cIAP1 Blocking Peptide
- Known as:
- cIAP1 Blocking Peptide
- Catalog number:
- 33r-10656
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- cIAP1 Blocking Peptide
Ask about this productRelated genes to: cIAP1 Blocking Peptide
- Gene:
- BIRC2 NIH gene
- Name:
- baculoviral IAP repeat containing 2
- Previous symbol:
- API1
- Synonyms:
- cIAP1, hiap-2, MIHB, RNF48, c-IAP1
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-05
Related products to: cIAP1 Blocking Peptide
Related articles to: cIAP1 Blocking Peptide
- Liver cancer remains one of the leading causes of cancer-related mortality worldwide, with its progression driven by uncontrolled cell proliferation and evasion of apoptosis. N1-methyladenosine (mA) is a prevalent RNA modification implicated in cancer progression, yet its role in liver cancer remains unclear. Here, we report a significant reduction in mA levels in liver cancer tissues, which contributes to apoptosis evasion in liver cancer cells. We demonstrate that ALKBH3, an mA demethylase, regulates apoptosis by modulating BIRC2 expression. Specifically, ALKBH3 depletion destabilizes BIRC2 mRNA by promoting its degradation, facilitated by mA modifications at positions A98/99/100 in the 5'-UTR of BIRC2. These modifications enhance the interaction between BIRC2 mRNA and the YTHDF3/CNOT1-XRN2 complex, thereby driving mRNA degradation. In vitro, in vivo, and clinical analyses validate the critical role of the mA/BIRC2 axis in regulating apoptosis and tumor progression in liver cancer. Our findings underscore the therapeutic potential of targeting the mA/BIRC2 axis to overcome apoptosis resistance in liver cancer, offering new avenues for intervention in this malignancy. - Source: PubMed
Publication date: 2026/04/16
Wu YingminZhang ShenjieZhang ShilongLu JieyuYang YuntaoZeng ZhiruiLei ShanMi RuiZhang YeweiGe LichenChen TengxiangLi Haiyang - Coexisting myocardial infarction (MI) and type 2 diabetes mellitus (T2DM) is a common condition. We aimed to investigate the association between MI and type 2 diabetes (T2D) with mitophagy-related differentially expressed genes (MRDEGs) and the impact thereof on disease progression. - Source: PubMed
Publication date: 2026/04/08
Yang YingWan FeiyanXu XuelianXu WeiJiang LingliPan Pei - Early detection of cancer is essential for effective treatment. However, current prostate cancer screening methods lack sufficient sensitivity and specificity, leading to overdiagnosis and unnecessary treatment. There is also an unmet need to distinguish clinically significant from insignificant prostate cancer. To identify complementary biomarkers for improved screening and diagnosis, we performed transcriptional profiling of cancer-associated transcripts in circulating extracellular vesicles (EVs) isolated from peripheral blood of patients with suspected prostate cancer prior to biopsy and healthy donors. Expression data for 2549 mRNAs were obtained from 28 men. CAPN5 expression was significantly lower, whereas BIRC2, CASP3, CD63, FMO5, IRF6, PFDN1, PRDX6, PSMD2, RIT1, S100A2, THBS1, and XRCC2 were significantly elevated in EVs from patients with significant prostate cancer (n = 14) compared with cancer-free individuals and patients with insignificant disease (n = 14). Candidate biomarkers were subsequently evaluated by in silico validation using the The Cancer Genome Atlas (TCGA) prostate adenocarcinoma dataset and the GEO dataset GSE70768 containing benign and malignant prostate tissues. This analysis identified CASP3, XRCC2, and RIT1 transcripts in circulating EVs as promising biomarkers for the early detection of significant prostate cancer. - Source: PubMed
Publication date: 2026/03/26
Werner StefanTennstedt PierrePose Randi CMüller ChristianBesler KatharinaSchneegans SvenjaAlawi MalikRoesch Marie CPeine SvenBonci DesireeBudna-Tukan JoannaLianidou EviAlix-Panabières CatherineTilki DeryaPantel Klaus - Ewing sarcoma (EwS) is a highly aggressive pediatric malignancy driven by EWSR1::ETS fusion oncoproteins -primarily EWSR1::FLI1- which deregulate genes essential for differentiation, proliferation, and cell survival. To uncover key downstream targets of this fusion involved in cell differentiation, we combined transcriptomic profiling of EwS cell lines following EWSR1::ETS inhibition with gene ontology analysis, a clinically annotated gene expression dataset derived from EwS patient material and network analyses. This integrative approach identified inhibitor of apoptosis protein 1 (cIAP1, alias BIRC2) as an EWSR1::FLI1-suppressed gene. Despite its known oncogenic role in many cancers, cIAP1 showed minimal expression in EwS. Using inducible cIAP1 re-expression models in EwS cells, we demonstrated that cIAP1 re-expression suppresses proliferation, clonogenic growth, and 3D spheroid formation in vitro. Transcriptomic and proteomic analyses revealed that low cIAP1 expression enhances proliferation-related gene signatures, which are inhibited upon cIAP1 re-expression. In vivo xenograft models revealed that cIAP1 re-expression significantly reduces tumor growth, mitotic activity, and Ki-67 positivity, while increasing tumor necrosis and apoptosis. These findings highlight an unexpected tumor-suppressive role for cIAP1 in fusion-driven EwS, contrasting with its pro-survival function in other cancers. Collectively, our results identify cIAP1 as a prognostically relevant, EWSR1::FLI1-regulated hub whose re-expression disrupts tumor progression, offering a potential therapeutic strategy to restore tumor-suppressive pathways in EwS. - Source: PubMed
Publication date: 2026/03/02
Cidre-Aranaz FlorenciaGeyer Florian HHölting Tilman L BHanssen Kimberley MFaehling TobiasRitter AlinaZimmermann MalenkaMao LianghaoAlonso JavierSastre AnaJayavelu Ashok KumarKnott Maximilian M LMusa JulianGrünewald Thomas G P - The cathepsin gene family plays an important role in the immune function of vertebrates. However, limited research has been reported on teleosts. In this study, we identified eighteen Lccathepsin genes in the large yellow croaker (Larimichthys crocea). The phylogenetic tree indicated that Cathepsin family members were highly conserved in fish. Motif and gene structure analysis showed LcCathepsins could be divided into three subfamilies and different subfamilies' members have similar structure. During Pseudomonas plecoglossicida infection, we found most Lccathepsin family members were significantly changed, except for LccathepsinDb, LccathepsinF, LccathepsinO, LccathepsinSa, and LccathepsinE. Under hypoxic stress, LccathepsinE and LccathepsinH in three tissues (blood, gills, and liver) and LccathepsinB in two tissues (blood and gills) were significantly changed. Additionally, the protein-protein interaction network demonstrated that LcCathepsins widely interacted with immune-related factors, including Bcl2, Birc2, Birc5a and so on. To explore the functional role of LcCathepsinB during infection, we utilized the inhibitor CA-074Me to assess its effects on apoptosis under P. plecoglossicida stress. Treatment with CA-074Me could reduce the expression levels of inflammation (il1β, tnfα, and il6) and apoptosis-related genes (cytc, casp3, casp9, bax) after infection. The Western blotting results were consistent with qRT-PCR data, showing that P. plecoglossicida infection increased Casp3 activity in PCK cells, whereas CA-074Me decreased Casp3 expression. Furthermore, the PI staining clarified that CA-074Me could rescue PCK cells from death induced by bacterial infection. Collectively, this study provided a foundational investigation into cathepsin genes in the large yellow croaker response to hypoxic and P. plecoglossicida stress, and served as a reference for the discovery of molecular targets to bolster disease resistance in large yellow croaker aquaculture. - Source: PubMed
Publication date: 2026/02/25
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