TRIM67 Antibody (C-term)
- Known as:
- TRIM67 Antibody (C-terminus)
- Catalog number:
- AP10325b-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- TRIM67 Antibody (C-term)
Related genes to: TRIM67 Antibody (C-term)
- Gene:
- TRIM67 NIH gene
- Name:
- tripartite motif containing 67
- Previous symbol:
- -
- Synonyms:
- TNL
- Chromosome:
- 1q42.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-19
- Date modifiied:
- 2014-11-19
Related products to: TRIM67 Antibody (C-term)
Related articles to: TRIM67 Antibody (C-term)
- Propofol, an intravenous anesthetic, exhibits cerebroprotective effects against cerebral infarction (CI); however, its underlying mechanisms, particularly those involving ferroptosis, remain incompletely understood. This study employed oxygen-glucose deprivation/reperfusion (OGD/R)-treated SK-N-SH cells and middle cerebral artery occlusion (MCAO) rat models to investigate propofol's actions in vitro and in vivo. Propofol alleviated OGD/R-induced neuronal injury by enhancing cell viability, suppressing apoptosis, and reducing the release of inflammatory cytokines interleukin-6 (IL-6) and IL-1β. Importantly, propofol significantly suppressed ferroptosis, as evidenced by decreased levels of reactive oxygen species (ROS), Fe, and malondialdehyde (MDA), as well as restored mitochondrial membrane potential. Mechanistically, propofol up-regulated the expression of tripartite motif-containing 67 (TRIM67), which bound to voltage-dependent anion channel 1 (VDAC1), promoting its K63-linked polyubiquitination and proteasomal degradation. Conversely, VDAC1 overexpression or TRIM67 knockdown reversed the protective effects of propofol. Consistent with the in vitro results, propofol reduced cerebral infarct volume, improved neurological function, and suppressed neuroinflammation, effects that were concomitant with increased TRIM67 and decreased VDAC1 protein expression in brain tissues. In conclusion, this study reveals the TRIM67/VDAC1 pathway as a novel mechanism underlying propofol's cerebroprotective effects, thereby identifying a potential therapeutic target for CI. - Source: PubMed
Jia WangLiu YinhuaLiu ZhongyuSun Donghui - Hepatocellular carcinoma (HCC) remains a significant health concern, given its rising incidence and the increasing complexity associated with its management. The exploration of novel intervention approaches, particularly in the realm of specific biological target therapy, underscores the imperative to identify new biological targets associated with HCC. - Source: PubMed
Publication date: 2026/04/27
Zhou ZhuangZhang Shi-YiJiang Ying-SongPeng Da-DiHuang Zuo-TianLi Kai-LiZong Ke-ZhenWu Zhong-Jun - NFS1 cysteine desulfurase (NFS1) a critical enzyme in iron‑sulfur (Fe-S) cluster biogenesis and mitochondrial iron homeostasis, plays a pivotal role in the dysregulation of iron metabolism, a recognized hallmark of cancer. However, the specific role and regulatory mechanisms of NFS1 in colorectal cancer (CRC) remain poorly understood. This study aimed to elucidate the function of NFS1 in CRC and to uncover the upstream molecular pathways governing its expression. - Source: PubMed
Publication date: 2026/04/30
Wang BingHuang XiaofangXing YulongJiao WeiJiang JianhuaLiu GangLi GuochaoLi QinquanYang ChunyuShi Lianghui - Ischemic stroke is a devastating condition with limited treatment options, where neuroinflammation plays a pivotal role in secondary brain injury. Neural cell adhesion molecule 1 (NCAM1) is implicated in neural development and plasticity, but its specific role in microglia during ischemic stroke remains unclear. Here, we demonstrate that microglial NCAM1 expression is significantly downregulated in the acute phase of ischemic stroke in both human patients and a mouse transient middle cerebral artery occlusion (tMCAO) model. Using microglia/macrophage-specific NCAM1-overexpressing mice, we show that NCAM1 overexpression reduces infarct volume, improves neurological deficits, and enhances long-term functional recovery. Mechanistically, NCAM1 directly interacts with the E3 ubiquitin ligase TRIM67 via its cytoplasmic domain. This NCAM1-TRIM67 complex enhances K63-linked ubiquitination while suppressing K48-linked ubiquitination of IκBα, thereby stabilizing IκBα protein, preventing NF-κB p65 nuclear translocation, and ultimately inhibiting NF-κB-driven neuroinflammation and apoptosis. Furthermore, through molecular docking and high-throughput screening, we identified DB07993 as a potent NCAM1 agonist. DB07993 treatment mimicked the neuroprotective effects of NCAM1 overexpression in vitro and in vivo, primarily through activation of the NCAM1-TRIM67-IκBα axis. Our study unveils a novel regulatory mechanism where microglial NCAM1 serves as a critical brake on post-stroke neuroinflammation and identifies DB07993 as a promising lead compound for developing NCAM1-targeted stroke therapies. - Source: PubMed
Publication date: 2026/03/14
Yu ZongdongYu LuliLu WeiChen PengYan HuanJiang Yong'an - Cerebral infarction is one of the most common ischemic cerebrovascular diseases that can lead to neurological deficits. Remimazolam (RE) is a sedative agent that has been shown to improve neurological disorders. However, the underlying molecular mechanism of RE for the treatment of cerebral infarction remains to be further explored. Oxygen-glucose deprivation/reperfusion (OGD/R) cell model and middle cerebral artery occlusion (MCAO) rat model were constructed. Cell proliferation, apoptosis, and inflammation were evaluated using CCK8 assay, EdU assay, flow cytometry, and ELISA. Ferroptosis-related markers were assessed by commercial kits. The expression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) and tripartite motif-containing 67 (TRIM67) was examined by qRT-PCR or western blot. The interaction between TRIM67 and ACSL4 was confirmed by Co-IP assay. Cerebral injury in MCAO rat model was assessed by histological staining and neurological score. RE treatment enhanced proliferation, repressed apoptosis, inflammation and ferroptosis in OGD/R-induced SK-N-SH cells. RE decreased ACSL4 protein expression, and ACSL4 overexpression could reverse the anti-apoptosis, anti-inflammation and anti-ferroptosis roles of RE in OGD/R-induced SK-N-SH cells. TRIM67 reduced ACSL4 expression by increasing its ubiquitination and degradation. TRIM67 alleviated OGD/R-induced neuronal injury by downregulating ACSL4. RE enhanced TRIM67 protein expression, and TRIM67 knockdown also reversed the neuroprotective effect of RE. Also, RE relieved cerebral injury in the MCAO rat model via promoting TRIM67 expression to repress ACSL4. RE alleviated OGD/R-induced apoptosis, inflammation and ferroptosis through promoting TRIM67-mediated degradation of ACSL4, which provided a possible path for additional research in the therapies of cerebral infarction. - Source: PubMed
Xiao GaopengZhang YongqinYang JiHe JigangZhang YouwuQin WenYu LiuqiongWang LingLi YujinBai Yuncheng