C1orf85 ELISA kit
- Known as:
- C1orf85 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-C1orf85-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- C1orf85 ELISA kit
Related genes to: C1orf85 ELISA kit
- Gene:
- GLMP NIH gene
- Name:
- glycosylated lysosomal membrane protein
- Previous symbol:
- C1orf85
- Synonyms:
- MGC31963, NCU-G1
- Chromosome:
- 1q22
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-27
- Date modifiied:
- 2015-01-09
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- Low-grade glioma (LGG) is a highly heterogeneous tumor, and this study aims to develop a metabolism-based classifier to identify patients with distinct prognostic risks and treatment responses for precision therapy. We utilized gene expression profiles, mutation, and clinical data from the TCGA-LGG cohort. Unsupervised clustering was applied to identify metabolism subtypes, and differences in clinical features, survival, and drug sensitivity were analyzed. Four key feature genes—SNAP91, TAGLN2, GLMP, and MCUB—were identified through machine learning, and an artificial neural network (ANN) classifier was constructed to accurately classify LGG patients into two metabolism subtypes. The results revealed significant differences in gene expression profiles and mutational landscapes between the subtypes. The metabolism subtype is a clinically independent prognostic predictor of LGG, subtype C2 has a poorer prognosis. Drug sensitivity analysis showed that subtype C2 had lower 50% inhibitory concentration(IC50) and area under curve(AUC) values for TMZ. Subsequent experimental validation revealed that high expression of TAGLN2 drove tumor progression by reprogramming cellular metabolism, including enhancing oxidative phosphorylation and activating the PI3K/Akt signaling pathway in LGG cells. Our findings highlight the potential of metabolism subtyping as a tool for precision treatment strategies in LGG. - Source: PubMed
Publication date: 2026/04/21
Tan YiqiZeng LeZhang GanghuaFang JianingYin ZhijingDeng WenzhiCao KeJiang Jiaode - Glucosamine (GlcN) is an essential amino monosaccharide widely used in pharmaceuticals, nutraceuticals, and cosmetics. Microbial fermentation presents a sustainable alternative to its traditional chemical production. However, in , competitive carbon flux towards ethanol significantly limits GlcN yields. In this study, an strain for GlcN biosynthesis was engineered by integrating heterologous (glucosamine-6-phosphate deaminase) and (glucosamine-6-phosphate phosphatase) genes. To redirect carbon flux, the pyruvate decarboxylase genes , 5, and were sequentially knocked out using the Clustered Regularly Interspaced Short Palindromic Repeats Cas9 (CRISPR-Cas9) approach, generating strains , , and . achieved a GlcN titer of 2.20 ± 0.11 g/L, a 1.54-fold increase over the parental strain, while its ethanol yield decreased by 26%. This enhancement was achieved without significantly affecting cell growth or glucose consumption. Comparative transcriptomics between the triple-knockout and parental yeasts revealed 892 differentially expressed genes. Pathways related to glycolysis and ethanol formation were predominantly downregulated, whereas pathways potentially supporting GlcN synthesis were upregulated. The engineered strain demonstrated high genetic stability over 50 generations. Our findings demonstrate that disrupting ethanol formation is an effective strategy to enhance GlcN production in , providing valuable insights for carbon flux redistribution. - Source: PubMed
Publication date: 2026/03/30
Ke MingsiZheng XinyueFeng JiaqiCheng JieshunYang Peizhou - Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) restricts the long-term efficacy of treatment in patients with lung cancer. Here, we report that the EGFR-TKI resistance mechanism is mediated by lysosome-related regulation. The overexpression of glycosylated lysosomal membrane protein (GLMP), a lysosomal membrane protein, promotes resistance to Osimertinib both in vitro and in vivo. Mechanistically, GLMP could regulate the ubiquitination of RhoA and promote resistance by activating the epithelial-mesenchymal transition (EMT), which involves the RhoA pathway and activates the late stage of autophagy. Inhibition of the RhoA pathway alone enhances the initiation stage of autophagy. Lysosomal hyperactivity in TKI-resistant cells sustains the flow of autophagy. Therefore, the combined inhibition of the RhoA pathway and autophagy can effectively attenuate EGFR-TKI resistance. Our findings provide a potential therapeutic strategy to overcome resistance to EGFR-TKIs. - Source: PubMed
Publication date: 2025/11/26
Liang XiaoXu JialiShu SuhuiLv WeiYin DandanMiao SunanLu XiyiZhang ChenLiu XinyinDai JialiLi JunWu WeibingZhang ErbaoGuo Renhua - Glucosamine (GlcN) is a high-value compound with significant health applications. GlcN is widely used in the food and health industry as a food additive or functional food. The development of a green, efficient, and safe method for GlcN production is of great significance due to the complexity of traditional production methods, environmental pollution, and sensitization of raw materials. In this study, genes , , , , and were knocked out using the Clustered Regularly Interspaced Short Palindromic Repeats Cas9 (CRISPR-Cas9) method. In addition, three key enzyme genes, glucosamine-6-phosphate deaminase , glucosamine-6-phosphate phosphatase , and ammonium transporter , were introduced to construct engineered strains for GlcN synthesis in the presence of high-concentration inorganic ammonium ions. The results indicated that HPG5 with , , and integration and simultaneous deletion of , , , , and achieved the highest GlcN yield (1.95 ± 0.02 g/L) during fermentation with 10 g/L (NH)SO, which was 2.47-fold higher than the control. The conversion rate of glucose to GlcN in HPG5 was 9.75% in liquid YPD medium containing 20 g/L of glucose and 10 g/L of (NH)SO. Thus, the results indicated that HPG5 could effectively produce GlcN in the presence of high-concentration ammonium sulphate. This study provides a promising alternative, HPG5, for GlcN production. - Source: PubMed
Publication date: 2025/08/10
Yang PeizhouKe MingsiFeng JiaqiZheng ZhiJiang Shaotong - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which drove the 2019 coronavirus disease (COVID-19) pandemic, continues to engender inquiries into the role of host genetic factors in disease susceptibility. Despite the identification of over 1,000 genes potentially associated with SARS-CoV-2 and COVID-19, the mechanisms connecting genetic variants to phenotype remain elusive. To shed light on these mechanisms, we undertook an integrated analysis, merging data from whole genome association analyses of COVID-19 with methylome and transcriptomic. The study includes African American adults from the GENE-FORECAST study, encompassing 371 individuals with whole genome sequencing (WGS), 203 with DNA methylation, and 321 with RNA sequencing (RNA-Seq) of blood. About 53.3% of participants reported COVID-19. Significant loci associated with COVID-19 were examined within the framework of methylation quantitative trait loci (mQTL), which are located near the gene-of-orig (-mQTL) and expression quantitative trait loci (eQTL), which are located near the gene-of-origin (-eQTL), enabling analysis to assess mediators between genetic variants and COVID-19 status. Our analysis identified four intronic variants and confirmed a missense variant, rs1052067, in associated with COVID-19. Causal mediation analysis revealed that the combination of genetic variants within , epigenomics, and transcriptomics mapped four pathways influencing COVID-19 status. These pathways include: rs9659072→DNAm at chr1:156285845 (annotated to )→ENSG00000198715:13 (annotated to glycosylated lysosomal membrane protein, ); rs12083543→DNAm at chr1:155951748 ()→ENSG00000198715:13 (); rs1052067→DNAm at chr1:155951748 ()→ENSG00000198715:13 (); rs1543294→ENSG00000198715:13 ()→DNAm at chr1:156077518 (). Through integrated multiomics analyses, we identified genetic variants whose effects on COVID-19 susceptibility are mediated by changes in DNA methylation and mRNA expression. These findings offer insights into potential mechanistic pathways that merit further exploration. The study investigates host genetic factors influencing COVID-19 susceptibility by integrating WGS, epigenomics, and transcriptomic data. It identified that PMF1 is linked to COVID-19. Mediation analysis revealed that genetic variants in PMF1 affect COVID-19 status via combinations of one transcript (annotated to GLMP) and three DNAm sites (annotated to ARHGEF2, TMEM79, MEX3A). The findings highlight the role of lysosomal pathways and transmembrane proteins in disease susceptibility, offering new insight into potential therapeutic targets for COVID-19. - Source: PubMed
Publication date: 2025/07/01
Chen GuanjieDeRoo Lisa AGoodney GabrielDoumatey Ayo PZhou JieAdeyemo Adebowale ARotimi Charles NGaye Amadou