Ask about this productRelated genes to: CDKL3 antibody
- Gene:
- CDKL3 NIH gene
- Name:
- cyclin dependent kinase like 3
- Previous symbol:
- -
- Synonyms:
- NKIAMRE
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-04
- Date modifiied:
- 2016-01-07
Related products to: CDKL3 antibody
Related articles to: CDKL3 antibody
- Epithelial ovarian cancer (EOC) remains one of the most lethal gynecological malignancies. Although treatment options for newly diagnosed advanced EOC include primary debulking surgery (PDS) or neoadjuvant chemotherapy (NACT) followed by interval debulking surgery (IDS), the comparative effectiveness of these strategies remains uncertain across different disease stages. - Source: PubMed
Publication date: 2025/08/27
Jin YingShan YingGuo WenDong YuLi YanWang WeiYin JieLiang YimingGu YuPan LingyaLiang Han - Melanoma is a type of skin cancer originating from melanocytes with a high risk of gastrointestinal tract metastasis. The abnormal expression of cyclin-dependent kinase-like 3 (CDKL3) is involved in several tumor progression. However, the role of CDKL3 in malignant melanoma has never been reported and remains unknown. In this study, the expression of CDKL3 was revealed using clinical human malignant melanoma tissues and normal skin tissues. The effects of CDKL3 on malignant melanoma cell phenotypes was evaluated in vitro and in vivo via establishing CDKL3 deficiency cell models. Our results indicated that CDKL3 was highly expressed in malignant melanoma tissues, especially in advanced malignant melanoma tissues, in comparison with normal skin tissues. Moreover, CDKL3 knockdown significantly suppressed the proliferation, migration and invasion of malignant melanoma cells, and induced cell apoptosis. The indispensable role of CDKL3 on tumorigenesis was confirmed through in vivo experiments. Finally, we showed that CDKL3 promoted malignant melanoma progression via targeting autophagy related 5 (ATG5). CDKL3 induced melanoma cell autophagy through an ATG5-dependent manner. In conclusion, these results showed the promoting role of CDKL3 in proliferation and migration of malignant melanoma cells. The CDKL3 may be a novel biomarker for malignant melanoma progression and the potential therapeutic target for patients with malignant melanoma. - Source: PubMed
Publication date: 2025/06/26
Chen QiYu WenyuanGu YifeiCao ShikunXie XiaomingWu Lijun - CDKL3 (Cyclin-Dependent Kinase-Like 3) is a serine/threonine kinase that belongs to the cyclin-dependent kinase-like (CDKL) family. The first cloning of human CDKL3 was achieved in 1999. Despite the fact that the CDKL3 sequence shares features of both the MAPK (Mitogen-Associated Protein Kinase) and CDK (Cyclin-Dependent Kinase), suggesting that it may have important physiological functions, CDKL3 has long been under-explored. Over the past two decades, studies have revealed the involvement of CDKL3 in cell cycle regulation and cancer progression. However, the in-depth mechanism by which it exerts these effects remains to be elucidated. Recently, we have performed systematic studies on CDKL3, providing a comprehensive revelation of the pivotal role of CDKL3 in cell cycle regulation, metabolic disease, cancer initiation and progression. We hence review CDKL3 in terms of its molecular mechanism, function and the relevance of CDKL3 to other proteins, and discuss the future perspectives in studying CDKL3. - Source: PubMed
Publication date: 2025/05/29
Ma LanjingZhang HaijiaoPang ZhongqiuSheng Ren - Clear cell renal cell carcinoma (ccRCC) is the predominant human renal cancer with surging incidence and fatality lately. Hyperactivation of hypoxia-inducible factor (HIF) and mammalian target of rapamycin (mTOR) signaling are the common signatures in ccRCC. Herein, we employed spontaneous ccRCC model to demonstrate the indispensability of an underappreciated Ser/Thr kinase, CDKL3, in the initiation and progression of ccRCC. Ablation of CDKL3 does not affect normal kidney, but abrogates Akt-mTOR hyperactivity and thoroughly prevents the formation and growth of the HIF-agitated ccRCC in vivo. Remarkable clinical correlations also supported the oncogenic role of CDKL3. Mechanism-wise, cytosolic CDKL3 unexpectedly behaves as the adaptor to physically potentiate mTORC2-dependent Akt activation without functioning through kinase activity. And mTORC2 can phosphorylate and stabilize CDKL3 to form a positive feedback loop to sustain the cancer-favored Akt-mTOR overactivation. Together, we revealed the pathological importance and molecular mechanism of CDKL3-mediated Akt-mTOR axis in ccRCC initiation and progression. - Source: PubMed
Publication date: 2025/02/12
Ma LanjingPang ZhongqiuZhang HaijiaoYang XuelingZheng ShaoqinChen YiDing WeijieHan QingZhang XiCao LiuFei TengWang QiangGao DamingHe AinaHu Ke-BangLi XuexinSheng Ren - Pulmonary hypertension (PH) is a malignant cardiovascular disease with a complex etiology. 5-Methylcytosine (m5C) is a post-transcriptional RNA modification identified in both stable and highly abundant RNAs, with a lower frequency of occurrence in circular RNAs (circRNAs). Nevertheless, the function of m5C-modified circRNAs in the pathogenesis of PH remains uncertain. The objective of this study was to investigate the biological role and molecular mechanisms of m5C-modified circRNA-CCNL2 in hypoxic PH pulmonary vascular remodeling. Our findings revealed that hypoxia downregulates circCCNL2 expression, and overexpression of circCCNL2 attenuates PH progression and inhibits the proliferation of pulmonary artery smooth muscle cell (PASMCs). Bioinformatics predictions indicated the presence of m5C modification sites in circCCNL2, which NSUN2 mediated. The downregulation of NSUN2 resulted in a reduction in m5C modification of circCCNL2. It was also observed that the stability of circRNAs was associated with the proliferation of PASMCs. From a mechanistic standpoint, low expression of circCCNL2 resulted in reduced binding of FXR2, while increased association of free FXR2 with CDKL3 led to enhanced proliferation of PASMCs. Notably, circCCNL2 expression was found to be regulated by alternative splicing involving SRSF2, with reduced pre-CCNL2 splicing resulting from low SRSF2 expression, ultimately leading to decreased circCCNL2 expression. This is the first demonstration that m5C-modified circCCNL2 can slow the development of PH and inhibit the proliferation of PASMCs by binding to FXR2. These findings offer new insights into the regulation of circRNAs through m5C modifications and the role of epigenetic reprogramming in PH. - Source: PubMed
Publication date: 2025/01/10
Sun HanliangLiao XueyinWang ShanshanYuan HaoBai JuneFeng HaoxueLi MengnanSong XinyueMa CuiZhang LixinZhao XijuanZheng XiaodongZhu Daling