Human Polyclonal XIAP Ab
- Known as:
- Human Polyclonal XIAP Antibody
- Catalog number:
- a0383
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal XIAP
Related genes to: Human Polyclonal XIAP Ab
- 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: Human Polyclonal XIAP Ab
Related articles to: Human Polyclonal XIAP Ab
- 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 genes, are cellular checkpoints that can regulate and inhibit pro-apoptotic caspase signaling. Overexpression of 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: , , , , , , , , , and . 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 ( = 0.049), ( = 0.008), and ( = 0.032) was significantly higher in tumors negative for Ki67, whereas the remaining genes showed no significant correlation with Ki67 expression. In contrast, (=-0.478 < 0.05) and (=-0.536 < 0.05) expression levels were negatively correlated with overall survival. A similar negative association was observed between progression-free survival and the expression of (=–0.481, < 0.05) and (=-0.540, < 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 - Aminoglycoside antibiotics are essential in managing many life-threatening diseases. However, their derivatives, such as neomycin, are associated with severe side effects such as persistent sensorineural hearing loss. Therefore, it is essential to elucidate the molecular and biochemical mechanisms of aminoglycoside-induced ototoxicity and identify targets for alleviating ototoxic injury. Here, we provide a detailed cochlear cell atlas of neomycin-induced acute and chronic ototoxicity-related changes through single-nucleus RNA sequencing profiling. Utilising this cochlear cell atlas, we used the Augur and scDist algorithms to evaluate cell-type-specific susceptibility to neomycin injury. We observed aberrant expression of X-linked inhibitor of apoptosis (Xiap)-associated factor 1 (Xaf1) in neomycin-exposed cochleae using the cochlear cell atlas, and we identified a novel role for Xaf1 in facilitating PANoptosis through overexpression and knockdown assays in vitro. Finally, we assessed the protective role of Xaf1 against neomycin-induced ototoxicity by Xaf1 knockdown in cochlear hair cells using adeno-associated virus-based gene delivery. Mechanistically, Xaf1 orchestrates PANoptosis activation through direct interaction with and transcriptional regulation of ZBP1, establishing its hierarchical position upstream in the signalling cascade. This study presents detailed cochlear cellular maps of neomycin-induced ototoxicity and serves as a valuable resource for identifying transcriptome-wide disease-driving perturbations at the single-cell level. More importantly, we identified Xaf1 as a critical target for modulating the PANoptosis pathway, offering a promising treatment strategy for aminoglycoside-induced ototoxicity. - Source: PubMed
Publication date: 2025/07/02
Wang XinlinXiao HairongWu JihengLin YanqinAo YihengYe ZixuanTan XinKong FanliangChen XinChai RenjieZhang Shasha - Tripartite motif-containing 47 (TRIM47) is a member of the TRIM family, which has E3 ligase activity and has been demonstrated to be involved in tumor development. In this work, we found that TRIM47 is highly expressed in head and neck squamous cell carcinomas (HNSCC) tissues. TRIM47 overexpression promoted HNSCC cell proliferation. Downregulation of TRIM47 suppressed HNSCC cell proliferation and promoted apoptosis and autophagy. TRIM47 suppression caused cell proliferation inhibition and apoptosis promotion could be reversed by 3-MA, an autophagy inhibitor. In mechanism, TRIM47 interacted with XIAP-associated factor 1 (XAF1), promoting its ubiquitination and degradation. XAF1 promoted HNSCC cell apoptosis and autophagy. TRIM47 overexpression caused cell proliferation promotion and autophagy inhibition could be reversed by XAF1 overexpression. Animal experiments confirmed that the knockdown of TRIM47 inhibits tumor growth . Ultimately, TRIM47 promotes the ubiquitination and degradation of XAF1 and suppresses apoptosis and autophagy to promote the progression of HNSCC. - Source: PubMed
Publication date: 2024/12/13
Yu ChangyunZhang ChenZhang QianqianZhang CaiHan JingjieLi Jinying