IAP4 _ BIRC5
- Known as:
- IAP4 _ BIRC5
- Catalog number:
- NB110-92717SS
- Product Quantity:
- 0.025 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IAP4 _ BIRC5
Related genes to: IAP4 _ BIRC5
- 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
Related articles to: IAP4 _ BIRC5
- Messenger RNA (mRNA) imaging in tumor cells plays a crucial role in monitoring the occurrence and development of tumors. However, achieving highly specific and sensitive mRNA imaging remains a significant challenge due to the complex intracellular environment and high background signal. Here, we engineered a CRISPR/Cas12a2 system with an RNA blocking strand that binds to CRISPR RNA (crRNA). After glutathione (GSH) stimulation, the RNA blocking strand is cleaved, allowing the release of crRNA and restoring the capability of CRISPR/Cas12a2 ribonucleoprotein (RNP). Furthermore, we developed a nanoprobe (termed eRNP-FHR) by converging engineered Cas12a2 RNP (eRNP) with framework-hotspot reporters (FHR). FHR features four vertices that modify the sgc8 aptamer to specifically target the protein tyrosine kinase 7 receptor on the surface of tumor cell membranes, link to the eRNP by hybridizing with crRNA, and incorporate fluorescence quenching groups. The eRNP-FHR precisely targets tumor cells through aptamer-mediated endocytosis, specifically recognizes mRNA upon GSH stimulation, and simultaneously cleaves FHR to release a significant fluorescent signal. Excitingly, eRNP-FHR successfully achieved imaging of baculoviral IAP repeat-containing 5 mRNA in pancreatic tumor cells, accurately distinguishing pancreatic tumor cells from normal cells. In a murine pancreatic tumor model, eRNP-FHR exhibited excellent mRNA imaging, highlighting significant potential for precise tumor diagnosis. - Source: PubMed
Publication date: 2026/05/26
Li JunruJi ChenYang WenzhiHan YongmingZhao PeipeiCai XiaohanTian SiqiZhu WenjingZhang JingjingXu JinxinyiYang WeiqiangLi FengqinLiu Peifeng - Insulin signaling regulates cellular metabolism in an epigenetic manner, but its role in the immune cell homeostasis remains unknown. High plasma insulin obstructs efficient insulin signaling and rewires metabolic activity in autoimmunity. In this study, we explored the functional consequences of insulin signaling for the metabolism and phenotype of effector CD4 T cells in blood and synovial tissue of patients with rheumatoid arthritis (RA). Transcriptome profiling of CD4 cells in RA blood and synovia revealed high metabolic activity and effector function of the survivin/BIRC5PD1 T peripheral helper cell population. Low insulin signaling and deficient histone acetylation in RA T cells amplified proinflammatory IFNγ and TNF expression. Co-deposition of survivin with acetylated histone H3K27 on regulatory chromatin controlled the transcription of histone acetylation complex subunits and insulin-dependent genes. Insulin stimulation and histone deacetylase inhibition induced an increase in histone acetylation. In CD4 cell cultures and in aggressive PD1Tph cells in RA synovial tissue, exposure to insulin synergized with inhibition of histone deacetylation to upregulate IL7 production suppressing IFNγ and PD1. This activated IL7R-signaling mediators STAT5A/B, BCL2, and promoted acquisition of CD27CD45RO central memory phenotype in the PD1Tph cells. Likewise, the CD4 cells in hyperinsulinemic T2D patients showed enrichment of IL7RT cell cluster. In RA patients, antagonizing folate transport and JAK/STAT signaling activated insulin signaling and histone acetylation-dependent metabolism of CD4 cells. Concomitant with CTLA4-dependent signaling, this enabled the adoption of an incipient IL7R T cell phenotype. This study demonstrates that insulin binds together metabolic activity and histone acetylation in CD4 cells. Sufficient insulin signaling promotes IL7R memory phenotype accrual in aggressive PD1Tph cells. Hence, achieving insulin sensitivity via histone acetylation disarms effector CD4 T cell function and presents an attractive interventional goal to restore immune cell homeostasis in RA. - Source: PubMed
Publication date: 2026/05/25
Chandrasekaran VenkataragavanErlandsson Malin CSvensson DavidMalmhäll-Bah EricSilfverswärd Sofia TöyräPullerits RilleKatona GergelyBokarewa Maria I - The treatment of head and neck squamous cell carcinoma (HNSCC) is particularly difficult because of its aggressive nature, complex anatomical location, and high recurrence and metastasis rates. This study investigated the relationship between glycosylation and mitophagy-related genes in HNSCC. - Source: PubMed
Publication date: 2026/04/28
Lu QiaolingYing LiLing LangHui WuWang Xinbin - To investigate the role of peroxiredoxin isoforms (Prdx) in the radioresistance of cancer cells, the expression of Prdx1-6, DNA repair genes, and apoptosis regulators was studied in human cancer cell lines with varying radiosensitivities (A549, Caco-2, and MCF-7) after exposure to ionizing radiation. A correlation was found between high constitutive Prdx1-6 expression levels and increased radioresistance. Predominantly cytosolic isoforms Prdx2 and Prdx6 demonstrated pronounced induction after irradiation, indicating their critical role in protecting against radiation-induced oxidative stress. Most radiosensitive A549 cells exhibited the lowest baseline Prdx expression and the most pronounced transcriptional changes after irradiation, whereas MCF-7 and Caco-2 cells had higher constitutive expression and a weaker response to radiation. Mitochondrial Prdx3 and Prdx5, as well as ER-localized Prdx4, exhibited relatively stable expression. A549 cells demonstrated the highest induction of DNA repair genes, which may indicate more severe DNA damage. In contrast, MCF-7 cells were characterized by high basal expression of repair genes and elevated γH2AX levels before irradiation, which may reflect their "readiness" for repair and explain their higher radioresistance. Furthermore, radioresistant MCF-7 cells had increased expression of anti-apoptotic genes (BCL2, MCL1, BIRC5), suppressing the mitochondrial apoptotic pathway. Meanwhile, A549 cells showed higher induction of pro-apoptotic genes (PUMA, NOXA, BAK1) and activation of caspase-3, which correlates with their increased radiosensitivity. Therefore, peroxiredoxins protect cells from radiation exposure, either by being constitutively expressed or by being highly inducible in response to radiation, and promote cell survival after irradiation. This makes them attractive targets for overcoming cancer cell radioresistance. - Source: PubMed
Publication date: 2026/05/22
Sharapov M GGoncharov R GKarmanova E EParfenyuk S BGlushkova O VLunin S M - : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
Rutecki SzymonKrawiec AdriannaLeśniewska-Bocianowska AgnieszkaMatuszewska JuliaNaumowicz ErykSzubert SebastianKsiążek KrzysztofMikuła-Pietrasik Justyna