CDK10 _ PISSLRE
- Known as:
- CDK10 _ PISSLRE
- Catalog number:
- Y214251
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CDK10 _ PISSLRE
Related genes to: CDK10 _ PISSLRE
- Gene:
- CDK10 NIH gene
- Name:
- cyclin dependent kinase 10
- Previous symbol:
- -
- Synonyms:
- PISSLRE
- Chromosome:
- 16q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-30
- Date modifiied:
- 2016-06-08
Related products to: CDK10 _ PISSLRE
Related articles to: CDK10 _ PISSLRE
- Bone remodeling is a critical process for skeletal health, and its dysregulation can lead to diseases like osteoporosis. While several Cyclin-Dependent Kinases (CDKs) are known to regulate bone metabolism, the function of CDK10 remains uncharacterized in this context. Human mutations in cause the Al Kaissi syndrome, which involves severe skeletal defects, suggesting a role for CDK10 in bone. The objective of this study was to investigate the functional role of CDK10 in bone remodeling in mice . - Source: PubMed
Publication date: 2025/12/22
Yu DaiyangTanaka TomoyukiMiyakoshi YuriKato TsuyoshiOchi HirokiSato ShingoYoshii ToshitakaAl Kaissi AliKaldis PhilippInose Hiroyuki - - Source: PubMed
Firmino Natalie SWest Nathaniel R - Cancer immunotherapies have revolutionized cancer treatment, yet many patients fail to respond. Activating innate immunity offers a promising approach to enhance therapeutic efficacy, but the signaling kinases directly regulating this process to boost antitumor responses remain elusive. Here we conduct an in vivo kinome CRISPR screen and identify CDK10 as a key suppressor of tumor immune surveillance. Mechanistically, CDK10 phosphorylates DNMT1 and RAP80 to reduce the accumulation of double-stranded RNA and R-loops, which alleviates the activation of innate immune pathways mediated by MDA5 and cGAS. Kinase inhibitor screens identify NVP-AST487 and ponatinib as selective CDK10 inhibitors. Both genetic and pharmacological inhibition of CDK10 activates MDA5 and cGAS pathways, fostering an immunoactive tumor microenvironment that enhances cancer immunotherapy in multiple mouse tumor models. Clinically, low CDK10 expression in tumors correlates with better immunotherapy responses. These findings establish CDK10 as a pivotal modulator of tumor immunity and a potential therapeutic target. - Source: PubMed
Publication date: 2026/01/08
Xu GaoshanGuo FushengHe ChuanWang XiyongXiang BolinFan LifangChen BaoxiangPeng JiakunSun YishuangShi JieXing XixinYao YingmengDai PanpanLi HaiouXiong WenjunLiu HudanXiao RuiQing GuoliangJiang CongqingJiang BaishanLei XiaoguangZhang Jinfang - CDK11 is an essential cyclin-dependent kinase in higher eukaryotes, yet its specific substrates and functional roles have remained elusive. Our findings reveal that CDK11 is functionally analogous to the yeast Bur1 kinase, phosphorylating the repeat region of hSpt5 and the linker domain of Rpb1 in RNA Polymerase II (Pol II). Inhibition of CDK11 results in a significant reduction of active Pol II not only at transcription start sites but also along gene bodies. Further investigation finds that CDK11 is crucial for the phosphorylation and activation of CDK12, which is essential for the elongation of Pol II. Moreover, we find that CDK10 can partially compensate for the function of CDK11. Combining with earlier functional elucidation of CDK9 from us, the consequent roles of CDK7/8, CDK9, CDK10/11, and CDK12/13 in transcription regulation in metazoans are established. - Source: PubMed
Publication date: 2025/09/28
Liu HaolinLi LingboGao JunfengLeach SoniaWei PengchengZhang QianqianHuang HuaHoules ThibaultRoux Philippe PZhang Gongyi - To resolve the ambiguous causal relationship between sleep disturbances and neurodegenerative diseases such as Alzheimer's disease (AD), we conducted a multi-stage genetic and multi-omics investigation. Our large-scale bidirectional Mendelian randomization analysis identified a robust, asymmetrical pattern of genetic association, providing strong genetic evidence suggesting that liability for neurocognitive decline and AD is associated with sleep disturbances, with substantially weaker evidence for the reverse direction. To identify the underlying molecular drivers, a multi-omics Summary-data-based MR (SMR) analysis prioritized high-confidence causal genes, including , , , and . The predictive power of this gene signature was confirmed using machine learning models (ROC-AUC > 0.8), while functional validation through bulk and single-cell transcriptomics uncovered profound, cell-type-specific dysregulation in the AD brain, most notably opposing expression patterns between neurons and glial cells (e.g., was upregulated in excitatory neurons but downregulated in glia). Functional enrichment and network analyses implicated two core pathways-nucleotide metabolism centered on and synaptic function involving -and our investigation culminated in the identification of a promising therapeutic interaction, with molecular docking validating high-affinity binding between Ecdysterone and COX6B1 (docking score = -5.73 kcal/mol). Collectively, our findings strengthen the evidence that sleep disruption as a likely consequence of neurodegenerative processes and prioritize a set of validated, cell-type-specific gene targets within critical pathways, offering promising new avenues for therapeutic development. - Source: PubMed
Publication date: 2025/11/20
Du YananXia Xiao-YongNi ZhuFan Sha-ShaHe JunwenHe YangMeng Xiang-YuWang XuXu Xuan