CCNB1 & PKMYT1 Protein Protein Interaction Antibody Pair
- Known as:
- CCNB1 & PKMYT1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0004
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCNB1 & PKMYT1 Protein Interaction Antibody Pair
Ask about this productRelated genes to: CCNB1 & PKMYT1 Protein Protein Interaction Antibody Pair
- 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
- Gene:
- PKMYT1 NIH gene
- Name:
- protein kinase, membrane associated tyrosine/threonine 1
- Previous symbol:
- -
- Synonyms:
- MYT1, PPP1R126
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-20
- Date modifiied:
- 2014-11-19
Related products to: CCNB1 & PKMYT1 Protein Protein Interaction Antibody Pair
Related articles to: CCNB1 & PKMYT1 Protein Protein Interaction Antibody Pair
- Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer and lacks effective biomarkers. This study seeks to unravel the expression status and the prospective transcriptional mechanisms of EZH1/EZH2 in TNBC tissue samples. Moreover, another objective of this study is to reveal the prognostic molecular signatures for risk stratification in TNBC patients. - Source: PubMed
Publication date: 2022/07/12
Peng WeiTang WeiLi Jian-DiHe Rong-QuanLuo Jia-YuanChen Zu-XuanZeng Jiang-HuiHu Xiao-HuaZhong Jin-CaiLi YangMa Fu-ChaoXie Tian-YiHuang Su-NingGe Lian-Ying - This article is dedicated to finding important genes related to the prognosis of lung adenocarcinoma (LUAD), looking for a new gene that may affect tumor radiosensitivity, and conducting basic experiments to verify the relationship between this gene and the radiosensitivity of LUAD. - Source: PubMed
Publication date: 2020/04/29
Long Huan-PingLiu Jia-QingYu Yang-YangQiao QiaoLi Guang - Prostate cancer (PCa) is the third most common malignancy worldwide. Novel and effective therapeutic targets are needed for PCa. The purpose of this study was to discover novel therapeutic targets for PCa by performing advanced analysis on PCa RNA sequencing (RNAseq) data from The Cancer Genome Atlas (TCGA). Weighted correlation-network analysis (WGCNA) was performed on the RNAseq data of tumor samples, and the module most relevant to the Gleason score was identified. Combining differential gene-expression analysis and survival analysis, we narrowed down potential therapeutic target genes and found that PKMYT1 might be one. Subsequently, functional studies (i.e., cell-proliferation assays, cell cycle analysis, and colony-formation assays) demonstrated that knockdown of PKMYT1 significantly inhibited the growth of PCa cells. Further investigation illustrated that PKMYT1 promoted the growth of PCa cells through targeting CCNB1 and CCNE1 expression. In addition, fostamatinib, an inhibitor of PKMYT1, effectively inhibited the proliferation of PCa cells. Taken together, our results suggest that PKMYT1 is a gene associated with malignancy of PCa and is a novel therapeutic target. - Source: PubMed
Publication date: 2020/03/29
Wang JiananWang LinChen SaipengPeng HuahongXiao LongfeiE Du Liu YanLin DongWang YuzhuoXu YongYang Kuo - The role and mechanism of hsa_circRNA_104433 in gastric cancer (GC) are further elucidated. - Source: PubMed
Publication date: 2020/01/06
Wei WeiyuanMo XianweiYan LinhaiHuang MingweiYang YangJin QinwenZhong HuageCao WenlongWu KunWu LiuchengLi ZhaoWang TinganQin YuzhouChen Jiansi - 1,25-dihydroxyvitamin D3 (1,25[OH]2VD3) has an antiproliferative effect on keratinocyte growth, and its derivatives are used for the treatment of psoriasis. It was reported previously that 1,25[OH]2VD3 induced cell cycle arrest not only at the G0/G1 phase but also at the G2/M phase. However, the mechanism of 1,25[OH]2VD3-induced G2/M phase arrest in keratinocytes has not been fully understood. The addition of 10(-8) to 10(-6) M 1,25[OH]2VD3 to cultured normal human keratinocytes enhanced the expression of Myt1 mRNA preceding Wee1 mRNA; 10(-6) M 1,25[OH]2VD3 unregulated Myt1 mRNA from 6 h to 24 h and Wee1 mRNA from 12 to 48 h. Interestingly, the levels of phosphorylated Cdc2 were increased between 6 h and 48 h after 1,25[OH]2VD3 treatment, although the expression levels of Cdc2 mRNA and its protein production were reduced. 1,25[OH]2VD3 also decreased the expression of cyclin B1, which forms a complex with Cdc2. These data indicated that the increase of Myt1 and Wee1 induced the phosphorylation of Cdc2 leading to G2/M arrest. In conclusion, the induction of Cdc2 phosphorylation due to the increase of Wee1 and Myt1 as well as the reduction of Cdc2 and cyclin B1 are involved in 1,25[OH]2VD3-induced G2/M arrest of keratinocytes. - Source: PubMed
Dai XiujuYamasaki KenshiYang LujunSayama KojiShirakata YujiTokumara ShoYahata YokoTohyama MikikoHashimoto Koji