Ubiquitin E3 ligase XIAP
- Known as:
- Ubiquitin E3 ligase XIAP
- Catalog number:
- 80401
- Product Quantity:
- 20 µg
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- Ubiquitin E3 ligase XIAP
Related genes to: Ubiquitin E3 ligase XIAP
- Gene:
- XAF1 NIH gene
- Name:
- XIAP associated factor 1
- Previous symbol:
- -
- Synonyms:
- BIRC4BP, XIAPAF1, HSXIAPAF1
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-03-04
- Date modifiied:
- 2017-05-22
- Gene:
- XIAP NIH gene
- Name:
- X-linked inhibitor of apoptosis
- Previous symbol:
- API3, BIRC4
- Synonyms:
- hILP, ILP-1
- Chromosome:
- Xq25
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2019-04-23
Related products to: Ubiquitin E3 ligase XIAP
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- Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the JNK western blotting data shown in Fig. 2E on p. 1138 were strikingly similar to the JNK western blotting data shown in Fig. 4D on p. 1139, even though the experimental conditions reported for these figure parts were apparently different. The authors have been contacted by the Editorial Office to offer an explanation for the apparent re‑use of the same data in this paper, and the authors have replied to explain that these studies were performed several years ago, that they no longer have access to the original data, and moreover, that they are not in a position to repeat any of these experiments. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem associated with the abovementioned data. [Oncology Reports 36: 1135‑1142, 2016; DOI: 10.3892/or.2016.4895]. - Source: PubMed
Publication date: 2026/09/18
Chung Yoon HeeKim Daejin - Atherosclerosis (AS) is driven by chronic vascular inflammation, yet the relationship between immune activity within atherosclerotic lesions and systemic immune signals in peripheral blood remains poorly defined. In this study, we performed an integrative multi-cohort analysis of gene expression profiles from atherosclerotic tissues, peripheral blood, and single-cell transcriptomic datasets to characterize spatial immune heterogeneity in AS. Differential expression and enrichment analyses revealed divergent immune-related transcriptional patterns between plaques and blood, indicating a dissociation between local and systemic immune responses. Using weighted gene co-expression network analysis and multiple machine learning approaches, we identified a 5-gene signature (with XAF1 [XIAP-associated factor 1], RNF213 [ring finger protein 213], OAS2 [2'-5'-oligoadenylate synthetase 2], and OAS3 [2'-5'-oligoadenylate synthetase 3] upregulated, and BEND5 [BEN domain containing 5]) downregulated in plaques) that robustly distinguished atherosclerotic from control samples across multiple vascular beds. This gene signature demonstrated strong diagnostic performance in tissue datasets. While its diagnostic accuracy was attenuated in peripheral blood, it retained moderate prognostic value for ischemic stroke risk, suggesting its utility as a hypothesis-generating tool for noninvasive risk stratification. Together, these findings highlight spatially distinct immune programs in AS and support the use of integrated tissue- and blood-based gene signatures for improved disease diagnosis and risk stratification. - Source: PubMed
He RuiqiaoHuang WenlinHu LiangqiaoFang YongyouYang Fei - Lung adenocarcinoma (LUAD) is the most prevalent subtype of lung cancer, the leading cause of global cancer-related mortality. Genetic mutations play critical roles in LUAD pathogenesis. This study aims to investigate the role of XIAP-associated factor 1 (XAF1) rs117407731, a nonsense mutation in certain splice variants (p.22W>*, TGG to TGA), in LUAD susceptibility and cellular function. Genotyping of XAF1 rs117407731 was conducted using blood samples of 103 LUAD patients and 229 healthy individuals. Multivariate logistic regression analysis was carried out to identify independent factors associated with LUAD risk. Immunofluorescence staining showed the expression of XAF1 and XIAP in LUAD tissues. TUNEL staining was employed for cell apoptosis analysis in patient LUAD tissues or mouse tumors. A549 cells were transduced with lentiviral vectors carrying wild-type or mutant XAF1 (XAF1-WT or XAF1-MUT) for functional experiments. XAF1 rs117407731 significantly increased susceptibility to LUAD. XAF1 protein expression was reduced, XIAP expression was elevated, and cell apoptosis was decreased in LUAD tissues from rs117407731 carriers. Overexpressing XAF1-MUT abated XAF1-mediated impairment of A549 cell proliferation and enhancement of apoptosis in vitro. XAF1-MUT overexpression impaired tumor suppression in the xenograft mouse model. XAF1 rs117407731 contributes to LUAD risk by impairing XAF1-mediated apoptosis. - Source: PubMed
Publication date: 2026/04/24
Xu GuanxinZhang HangZhang SaiYu Danqing - Non-small cell lung cancer (NSCLC) continues to be the primary contributor to deaths associated with cancer. Current treatments are often limited by drug resistance and toxicity, highlighting the need for novel therapeutic approaches. Building on previous findings demonstrating that Gamabufotalin (CS-6) is effective against hepatocellular carcinoma, this study explores its mechanism of action in NSCLC. The findings indicate that CS-6 suppresses the proliferation and migratory capacity of NSCLC cells in a concentration-dependent manner, while significantly inducing apoptosis. The 48-hour half-maximal inhibitory concentration (IC) ranged from 30 to 80 nM. In xenograft models, CS-6 effectively suppressed tumor growth (P < 0.05) without causing significant systemic toxicity at effective doses (25 mg/kg and 50 mg/kg). Mechanistically, coiled-coil-helix-coiled-coil-helix domain-containing protein 2 (CHCHD2) was identified as the direct molecular target of CS-6 through Limited Proteolysis-Mass Spectrometry (LiP-MS), validated by cell thermal shift assay (CETSA), MicroScale Thermophoresis (MST), and Surface Plasmon Resonance (SPR). CHCHD2, also known as mitochondrial nuclear retrograde regulator 1 (MNRR1), is a bi-organelle regulator located primarily in the mitochondrial intermembrane space, where it controls respiratory chain stability and cristae structure, thereby regulating cell survival and apoptosis[1-3]. CHCHD2 is essential for NSCLC cell survival, as both its knockdown and overexpression reduced the efficacy of CS-6. Furthermore, transcriptomic analysis revealed that targeting CHCHD2 with CS-6 activates interferon signaling and significantly upregulates the tumor suppressor X-linked inhibitor of apoptosis (XIAP)-associated factor 1 (XAF1). In conclusion, these findings establish the mitochondrial CHCHD2-XAF1 axis as a key mediator of CS-6 activity, thereby highlighting CS-6 as a promising candidate for targeted therapy in NSCLC. - Source: PubMed
Publication date: 2026/02/13
Cai YisiWang XiaoweiXu DieSong YinghuiZhu LemeiPeng WeijunChen Bolin - Inhibitors of apoptosis proteins (IAPs), coded by BIRC genes, are cellular checkpoints that can regulate and inhibit pro-apoptotic caspase signaling. Overexpression of BIRC genes has been associated with cancer progression, multidrug resistance, poor prognosis, and shorter survival in several types of cancer. Using quantitative real-time polymerase chain reaction, we examined the expression of IAP family genes and their regulators: NAIP, BIRC2, BIRC3, XIAP, BIRC5, BIRC6, BIRC7, CASP3, CASP9, DIABLO and XAF1. We also evaluated the impact of clinical parameters (programmed death receptor 1 [PD1] expression, oligodendrocyte transcription factor 2 [Olig2] expression, Ki-67 antigen expression, tumor protein p53 expression in tumor cells, patient survival time, and progression-free survival) on gene expression levels. The expression of BIRC3 (p = 0.049), NAIP (p = 0.008), and XAF1 (p = 0.032) was significantly higher in tumors negative for Ki67, whereas the remaining genes showed no significant correlation with Ki67 expression. In contrast, BIRC2 (r=-0.478 p < 0.05) and BIRC3 (r=-0.536 p < 0.05) expression levels were negatively correlated with overall survival. A similar negative association was observed between progression-free survival and the expression of BIRC2 (r=–0.481, p < 0.05) and BIRC3 (r=-0.540, p < 0.05). To our knowledge, this is the first study to comprehensively assess the relationship between the expression of IAP family genes and their regulators in a homogeneous group of patients diagnosed with pediatric high-grade gliomas (pHGGs). Our findings provide new insights into molecular mechanisms involved in the pathogenesis of pHGGs, however, these preliminary results require confirmation in larger and more detailed studies. - Source: PubMed
Publication date: 2026/01/30
Petniak AlicjaGil-Kulik PaulinaZarychta JuliaKowalczyk AdrianTrubicka JoannaPerek-Polnik MartaGrochowski CezaryMaciejewski RyszardGrajkowska WiesławaKocki Janusz