IAP4 _ BIRC5 pThr34 Control Peptide
- Known as:
- IAP4 _ BIRC5 pThr34 Control Peptide
- Catalog number:
- AP10287CP-N
- Product Quantity:
- 0.25 mg
- Category:
- Peptides
- Supplier:
- ACR
- Gene target:
- IAP4 _ BIRC5 pThr34 Control Peptide
Ask about this productRelated genes to: IAP4 _ BIRC5 pThr34 Control Peptide
- Gene:
- BIRC5 NIH gene
- Name:
- baculoviral IAP repeat containing 5
- Previous symbol:
- API4
- Synonyms:
- EPR-1, survivin
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-04
Related products to: IAP4 _ BIRC5 pThr34 Control Peptide
Related articles to: IAP4 _ BIRC5 pThr34 Control Peptide
- Ultra-high dose rate FLASH radiotherapy can mitigate normal tissue toxicity while sustaining tumor control, yet the associated molecular mechanisms are still unclear. This study aimed to evaluate the differential DNA damage and transcriptomic responses of MRC-5 cells to FLASH versus conventional (CONV) irradiation. To address this, MRC-5 cells were exposed to X-rays irradiation at either FLASH dose rate or CONV dose rate. γH2AX/phosphorylated 53BP1 immunofluorescence was performed to detect early-stage DNA double-strand breaks. Transcriptome sequencing was implemented to characterize the transcriptomic expression profiles of the cells. Interaction patterns among differentially expressed genes (DEGs) were investigated via protein-protein interaction (PPI) network analysis. The expression levels of the screened core DEGs were validated via quantitative real-time PCR (RT-qPCR). Results showed that at high doses (8 Gy and 12 Gy), the FLASH group exhibited significantly fewer early-stage DNA double-strand breaks than the CONV group. Its transcriptomic profile was more analogous to that of nonirradiated cells, with differential regulation in DNA damage response (DDR)-related pathways; 9 core DEGs (CCNA2, CCNB1, CCNB2, RAD51, EXO1, BIRC5, BUB1, CDC6, CDC20) were screened out via PPI network analysis, and RT-qPCR verified that their downregulation was less extensive in the FLASH group relative to the latter. Collectively, X-ray FLASH irradiation alleviates MRC-5 cell damage by regulating DNA double-strand break repair and other DDR-related pathways, along with the nine core DEGs, providing a molecular basis for FLASH radiotherapy's normal tissue protective effect. - Source: PubMed
Publication date: 2026/06/15
Jiang YiWang XiaofengYang ChongkaiWu JiangpingChen YaotianLi JieWang QingZhu Wenkun - Glioma represents the most prevalent and lethal primary malignant tumor of the central nervous system, characterized by remarkable cellular heterogeneity and poor prognosis. Comprehensive characterization of glioma at single-cell resolution is essential for identifying novel therapeutic targets and improving patient outcomes. - Source: PubMed
Publication date: 2026/05/28
Gu ChengcongWu XiaojinYang Liang - Synthetic polyinosinic:polycytidylic acid (poly(I:C)) offers an attractive cancer therapeutic by operating on two fronts at once, combining direct tumor cell killing with immunostimulatory activity. Yet, these dual functions can only be efficiently harnessed when intracellular delivery is sufficiently effective to enable poly(I:C) to reach and activate its intracellular receptors. We addressed this delivery challenge by developing pH-responsive formulations using lipoamino fatty acid xenopeptide (LAF-XP) carriers, composed of polar cationizable succinoyl tetraethylene pentamine (Stp) and apolar cationizable LAF building blocks in defined architectures. In particular, poly(I:C)-lipid nanoparticles (LNPs) formulated with bundle LAF-Stp XP carriers displayed increased anti-tumoral activity at decreased dosage across multiple cancer cell models, compared to control formulations. In parallel, LAF-XP LNP-delivered poly(I:C) activated immune responses, including CXCL10 production by tumor cells, and activation of peripheral blood mononuclear cells (PBMCs), characterized by increased phenotypic markers (CD69 and LAMP-1/CD107a) and functional molecules (e.g., IFN-γ and granzyme B). Conditioned supernatant of pre-stimulated PBMCs with poly(I:C) reduced cancer cell viability, highlighting the contribution of PBMC-released factors to cancer cell death. Of particular novelty is the combination of poly(I:C) with siRNA-mediated survivin knockdown to increase apoptosis in cancer cells using the bundle LAF-XP LNP. Collectively, our findings establish efficient LAF-XP LNPs as a versatile platform that supports multi-layered therapeutic strategies. - Source: PubMed
Publication date: 2026/05/30
Yazdi MinaHasheminejad ZahraHachani KhouloudKache JoyceGrau MelinaWollenberg BarbaraBashiri Dezfouli AliWagner Ernst - Cisplatin (Cis) resistance and dose-limiting toxicity remain major challenges in the treatment of cervical cancer, necessitating the development of more effective combination strategies. The effects of gallic acid (GA), alone and in combination with Cis, were evaluated in HeLa cervical cancer cells using cell viability, apoptosis, gene expression, caspase activity, and cytokine profiling assays. Drug interactions were assessed using the Chou-Talalay method. The GA+Cis combination was associated with enhanced cytotoxicity compared to single-agent treatments, with combination index (CI) values ranging from 0.61 to 0.92, indicating synergistic interactions. Selectivity index (SI) values exceeding 2 at 48 h suggested preferential cytotoxicity toward cancer cells. The combination treatment significantly increased apoptotic cell populations and was accompanied by elevated caspase-3 and caspase-9 activities. Gene expression analysis revealed increased BAX and CASP3 levels, along with decreased BCL2 and BIRC5 expression, resulting in an increased BAX/BCL2 ratio. In addition, cell cycle analysis indicated accumulation in the G2/M phase, while cytokine profiling demonstrated reduced levels of pro-inflammatory cytokines and increased IL-10 levels under combination treatment conditions. These findings suggest that GA enhances the biological activity of Cis in cervical cancer cells through coordinated modulation of apoptosis, cell cycle dynamics, and inflammatory signaling. However, these results are based on in vitro observations, and further in vivo and mechanistic studies are required to confirm the therapeutic potential of this combination strategy. - Source: PubMed
Publication date: 2026/05/23
Ozan ElifTuncer Mehmet CudiÖzdemir İlhan - Retinoblastoma is the most common pediatric intraocular malignancy, although it remains a rare disease overall, yet the molecular targets and therapeutic vulnerabilities sustaining its most aggressive proliferative cell states remain incompletely defined. We aimed to identify actionable molecular regulators and potential therapeutic targets of malignant retinoblastoma progression using integrated single-cell transcriptomics and functional validation. - Source: PubMed
Publication date: 2026/05/21
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