Ask about this productRelated genes to: BIRC7 antibody
- Gene:
- BIRC7 NIH gene
- Name:
- baculoviral IAP repeat containing 7
- Previous symbol:
- -
- Synonyms:
- mliap, ML-IAP, KIAP, RNF50
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-06
- Date modifiied:
- 2016-10-05
Related products to: BIRC7 antibody
Related articles to: BIRC7 antibody
- 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 - - Source: PubMed
Publication date: 2026/04/17
G Farag NesmaO Mohamed AmanyAbdel-Aleem MahmoudS El-Deeb ThoryaA Elghazally ShimaaG Elnaggar MohamedAl-Husseini AbdulmonemA Gaber Marwa - Programmed Death-Ligand 1 (PD-L1) promotes tumor progression through several mechanisms, including its intrinsic effect on breast cancer cell proliferation via the S-Phase Kinase-Associated Protein 2 (SKP2)-p21/p27 (SKP2-p21/p27) axis. However, the specific regulatory signaling through which PD-L1 influences the SKP2-p21/p27 axis to drive cell proliferation remains unclear. To investigate how PD-L1 mediates SKP2-dependent proliferation, proteomic analyses, gene-expression manipulation via knockdown or overexpression, Western blotting, quantitative immunofluorescence, colony-forming assays, real-time cell analysis, and Xenograft-derived cells were used. Proteomic data analysis identified several PD-L1 downstream targets as potential candidate regulators of the SKP2-p21/p27 axis and activators of the PI3K/AKT pathway. Candidate screening by gene knockdown, followed by analyses of SKP2, p21, and p27 protein expression, revealed Livin and Galectin-1 as upstream regulators of the SKP2-p21/p27 axis. Moreover, Western blotting and quantitative immunofluorescence in three breast cancer cell lines confirmed that PD-L1 is an upstream regulator of Livin, Galectin-1, and SKP2 protein expression. Mechanistically, Livin and Galectin-1 enhanced AKT phosphorylation (Ser473) to sustain PI3K/AKT pathway activation in a positive feedback loop to upregulate SKP2 expression. Functional assays, including colony-forming assays and real-time cell analyzer, demonstrated that Livin and Galectin-1 are critical for PD-L1-mediated, SKP2-dependent proliferation. These findings were corroborated in vivo using xenograft-derived cells. Overall, these findings delineate a tumor-intrinsic signaling axis in which PD-L1 upregulates Livin and Galectin-1 to sustain PI3K/AKT activity and drive SKP2-dependent cell proliferation. Targeting Livin and/or Galectin-1 may provide a rational strategy to disrupt PD-L1-associated proliferative signaling and improve combinatorial therapeutic approaches in breast cancer. - Source: PubMed
Publication date: 2026/03/17
Elfoly MarwaAlaiya AyodeleAl-Hazzani Amal AAl-Alwan MontherGhebeh Hazem - 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 - Lung adenocarcinoma (LUAD) is the most prevalent histological subtype of non-small cell lung cancer (NSCLC) and is characterized by high mortality and limited therapeutic efficacy in advanced stages. AVEN, an apoptosis inhibitor that interacts with Bcl-xL and Apaf-1 to suppress caspase activation, has been implicated in tumour progression and drug resistance in various cancers. However, its role in LUAD remains unclear. In this study, the prognostic importance, immune microenvironment association, and regulatory mechanisms of AVEN in LUAD were comprehensively investigated using bulk RNA sequencing (RNA-seq), single-cell RNA sequencing (scRNA-seq), and experimental validation. Analysis of the TCGA and GEO datasets revealed that AVEN expression was significantly upregulated in LUAD tissues compared with normal tissues and that high AVEN expression correlated with advanced T/N stage and pathological stage and was associated with poor overall survival (OS), disease-specific survival (DSS), and progression-free survival (PFS). Multivariate Cox regression identified AVEN expression as an independent prognostic factor, and a nomogram incorporating AVEN expression demonstrated high predictive accuracy for 1-, 3-, and 5-year OS. Functional enrichment analysis linked AVEN to keratinocyte differentiation, spliceosome activity, and cell cycle pathways, whereas the results of scRNA-seq highlighted its predominant expression in malignant epithelial cell subtypes (tS2), which is associated with aggressive proliferation and immune evasion. AVEN expression was positively correlated with Th2, NK CD56dim, and Tgd cell infiltration but negatively associated with TFH, eosinophil, and mast cell infiltration, suggesting its role in modulating the tumour immune microenvironment. Detection of clinical samples verified the high expression of AVEN in LUAD. In vitro, AVEN knockdown in A549 cells suppressed proliferation, migration, and invasion while promoting apoptosis. Furthermore, bioinformatics prediction and validation revealed that hsa-miR-30d-5p was an upstream regulator of AVEN, with its low expression in LUAD tissues inversely correlated with that of AVEN and predicting a favourable prognosis. Subsequent bioinformatics analysis further revealed that lncRNA-AC012236.1 functioned as an upstream regulator of hsa-miR-30d-5p. This lncRNA was found to be highly expressed in LUAD tissues, and its elevated expression was significantly associated with poor overall survival (OS) in LUAD patients. In conclusion, AVEN, as a promising diagnostic and prognostic biomarker in LUAD, affected tumour progression, immune infiltration and apoptosis resistance through the lncRNA-AC012236.1/hsa-miR-30d-5p-AVEN axis. These findings provided new insights into the pathogenesis of LUAD and highlighted potential therapeutic targets for improving patient prognosis. - Source: PubMed
Publication date: 2025/12/01
Yin RongjiangDong XinGuo ZijieWu JianmingDong MenghuaGu HuaWang ZhanqingDu Pengchao