CHFR antibody Polyclonal Antibodies Primary antibodies
- Known as:
- CHFR (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100470
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CHFR antibody Polyclonal Antibodies Primary antibodies
Related genes to: CHFR antibody Polyclonal Antibodies Primary antibodies
- 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 Polyclonal Antibodies Primary antibodies
Related articles to: CHFR antibody Polyclonal Antibodies Primary antibodies
- 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
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