, when PEX16 was overexpressed in melanocytes, there was a significant reduction in melanin content. The expression of PEX16 was detected in skin tissues. We found that PEX16 expression was higher in the areas with relatively lower pigmentation and decreased following ultraviolet B (UVB) irradiation. Furthermore, our findings suggest that PEX16 can inhibit melanogenesis by suppressing the Wnt/β-catenin signalling pathway. In conclusion, PEX16 can inhibit the Wnt/β-catenin signalling pathway, thereby reducing melanogenesis. Our research provides new insights for the clinical diagnosis and treatment of skin pigmentation disorders. - Source: PubMed
Duan XiaoleiHu YiboFu ChuhanChen JingHuang JinhuaDai XixiaZhao YuanyuanJiang LingZeng Qinghai - Thermal ablation (TA) (e.g., radiofrequency ablation [RFA]) is a critical curative therapy for hepatocellular carcinoma (HCC). However, the high recurrence rate of HCC after ablation remains a major clinical challenge. Hyperactive mRNA translation mediated by aberrant RNA modifications is vital for tumor heat stress adaptation. One of the most prevalent rRNA modifications is 18S rRNA N-methyladenosine (mA) modification catalyzed by methyltransferase 5 (METTL5); however, the role of METTL5-mediated rRNA modification in HCC recurrence after RFA remains unknown. Here, we found that the levels of METTL5 and 18S rRNA mA modification were significantly upregulated in post-RFA recurrent HCC and were further verified by insufficient RFA (iRFA) models in vitro and in vivo. Four mouse models, together with functional cell experiments, showed that METTL5 promoted HCC progression under heat stress. Mechanically, we demonstrated that heat-mediated METTL5 upregulation enhanced the PEX16 translation that promoted peroxisomal biogenesis and β-oxidation of very long-chain fatty acid, which promoted mitochondrial respiration to mediate HCC progression. Our study reveals the novel mechanistic insights in HCC recurrence after iRFA, demonstrating the important role of heat stress-mediated tumor metabolism adaptation by mRNA translation in HCC development. These findings identify METTL5 as a potential therapeutic target to prevent and treat HCC recurrence after TA. - Source: PubMed
Publication date: 2025/11/12
Xie ZonglinWang LinaWu YifanZhang YifanWang ShuoZeng XuezhenLiang RuimingLong JiantingGuo JianpingPeng SuiKuang MingLin ShuibinDai ZihaoChen Shuling - Peroxisomes are essential for the metabolism of very long-chain fatty acids (VLCFAs). Their biogenesis requires peroxins encoded by the PEX genes. While the significance of PEX14 has been established in the major rice pest the brown planthopper (Nilaparvata lugens), the role of PEX16 as a peroxisome biogenesis initiator remains uncharacterized in this pest. This study aimed to elucidate the functional importance of N. lugens PEX16 (NlPEX16) by comparing the impacts of disrupting NlPEX16 and NlPEX14. - Source: PubMed
Publication date: 2025/09/10
Liu YuqiongZhang QiqiangMao YiwenQiu ZhenghuiLin Xinda - Peroxisomal biogenesis disorders (PBD) are autosomal recessive diseases caused by mutations in specific PEX genes that impair peroxisome formation, leading to multi-systemic failure. Symptoms vary, even in patients with variants in the same PEX gene. Our goal is to select PEX mutations and use Drosophila to model a severity spectrum based on genotype-phenotype correlations. Utilizing KozakGAL4 (KZ) cassettes, we replaced the coding sequence of Pex with a GAL4 driver, ideal for making 'humanized' flies in which human PEX can replace the fly loss. We generated Pex2KZ and Pex16KZ lines and assessed them in various behavior assays, confirming their severe phenotypes. We performed rescue with human reference, variant PEX2 and PEX16 alleles, and phenotypic rescue was observed when human PEX2Ref or PEX16Ref were expressed in Pex2KZ or Pex16KZ flies, respectively. We identified a severity spectrum for PEX2 and PEX16 alleles, with some missense mutations exhibiting severity comparable to truncations. Alleles linked to mild PBD showed partial rescue, while variants associated with atypical ataxia could fully rescue. Drosophila humanization is an effective method to study the range of severity of PBD. - Source: PubMed
Publication date: 2025/07/28
Gomez Vanessa AKanca OguzJangam Sharayu VSrivastav SaurabhAndrews Jonathan CWangler Michael F - Peroxisomes are membranous organelles, and peroxisomal membrane protein 70 (PMP70), a peroxisome transporter, is used as a marker of peroxisomes. Like mitochondria, peroxisomes can also oxidize fatty acids and its rate limiting enzyme is acyl-CoA oxidase 1 (ACOX1). But unlike mitochondria, peroxisomes generate hydrogen peroxide (HO) by ACOX1, and the generated HO is locally detoxified by catalase. PPARα agonist WY-14,643 induces peroxisome proliferation as indicated by the induction of PMP70, ACOX1 and catalase were also induced. However, ACOX1 was induced to a greater extent than catalase. After WY-14,643 withdrawal, the induced ACOX1 started to decrease after 2 days; but catalase remained at higher levels up to10 days. While mRNA levels of ACOX1 were also induced by WY-14,643, mRNA levels of catalase were not induced by WY-14,643. In the livers collected from liver-specific PEX16 knockout (Pex16) mice, peroxisomes are absent but catalase and ACOX1 were somehow upregulated. The mRNA of ACOX1 was also spontaneously elevated, but the catalase mRNA was not changed. When PPARα was abrogated through crossing the Pex16 mice with Pparα mice to create the Pparα/Pex16 mice, the upregulated ACOX1 protein was suppressed in the Pparα/Pex16 mice, but catalase protein remained elevated. These results suggest that ACOX1 but not catalase is regulated by PPARα. - Source: PubMed
Publication date: 2025/06/25
Chen XueMazur AnnaXu WeiRisher W ChristopherDenning Krista LLu Yongke