Survivin _ BIRC5 Antibody
- Known as:
- Survivin _ BIRC5 Antibody
- Catalog number:
- AF2051a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Survivin _ BIRC5 Antibody
Related genes to: Survivin _ BIRC5 Antibody
- 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: Survivin _ BIRC5 Antibody
Related articles to: Survivin _ BIRC5 Antibody
- To investigate the effect of Interstitial photodynamic therapy (IPDT) on transplanted tumors of human lung adenocarcinoma A549 cells in nude mice. Twenty-four models of nude mice bearing A549 transplanted tumors were established, which were randomly and equally divided into four groups: the control group, the photosensitizer group, the laser group, and the IPDT group. Each group is treated according to the grouping principle. The tumor volume growth changes in each group were compared. The HE staining was performed to observe the pathomorphological changes of transplanted tumor cells in each group. The TUNEL assay was used to observe the apoptosis induced by IPDT. The qRT-PCR and western blot assays were used to detect the expression levels of Survivin, Caspase-3, Bax, Bcl-2, VEGF and HIF-1α genes in the transplanted tumor tissues. The results showed that the volume of the tumor volume in the IPDT group was noticeably smaller than that in the control, photosensitizer and laser groups, with statistically significant differences (P < 0.05). After HE staining of tumor tissues, there were various necrotic, disordered and foamy cells in the IPDT group. The cells in the other three groups were closely arranged with large hyperchromatic nuclei. The TUNEL assay revealed that more apoptotic cells with brown particles in the nucleus were found in the IPDT group. The results of qRT-PCR and western blot assays showed that compared with the other three groups, the expressions of Survivin, Bcl-2, VEGF, and HIF-1α in the IPDT group were decreased, while the expressions of Caspase-3 and Bax were increased. The differences were statistically significant (P < 0.05). IPDT could significantly inhibit the growth of A549 transplanted tumors in nude mice, which is possibly related to down-regulating the expression of apoptotic factors Survivin and Bcl-2 genes, up-regulating the expression of Caspase-3 and Caspase-9 genes, and down-regulating the expression of angiogenesis-related VEGF and HIF-1α genes. - Source: PubMed
Publication date: 2026/07/10
Zhang YuanyuanHan WeizhongNiu FangxiaZhang HuaDong YuxiaYang XiaohuiLin Cunzhi - Patients with advanced malignant adrenal tumors face poor prognoses with limited treatment options. Emerging data suggest that these rare tumors exhibit immunogenicity, potentially benefiting from intensified immunotherapy. - Source: PubMed
Publication date: 2026/07/06
Schultheiß ChristophBesemer BrendaWillscher EdithPaschold LisaMersceman TifannyTalpin AliceSerger ClaraZippelius AlfredBerruti AlfredoGrisanti SalvatoreMenke-van der Houven van Oordt Catharina WillemienBaudin EricLandwehr Laura-SophieCapdevila JaumeSubbiah VivekGranberg DanGedske Daugaard KirstenTriebig AlexandraGauduchon ThibaultDo Cao ChristineGarcia Marie-EveMagalhaes JoaoChêne LaurentBinder Mascha - Pulsed electromagnetic fields (PEMF) can be used to improve the efficacy of chemotherapeutic agents, such as doxorubicin (DOX). DOX induces mitotic slippage, leading to cell death in various cancers including breast cancer. Herein, we investigated whether PEMF exposure enhances DOX-induced mitotic slippage and subsequent cell death in breast cancer cells. - Source: PubMed
Woo Sung-HunLee Yong-HeumJung Byung ChulKim Yoon Suk - Adrenocortical carcinoma (ACC) is a rare but highly aggressive malignancy with limited treatment options. Anoikis plays a critical role in the progression of various cancers; however, its function in ACC remains unclear. - Source: PubMed
Publication date: 2026/06/11
Cao JuanXu MingZhou WenjunZhong ShuxiCao XiaoxuanXie HuipingShen Zhiming - Malignant rhabdoid tumor (MRT) is an aggressive pediatric cancer defined by biallelic loss of SMARCB1 and characterized by an unusually simple mutational landscape. Despite the absence of recurrent activating oncogenic mutations, MRT exhibits highly malignant behavior, creating a clinical paradox. Loss of SMARCB1 disrupts SWI/SNF-mediated chromatin organization, leading to enhancer redistribution and reorganization of transcriptional control. MRT therefore provides a defined model to examine how structural disruption of chromatin regulation sustains tumor maintenance in the absence of mutation-driven signaling activation. We propose that this epigenetic collapse reduces regulatory diversity and concentrates control of essential survival and cell-cycle programs within limited transcriptional nodes. We define this structural state as transcriptional bottleneck formation, in which tumor viability depends on concentrated transcriptional control rather than recurrent genetic alteration. Bottleneck nodes are characterized by enriched chromatin occupancy at survival and cell-cycle genes, limited compensatory regulation, and functional sensitivity to perturbation. In MRT, members of the RUNX family illustrate a representative concentrated transcriptional node linking chromatin reorganization to regulation of BIRC5 and related survival genes. This disease-focused perspective supports an architecture-centered therapeutic strategy aimed at disrupting concentrated transcriptional control. Identification of biomarkers reflecting this architectural state may facilitate selection of bottleneck-directed interventions in MRT. - Source: PubMed
Publication date: 2026/06/24
Masuda TatsuyaWatanabe TakayoshiOzaki ToshinoriKamikubo Yasuhiko