Bub3 (Phospho-Tyr207) Antibody
- Known as:
- Bub3 (Phospho-Tyr207) Antibody
- Catalog number:
- 11586
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- Bub3 (Phospho-Tyr207) Antibody
Related genes to: Bub3 (Phospho-Tyr207) Antibody
- Gene:
- BUB3 NIH gene
- Name:
- BUB3 mitotic checkpoint protein
- Previous symbol:
- -
- Synonyms:
- BUB3L
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-17
- Date modifiied:
- 2019-01-18
Related products to: Bub3 (Phospho-Tyr207) Antibody
Related articles to: Bub3 (Phospho-Tyr207) Antibody
- - Source: PubMed
Publication date: 2026/04/06
Zhu DingqiangLiang JinghuiLi JiachengYu WenhaoMa LuyuanTang ZhanpengLi RongyangQu ChenghaoHan JingyiWang DingxinLi LinTian Hui - The spindle assembly checkpoint (SAC) is vital for preventing oocyte aneuploidy, a leading cause of female infertility, miscarriages, and trisomy syndromes. However, whether deubiquitination participates in SAC regulation remains unknown. Here, we reveal that the deubiquitinase USP8 acts as a SAC regulator to prevent aneuploid egg formation. Mechanistically, depletion of USP8 inactivates the SAC, accelerates meiotic progression, and causes abnormal spindle assembly and chromosome alignment, ultimately leading to aneuploidy. Intriguingly, we identify USP8 in oocytes as a previously unidentified interaction partner of BUB3, a key component of the SAC, and demonstrate that USP8 stabilizes BUB3 through its deubiquitinating activity. Moreover, exogenous BUB3 rescues the defects observed in USP8-depleted oocytes. Together, our findings not only clarify that deubiquitination participates in regulating the SAC in oocytes but also uncover a unique role for USP8 in controlling the SAC via its interaction with BUB3. - Source: PubMed
Publication date: 2026/03/13
Zhou 周长银 ChangyinZhang 张雪 XueXu 许根露 GenluWang 王慧 HuiRan 冉宇婷 YutingLi 李昂 AngSun 孙青原 Qing-YuanOu 欧湘红 Xiang-Hong - Acrylamide is a synthetic material which is widely used in water treatment and paper manufacturing, and it is also generated from food formation, which shows neurological effects, skin irritation, or reproductive toxicity. Several studies focused on the effects of acrylamide on mitochondria and apoptosis in oocytes. In present study, we reported that acrylamide disturbed cell cycle progression of mouse oocyte meiosis. Our data showed that acrylamide caused both germinal vesicle (GV) breakdown and polar body extrusion defects. Further analysis indicated that acrylamide induced DNA damage in the GV oocytes, showing with increased γ-H2A.X expression, which active CHK2 for G2/M transition. This could be confirmed by the altered Cyclin B1 and CDK1 expression in oocytes. Besides, we found kinetochore-microtubule attachment was aberrant in metaphase I (MI) oocytes, which active spindle assembly checkpoint (SAC) for polar body extrusion, and this was confirmed by the consistent presentence of BubR1 and Bub3. This was due to the reduced tubulin acetylation-based microtubule stability, since HDAC6 and NAT10 expression was changed and cold treatment reduced the tubulin polymerization. Taken together, our study reported that acrylamide exposure disrupted cell cycle progression through DNA damage-based MPF activity and tubulin acetylation-based SAC activation in oocytes. - Source: PubMed
Publication date: 2026/01/30
Chen ShanshanWang Peng-XiaWang Yan-TingKe Xing-HeOu MinminSun Shao-ChenLiao Bi-YunChen Xuanyi - In colorectal carcinoma (CRC), 5-fluorouracil (5-FU) remains the cornerstone of adjuvant systemic therapy, with folic acid (FA) serving as an essential adjunct. Expression of genes related to the metabolism and action of 5-FU and FA can be influenced by patient- and tumor-specific biological factors. In this study, we explore differential gene expression profiles of 180 genes representing 14 different gene sets associated with different 5-FU and FA metabolism processes, at both gene and pathway levels across clinical and molecular subgroups. In 71 patients with CRC, paired tumors and normal colonic tissues were analyzed. In CRC tissue, several gene sets (including Cell Cycle Checkpoint, Oxidative Stress Response, and Signaling Pathway, etc.) were upregulated, while three gene sets (Apoptotic, Tumor Suppressor, and Endoplasmic Reticulum Stress) were downregulated. Kirsten rat sarcoma virus (), tumor protein p53 (), and microsatellite instability (MSI) status impacted gene expression across molecular subgroups. At the individual gene level, among cell cycle genes, the BUB3 mitotic checkpoint protein () was upregulated in MSI tumors compared to MSS, whereas SMAD family member 4 () was downregulated in MSS tumors compared to MSI. DNA fragmentation factor alpha () was downregulated in MSI and upregulated in MSS. Notably, thymidylate synthetase () was more upregulated in MSI tumors (1.65-fold; 95% CI: 1.27-2.13) compared to MSS (1.19-fold; 95% CI: 1.02-1.39). Dysregulation of these genes across these factors will broaden our understanding of 5-FU-based treatment in CRC. Furthermore, targeting dysregulated pathways could form the basis for improved precision therapies tailored to CRC subtypes. - Source: PubMed
Publication date: 2025/11/26
Islam Muhammad RafiqulJasmine FarzanaVasiljevs DaniilRaza MarufAlmazan ArmandoAhsan HabibulKibriya Muhammad G - - Source: PubMed
Shi XufanYu XingchenWang WenwenXiong FangyuanYuan XiaoHu QingSong XiaoyuDou ZhenYao XuebiaoZhang Liangyu