IAP4 _ BIRC5
- Known as:
- IAP4 _ BIRC5
- Catalog number:
- NB100-56167
- Product Quantity:
- 0.05 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
- High-grade serous ovarian carcinoma (HGSOC) features extensive intratumoral heterogeneity, frequent chemoresistance and poor prognosis. Tumor proliferation kinetics reflected by tumor doubling time (TDT) are linked to therapeutic response, yet molecular drivers of chemoresistance-associated proliferation remain incompletely defined. - Source: PubMed
Publication date: 2026/09/04
Zhang YanminWu SihuangLin HuizhuLi Ling - Diminished ovarian reserve (DOR) is associated with poor reproductive outcomes; however, the underlying molecular mechanisms-particularly those involving the regulation of granulosa cell (GC) function by exosomal microRNAs (miRNAs) derived from follicular fluid-remain unclear. This study integrated clinical analysis with molecular profiling to investigate the regulatory effects of DOR patient-derived follicular fluid exosomes on GC function. Clinical data confirmed significantly poorer embryological and clinical outcomes in DOR patients. Follicular fluid was collected from patients with normal ovarian reserve (NOR) and those with DOR. Exosomes and GCs were subsequently isolated from the respective follicular fluid samples. Molecular profiling of follicular fluid exosomes and GCs from both groups identified differentially expressed miRNAs and mRNAs via next-generation sequencing. Integrated bioinformatics analysis and dual‑luciferase reporter assays confirmed that exosomal hsa‑miR‑135a‑5p directly targets and suppresses BIRC5 expression in GCs. Functional experiments demonstrated that incubating NOR GCs with DOR exosomes not only significantly downregulated BIRC5 but also induced marked cellular autophagy and mitochondrial dysfunction. These findings reveal a novel exosome‑mediated regulatory pathway in which DOR follicular fluid exosomes deliver miR‑135a‑5p to recipient GCs, repress the anti‑apoptotic gene BIRC5, and disrupt cellular homeostasis, thereby providing a potential mechanistic explanation for the compromised follicular microenvironment and adverse clinical outcomes in DOR. - Source: PubMed
Ruan ZiyunLi ZhengdaShu JinhuiLin HuadanLi TianFeng YunWang XuWang CaizhuWu ZhulianHuang YulinXia MengZhao Xin - Corneal crosslinking (CXL) using riboflavin and ultraviolet A (UV-A) illumination is widely used to stabilize progressive ectatic corneal disorders such as keratoconus. However, the photochemical reaction generates oxidative stress and may induce apoptosis, while potential differences between healthy human corneal fibroblasts (HCF) and human corneal fibroblasts derived from keratoconus corneas (KC-HCF) remain insufficiently understood. This study examined in-vitro changes in pro- and anti-apoptotic markers in HCF and KC-HCF following riboflavin-UV-A illumination. - Source: PubMed
Publication date: 2026/09/03
Kahlert JulianBerger MaximilianSeitz BertholdChai NingSuiwal ShwetaSzentmáry NóraSchmitz FrankBerger Tim - EIF1, an RNA-binding protein implicated in multiple diseases, remains poorly characterized in diabetic retinopathy (DR). This study therefore investigated EIF1 expression and function in an in vitro model of DR pathogenesis. - Source: PubMed
Publication date: 2026/09/03
Li NaMa QianFan XinLiu QiLiu LiZhang ShengfuMa YalingXu HongxiaLi Xinyi - Neuroblastoma is a pediatric solid malignancy that primarily arises from poorly differentiated sympathoadrenal cells in the developing autonomic nervous system. The neuroblastoma genetic landscape is characterized by a paucity of somatic mutations and a far more common occurrence of chromosome copy number variations (CNVs). Two of the most common genetic abnormalities in neuroblastoma are the amplification of MYCN and the unbalanced gain of the long arm of chromosome 17 (17q+), both of which correlate with poor prognosis. Although mouse models exist for MYCN-driven neuroblastoma, no mouse models exist for 17q+. Thus, the mechanism by which 17q+ contributes to poor prognosis remains largely unknown. Here, we used a human pluripotent stem cell (PSC) model of neuroblastoma to show that 17q+ cooperates with MYCN amplification to accelerate tumorigenesis compared to MYCN amplification alone. We identified six genes on 17q that are upregulated in both our 17q+ PSC-derived tumors and 17q+ neuroblastoma patient tumors compared to WT 17q, correlate with poor prognosis in neuroblastoma patients, and are overexpressed at the protein level in our MYCN/17q+ tumors compared to MYCN alone. Of these six genes, knockdown of BIRC5, CDC6, IGF2BP1, or TK1 in MYCN/17q+ cells increases tumor latency in vivo and contributes to tumor progression through diverse mechanisms. Furthermore, knockdown of CDC6, IGF2BP1, and TK1 in neuroblastoma patient-derived xenografts with 17q+ slowed growth in vivo. Our findings provide new insights into potential candidate 17q drivers of neuroblastoma tumorigenesis and possible therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/08/26
Fang WanqiCheng BoPastor StevenZobel Michael JPorras TaniaWu Hong-WeiKondapally TaneeshRoberts Stephen SParekh ChintanTsai Jessica WTsakiridis AnestisBarbaric IvanaAsgharzadeh ShahabMaris John MHuang Miller