CCNB1 Antibody (Center)
- Known as:
- CCNB1 Antibody (Center)
- Catalog number:
- AP11096c
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCNB1 Antibody (Center)
Related genes to: CCNB1 Antibody (Center)
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
Related products to: CCNB1 Antibody (Center)
Related articles to: CCNB1 Antibody (Center)
- Glioblastoma (GBM) is the most aggressive primary brain malignancy, characterised by hypoxia-driven proliferation, therapeutic resistance and poor prognosis. While hypoxia-induced transcriptional changes are well documented, the temporal regulation of cell cycle genes under sustained hypoxia remains unclear. - Source: PubMed
Publication date: 2026/07/02
Sharma Manish KChongtham JonitaBhushan AshishChosdol KunzangSinha SubrataSrivastava Tapasya - O-GlcNAcylation is a post-translational modification (PTM) uniquely catalyzed by O-GlcNAc transferase (OGT), which has been linked to tumorigenesis and neurodegeneration. However, its roles in mammalian spermatogenesis remain unexplored. This study aims to elucidate the functional mechanisms of OGT in spermatogenesis and male fertility. - Source: PubMed
Publication date: 2026/07/03
Ding ZhimingWu CaiyunLi MinHu KaiqinLi XuanxiChen ZhenLi KuokuoCheng HuiruShen QunshanCao YunxiaXiang HuifenGuo Rui - Neoadjuvant chemotherapy (NAC) followed by radical cystectomy (RC) has been the standard care for muscle-invasive bladder cancer (MIBC) for two decades. One third of NAC-treated patients achieve pathologic complete response (pT0N0), a proxy for improved survival after RC. Predicting response already at transurethral resection of bladder tumor (TUR-BT) would enable selective use of NAC, minimizing exposure to ineffective therapy. We aimed to identify tumor mRNAs associated with response across multiple transcriptomic studies, prioritizing subsequent biomarkers for validation. Three NAC-treated cohort with tumor transcriptomic profiles were included. Differential mRNA-expression analysis and subtype classification according to the Lund Taxonomy were performed. Within each cohort and subtype, genes were ranked by differential expression, and integrated into a meta rank-score. Survival associations of top genes in the NAC-cohorts were used to select candidate biomarkers for protein validation. Proliferation/late cell-cycle gene predicted response in Urothelial-like subtype and cytotoxic T- and NK-cell-related genes predicted response in Basal/Squamous tumors. These findings were validated by immunostainings for CCNB1 and NKG7, respectively. This integrative framework suggests a complex picture in which two NAC-predictive signals identify responders in a subtype dependent manner. The framework can be updated as new datasets become available, providing dynamic exploration of NAC-predictive biomarkers in MIBC. - Source: PubMed
Publication date: 2026/07/03
Zadoroznyj AymericEriksson PontusBernardo CarinaTran LenaMattsson Carl-AdamFlaig Thomas WSeiler RolandTangen Catherine MBlack Peter CLerner Seth PMcConkey David JHöglund MattiasLiedberg FredrikSjödahl Gottfrid - Leukemia is a heterogeneous malignancy with poor outcomes in refractory cases, and fusion genes involving JAK2 are known oncogenic drivers. The ARHGEF2::JAK2 fusion gene combines hyperactive kinase signaling with cytoskeletal regulation, but its functional role in leukemia remains unclear. This study aimed to characterize the oncogenic mechanisms of ARHGEF2::JAK2 and identify key downstream targets. Ba/F3 cells transduced with ARHGEF2::JAK2 and mouse xenograft models were used to assess proliferation, apoptosis, and leukemogenic potential. RNA sequencing, qPCR, and Western blotting were used to analyze downstream targets, followed by functional validation via shRNA knockdown. Results showed that ARHGEF2::JAK2 conferred cytokine-independent growth, suppressed apoptosis, and drove aggressive leukemia in mice. Ruxolitinib ameliorates ARHGEF2::JAK2-induced leukemogenesis in vivo. Transcriptomic analysis identified CCNB1 as a critical downstream effector, and its knockdown reversed the oncogenic effects of ARHGEF2::JAK2, improving survival and reducing organ infiltration. These findings demonstrate that ARHGEF2::JAK2 promotes leukemogenesis via CCNB1 upregulation, suggesting CCNB1 as a potential therapeutic target. This study provides new insights into fusion-driven leukemia pathogenesis. - Source: PubMed
Publication date: 2026/07/03
Ma YananJiang YanWang LinlinCheng YuexinYang XiaofeiChen Suning - Psoriasis is a chronic immune-mediated inflammatory skin disorder characterized by excessive keratinocyte proliferation and persistent inflammation. Its multifactorial pathogenesis involves complex inflammatory mediators and signaling pathways. Current treatments remain limited by high recurrence and adverse effects, highlighting the need for safe and effective natural bioactive compounds for psoriasis prevention and management. In addition, cyclin B1 (CCNB1) has been reported as a hub gene associated with psoriasis; however, its mechanism of action remains unclear. - Source: PubMed
Publication date: 2026/06/27
Wang HuiqinDing YuanWang ZhenruiWang YiqiLiu YanwenMa YaqinWu Weidong