CDC2L1 antibody
- Known as:
- CDC2L1 (anti-)
- Catalog number:
- orb101250
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CDC2L1 antibody
Related genes to: CDC2L1 antibody
- Gene:
- CDK11B NIH gene
- Name:
- cyclin dependent kinase 11B
- Previous symbol:
- CDC2L1
- Synonyms:
- CDK11-p110, CDK11-p58, CDK11-p46
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-12
- Date modifiied:
- 2016-06-08
Related products to: CDC2L1 antibody
Related articles to: CDC2L1 antibody
- Gene-wise intratumor heterogeneity (ITH), defined as spatial variability in the expression of individual genes across tumor regions, remains incompletely characterized in non-small cell lung cancer (NSCLC). Identifying low-ITH genes as predictive biomarkers offers a promising strategy to enhance the reliability of immunotherapy outcome prediction. - Source: PubMed
Publication date: 2026/06/20
Yuan JianyeWeng ZelinLi ZhenguoChen RuiCheng ChaoYang WeixiongXie XiuyingLuo ChangWang TaoZhang ShuishenTan Zihui - Rhabdoid tumor of the kidney (RTK) is a highly aggressive pediatric malignancy characterized by biallelic loss, resulting in aberrant MYC pathway activation and cell cycle regulation. MYC-activated tumors are vulnerable in splicing functions and sensitive to splicing inhibitors. Therefore, in this study, cyclin-dependent kinase 11 (CDK11), which regulates both cell cycle and RNA splicing, was tested as a therapeutic target in RTK. - Source: PubMed
Publication date: 2026/01/14
Murakami YukiLam KamhungFukui ShinsukeHelmke ElizabethIczkowski Kenneth ALi YuejuSatake Noriko - Liver fibrosis is the initial stage of most liver diseases, and it is also a pathological process involving the liver in the late stages of many metabolic diseases. Therefore, it is important to systematically understand the pathological mechanism of liver fibrosis and seek therapeutic approaches for intervention and treatment of liver fibrosis. Disordered proteins and their post-translational modifications, such as phosphorylation, play vital roles in the occurrence and development of liver fibrosis. However, the regulatory mechanisms that govern this process remain poorly understood. In this study, we analyzed and quantified the liver proteome and phosphoproteome of carbon tetrachloride-induced early liver fibrosis model in mice. Proteomic analysis revealed that the pathways involved in extracellular matrix recombination, collagen formation, metabolism and other related disorders, and protein phosphorylation modification pathways were also significantly enriched. In addition, Western blotting and phosphoproteomics demonstrated that phosphorylation levels were elevated in the context of liver fibrosis. A total of 13,152 phosphosites were identified, with 952 sites increased, whereas only 156 sites decreased. Furthermore, the upregulated phosphorylation sites, which exhibited no change at the proteome level, mainly shared a common [xxxSPxxx] motif. Consequently, the kinase-substrate analysis ascertained the overactive kinases of these upregulated substrates, which ultimately led to the identification of 13 significantly altered kinases within this dataset. These kinases were mainly cataloged into the STE, CMGC, and CAMK kinase families. Among them, STK4 (serine/threonine-protein kinase 4), GSK3α (glycogen synthase kinase 3α), and CDK11B (cyclin-dependent kinase 11B) were subsequently validated though cellular and animal experiments, and the results demonstrated that their inhibitors could effectively reduce the activation of hepatic stellate cells and extracellular matrix production. These kinases may represent potential therapeutic targets for liver fibrosis, and their inhibitors may serve as promising antihepatic fibrosis drugs. - Source: PubMed
Publication date: 2025/05/12
Cheng XinyuKang LiLiu JinfangWang QingyeZhang ZhenpengZhang LiXie YupingChang LeiZeng DaobingTian LantianZhang LingqiangXu PingLi Yanchang - Hepatocellular carcinoma remains one of the most lethal cancers, characterized by poor prognosis and low life expectancy. Unfortunately, there are very few molecular therapeutic options available for it. Sorafenib is a current standard first-line treatment for advanced hepatocellular carcinoma, however, drug resistance significantly limits its therapeutic efficacy. - Source: PubMed
Wang XiaochenSu YijieLan BeiLi XuanyuanZhang BodiZhang LiangWang YingmeiZhang ChunzeXuan Chenghao - Cyclin-dependent protein kinases (CDKs) have been suggested as prospective therapeutic targets because they control processes vital to the survival and growth of cancer cells. However, research on the varied CDK expression profiles and prognostic factors in osteosarcoma is still lacking. - Source: PubMed
Publication date: 2024/10/02
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