CDC2L1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- CDC2L1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb101250
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CDC2L1 antibody Polyclonal Antibodies Primary antibodies
Ask about this productRelated genes to: CDC2L1 antibody Polyclonal Antibodies Primary antibodies
- 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 Polyclonal Antibodies Primary antibodies
Related articles to: CDC2L1 antibody Polyclonal Antibodies Primary antibodies
- 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
Mao JianshuiLi Hui-MinHuang Zhidan - We identified resistance mechanisms to abiraterone acetate/prednisone (AA/P) in patients with metastatic castration-resistant prostate cancer (mCRPC) in the Prostate Cancer Medically Optimized Genome-Enhanced Therapy (PROMOTE) study. We analyzed whole-exome sequencing (WES) and RNA-sequencing data from 83 patients with metastatic biopsies before (V1) and after 12 weeks of AA/P treatment (V2). Resistance was determined by time to treatment change (TTTC). At V2, 18 and 11 of 58 patients had either short-term (median 3.6 months; range 1.4-4.5) or long-term (median 29 months; range 23.5-41.7) responses, respectively. Nonresponders had low expression of TGFBR3 and increased activation of the Wnt pathway, cell cycle, upregulation of AR variants, both pre- and posttreatment, with further deletion of AR inhibitor CDK11B posttreatment. Deletion of androgen processing genes, HSD17B11, CYP19A1 were observed in nonresponders posttreatment. Genes involved in cell cycle, DNA repair, Wnt-signaling, and Aurora kinase pathways were differentially expressed between the responder and non-responder at V2. Activation of Wnt signaling in nonresponder and deactivation of MYC or its target genes in responders was detected via SCN loss, somatic mutations, and transcriptomics. Upregulation of genes in the AURKA pathway are consistent with the activation of MYC regulated genes in nonresponders. Several genes in the AKT1 axis had increased mutation rate in nonresponders. We also found evidence of resistance via PDCD1 overexpression in responders. - Source: PubMed
Sicotte HuguesKalari Krishna RQin SisiDehm Scott MBhargava VipulGormley MichaelTan WinstonSinnwell Jason PHillman David WLi YingVedell Peter TCarlson Rachel EBryce Alan HJimenez Raphael EWeinshilboum Richard MKohli ManishWang Liewei