CHFR antibody
- Known as:
- CHFR (anti-)
- Catalog number:
- orb100470
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CHFR antibody
Related genes to: CHFR antibody
- Gene:
- CHFR NIH gene
- Name:
- checkpoint with forkhead and ring finger domains
- Previous symbol:
- -
- Synonyms:
- FLJ10796, RNF196
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-14
- Date modifiied:
- 2017-12-06
Related products to: CHFR antibody
Related articles to: CHFR antibody
- Lung cancer (LC) is a well-known cause of cancer-related death worldwide. Early diagnosis of LC is an unmet need to improve the treatment response. In present study, we have analyzed the promoter methylation of a panel of genes in LC tissue and established tissue mirror biomarkers in plasma-derived circulating cell-free DNA (cfDNA). The mRNA expression of panel of genes ( and ) were analyzed in tumor tissue (TT) including Non-Small Cell Lung Cancer (NSCLC), and Small Cell Lung Cancer (SCLC) as compared to tumor-free tissue (TF) and correlated with gene promoter methylation in tissue-derived gDNA using methylation-specific PCR. The methylation analysis of genes were further analyzed in plasma-derived cfDNA of NSCLC and SCLC compared to healthy control. The methylation frequencies of and were significantly higher ( < 0.05 to < 0.001) in TT (59.45, 45.94 and 72.97%) compared to TF (21.42, 14.28 to 28.57%) respectively. Gene expressions in TT were down-regulated ( < 0.01) in contrast to TF and negatively correlated ( < 0.001) with hypermethylation, except which showed up-regulation with hypomethylation in TT of NSCLC. The methylation status in cfDNA exploits similar results as tissue sample, exhibited significant hypermethylation ( ≤ 0.05 to ≤ 0.001) in cfDNA of LC as compared to healthy control, and showed 58.33 to 76.47% positive predictive value and 51.47 to 66.33% negative predictive value. This study illustrated that gene promoter methylation analysis of the panel of genes in plasma samples has the potential for diagnosis of LC, and can be used as a tissue mirror biomarker. - Source: PubMed
Publication date: 2024/07/30
Karpathak SupriyaGarg RajivAhmad Mohammad KaleemSrivastava AnandQidwai TabishUbaid SabaSrivastav Anurag Kumar - Existing imaging and serum-marker assays miss many early liver cancers, especially in high-risk chronic liver disease carriers. We aimed to create a highly accurate, non-invasive, methylation-based liquid biopsy for early detection. - Source: PubMed
Zhang RuohanYang XinrongLi GuangmingDeng YinanLiu JibingGao HongjunZhao JieCheng JianwenZhao XiaofeiYang YangWu ZhenGu ShuangzhenWu YangMa ZhongyingLiu YanliKang YanZhou GuangpengLi HuaZhang YonghongHan XiaoliangFan JiaZhou JianDou KefengTao Kaishan - The link between neurodevelopment in infants exposed to maternal gestational diabetes mellitus (GDM) and fetal DNA methylation remains unexplored. We conducted this hypothesis-generating study to investigate the association between fetal DNA methylation and neurodevelopmental outcomes in children of mothers with GDM. We carried out a prospective, observational pilot cohort study comparing infants exposed to maternal GDM with an unexposed control group. Umbilical cord blood DNA methylation was assessed using targeted methylome sequencing covering 3.34 million CpG sites. Infant neurodevelopment was evaluated at age two years using the Bayley-III Scales. Bioinformatics processing identified differentially methylated regions (DMRs), followed by multiple enrichment analyses of DMR-associated genes and partial correlation analyses. Multi-dimensional enrichment analysis of the 1053 identified DMR-associated genes revealed a significant convergence of pathways related to neurogenesis, synaptic components, and axonal guidance. Infants born to mothers with GDM exhibited lower scores in cognitive, language, and motor domains, which were associated with identifiable DNA methylation signatures at birth. Significant correlations were observed in genes essential for brain scaffolding and synaptic circuitry, most notably , the alpha/beta clusters, and . Additionally, methylation patterns in and suggest a potential impact on blood-brain barrier integrity, while associations with and highlight a systemic metabolic 'cross-talk' influencing neurodevelopment. Although these pilot findings are hypothesis-generating and require further functional validation, this study provides pioneering evidence that neurodevelopmental alterations in the offspring of mothers with GDM are potentially associated with intrauterine epigenetic modifications detectable at birth. - Source: PubMed
Publication date: 2026/04/16
González-González Nieves LuisaArmas-González MarinaGonzález-Dávila EnriqueCastro-Conde José RamónGonzález-Campo CandelariaFlores CarlosLorenzo-Salazar José MiguelGonzález-Montelongo RafaelaMuñoz-Barrera AdriánPadrón-Pérez ErikaTascón-Padrón LauraOrribo-Morales Olivia - Palmitic acid (PA), a saturated fatty acid abundant in the diet and environment, has been closely associated with male reproductive dysfunction. However, the molecular basis of PA on the blood-testis barrier (BTB) disruption remains unclear. In this study, the chromatin remodeling factor SMARCD1 is identified as a key mediator of PA-induced testicular injury. PA exposure reduced the viability of Sertoli cells and Leydig cells, and markedly downregulated SMARCD1 expression. Although Smarcd1 haploinsufficient (Smarcd1) male mice maintained normal serum testosterone levels, they exhibited compromised BTB integrity in testicular tissue, as evidenced by reduced expression of the junctional markers ZO-1 and Cx43 in Sertoli cells. Importantly, PA exposure further aggravated BTB disruption in Smarcd1 mice, reflecting the impact of Smarcd1 gene heterozygous deletion on testicular barrier vulnerability under lipid stress. Mechanistically, PA can upregulate the expression of the E3 ligase CHFR, promote ubiquitination and degradation of SMARCD1 in Sertoli cells, thereby disrupting cellular junction function and BTB stability. Together, our findings confirm SMARCD1 as a key target of PA-induced male reproductive toxicity, reveal a previously unrecognized synergistic effect of epigenetic susceptibility and environmental lipid exposure, and suggest intervention directions for maintaining male reproductive health under lipid stress conditions. - Source: PubMed
Publication date: 2026/04/14
Liu YananChen YuanyuanZhang ChengchengMin ZiqianKang RongdaLiu NaYang LifangLi Dan - Vascular endothelial (VE)-cadherin is essential for maintaining endothelial junctional barrier integrity. The Angiopoietin-1 (Ang-1)/Tie2 axis induced Akt1 activation is crucial for maintaining endothelial junctional barrier by inhibiting FoxO1 and suppressing expression of Angiopoietin-2 (Ang-2), a Tie2 antagonist. Systemic inflammatory conditions such as sepsis, Akt1 expression is reduced, whereas FoxO1-dependent Ang-2 expression is increased, resulting in endothelial barrier dysfunction. We previously showed that the TLR4/FoxO1 axis induces the ubiquitin E3 ligase CHFR, which promotes endothelial barrier disruption by targeting VE-cadherin for ubiquitylation and degradation. However, little is known about Akt1 expression during vascular inflammation. Here, we identified FoxO1-dependent CHFR expression as a key mechanism driving K48-linked polyubiquitylation and proteasomal degradation of Akt1 in endothelial cells (EC). LPS-induced K -linked ubiquitylation of Akt1 was prevented in CHFR-depleted human EC and in endothelial-specific knockout ( ) mice. Accordingly, CHFR depletion increased Akt1 and VE-cadherin expression in both human lung EC and mice. mouse lungs also exhibited elevated Ang-1 and Tie2 expression, and Ang-1 stimulation induced sustained Akt1 phosphorylation in CHFR-deficient EC. Moreover, CHFR depletion prevented LPS-induced expression of FoxO1 and Ang-2 in EC. Mechanistically, CHFR interacted with phosphorylated Akt1 and mediated its ubiquitylation at lysine residues K30, K39, K154, and K268. Expression of a ubiquitylation-deficient Akt1 mutant prevented LPS-induced VE-cadherin degradation and vascular injury. Collectively, these findings identify CHFR as a critical regulator of endothelial inflammatory responses by controlling Akt1 stability and VE-cadherin expression during inflammation. - Source: PubMed
Publication date: 2026/03/31
Ansari Mohammad OwaisMo Gary C HJayathilaka LasanthiChen HuiMalik Asrar BTiruppathi Chinnaswamy