BIRC6 ELISA kit
- Known as:
- BIRC6 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BIRC6-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BIRC6 ELISA kit
Related genes to: BIRC6 ELISA kit
- Gene:
- BIRC6 NIH gene
- Name:
- baculoviral IAP repeat containing 6
- Previous symbol:
- -
- Synonyms:
- BRUCE
- Chromosome:
- 2p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2014-11-19
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- Pyroptosis, particularly gasdermin E (GSDME)-mediated programmed cell death, has emerged as a crucial determinant of chemosensitivity and antitumor immunity. Although baculoviral inhibitor of apoptosis protein (IAP) repeat-containing protein 6 (BIRC6) is a known inhibitor of apoptosis, its potential role in regulating the pyroptotic switch and cisplatin resistance in lung adenocarcinoma (LUAD) remains unclear. Therefore, in this study, we aimed to elucidate the molecular mechanism underlying BIRC6-mediated regulation of pyroptosis and cisplatin resistance in LUAD. - Source: PubMed
Publication date: 2026/05/21
Zhang TingChen MiaoLuo Peng-WeiHou Hui-JuanWang XinMa Yi-FanLiu TengDeng Shi-HuaWu Dong-MingXu Ying - Cell survival and death are the fundamental biological processes of life that involve both intracellular and extracellular dynamic events. How cells balance survival and death determines cell fate, and this question has attracted extensive research interest for decades yet remains largely unresolved. This review focuses on BRUCE, the only essential inhibitor-of-apoptosis (IAP) protein for survival. Based on recent structural discoveries regarding the autophagy-apoptosis switch, we provide novel mechanistic insights into this long-standing scientific question. BRUCE possesses a distinctive structure: its C-terminal UBC domain confers Ub conjugase (E2) and Ub-protein ligase (E3) activities, while its N-terminal region contains a baculoviral IAP repeat (BIR) domain. Benefiting from such distinctive structural properties. BRUCE centrally governs cell fate by modulating the transition from autophagy to apoptosis and maintaining genomic stability. At the organismal level, BRUCE sustains the homeostasis of reproductive and developmental processes by either inhibiting apoptosis or mediating substrate degradation. Aberrant BRUCE upregulation is widely implicated in diverse pathologies, including neurodevelopmental disorders and multiple malignancies. Nevertheless, research focusing on the targeted inhibition of BRUCE remains largely underexplored. A better understanding of the structural features and functional mechanisms of BRUCE will help elucidate how it exerts its pathogenic effects via regulation of cell survival and death. Such insights will lay a solid foundation for the future discovery and therapeutic application of specific BRUCE-targeted inhibitors. Outlooks and perspectives on the associated challenges are provided as well. - Source: PubMed
Publication date: 2026/05/18
Dong JiahuiXie XiufengWang YinJiang Tianxia - Premature ovarian insufficiency (POI), characterized by ovarian dysfunction before age 40, remains idiopathic in over 50% of cases, underscoring the urgent need to elucidate its genetic underpinnings. Here, we report a consanguineous Iranian family with five females diagnosed with POI, exhibiting elevated gonadotropins, undetectable anti-Müllerian hormone, and bilateral ovarian atrophy. Whole Exome Sequencing identified a novel homozygous missense variant in BIRC6 (NM_016252.4: c.11266C > T; p.Arg3756Cys), a gene encoding an apoptosis regulator. Segregation analysis confirmed an autosomal recessive inheritance pattern, with homozygosity exclusively in affected individuals. Functional studies in a CRISPR/Cas9-generated birc6 zebrafish model recapitulated POI phenotypes: homozygous females exhibited reduced fecundity, aberrant oocyte morphology, and elevated embryonic death. Transcriptional analysis revealed dysregulation of apoptotic (badb, sortilin, apc) and fertility-related (nanos1, vtg1) genes, alongside unaltered estradiol levels, implicating apoptosis-driven follicular atresia rather than endocrine dysfunction. Compensatory increase in egg production in mutants mirrored human POI progression, where initial irregular cycles culminate in follicular depletion. This study establishes BIRC6 as a novel POI candidate, links its anti-apoptotic function to ovarian homeostasis, and highlights zebrafish as a tractable model for dissecting POI mechanisms. Our findings expand the genetic landscape of infertility and suggest therapeutic potential for apoptosis modulation in fertility preservation. - Source: PubMed
Publication date: 2026/05/04
Kazerani MahsaCagiral UmutTabatabaei Seyedeh ZohaAkalper Remziye NurBora UgurBabashah SadeghOzhan GunesTotonchi Mehdi - Inhibitors of apoptosis proteins (IAPs) are endogenous apoptosis regulators conserved in many species. We used bioinformatics approaches, identified six members of the IAP gene family (named PtIAP-01 to PtIAP-06) in the genome of Portunus trituberculatus. We phylogenetically classified these PtIAPs into four distinct subfamilies, namely BIRC5, BIRC6, BIRC7-A, and BIRC7-B. All identified PtIAPs contained the characteristic baculoviral IAP repeat (BIR) domain. In addition, some PtIAP members were found to possess additional functional domains, including RING finger or UBC. The expression levels of the PtIAPs were tissue-specific. PtIAP-01 was highly expressed in immune-related tissues (intestine and hepatopancreas), PtIAP-05 dominated in muscle, while PtIAP-02, -03, -04, and -06 showed preferential expression in the eyestalk. Following Vibrio parahaemolyticus injection, the expression levels of PtIAP-01, -02 and -05 were significantly upregulated, reaching 1.64-, 3.48-, and 4.18-fold of the control group, respectively, indicating their potential involvement in anti-pathogen immunity. Fluorescence in situ hybridization (FISH), RNA interference (RNAi) and terminal deoxynucleotidyl transferase nick-end-labeling (TUNEL) apoptosis assays validated their function. FISH confirmed that PtIAP-01, -02, and -05 were in both the nucleus and cytoplasm of hepatopancreatic cells. Their fluorescence signals got stronger after V. parahaemolyticus infection (PtIAP-05 strongest). RNAi and TUNEL demonstrated that knockdown of PtIAP-01, -02, and -05 significantly increased the mortality and apoptosis rates of P. trituberculatus after V. parahaemolyticus challenge, and significant upregulation of downstream apoptotic effector genes (PtCaspase-1, -3, -8). These findings offer new insights into the innate immune mechanisms of crustaceans and lay a foundation for breeding disease-resistant strains. - Source: PubMed
Publication date: 2026/04/28
Pan JiayiPan HangfengZhang BingjieZhou XianfaLv JianjianWang XuezhongSun DongfangGao Baoquan - Tumor location influences survival in bladder cancer, potentially due to genetic heterogeneity driven by distinct embryological origins and structural compositions. We investigate location-specific somatic gene alterations (GAs) and their potential clinical implications in muscle-invasive bladder cancer (MIBC). - Source: PubMed
Publication date: 2026/03/09
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