Proteins CDK2, Human
- Known as:
- Proteins CDK2, Human
- Catalog number:
- C211
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CDK2 Human
Related genes to: Proteins CDK2, Human
- Gene:
- CDK2 NIH gene
- Name:
- cyclin dependent kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-28
- Date modifiied:
- 2016-06-10
Related products to: Proteins CDK2, Human
Related articles to: Proteins CDK2, Human
- Lung cancer is one of the most common malignancies and the leading cause of cancer-related mortality worldwide, posing a major public health challenge. Flavonoids, a large and diverse group of plant metabolites, exhibit various anticancer properties, making them promising candidates for therapeutic applications. This study evaluated the anticancer efficacy of methoxy flavonoids and elucidated their underlying mechanisms of action in A549 lung cancer cells. - Source: PubMed
Publication date: 2026/01/01
Singh DhirendraKumar AmitVerma InderjeetYadav GovindShukla Sanket - Autism Spectrum Disorder (ASD) is characterized by dysregulated signaling pathways, notably involving Glycogen Synthase Kinase 3 Beta (GSK3β). The present study investigates Rosmarinic acid (RA), a natural polyphenol, as a potential GSK3β inhibitor for ASD using an integrative in silico framework. Multiple sequence alignment across six species revealed high conservation of GSK3β's ATP-binding pocket, underscoring its therapeutic relevance and translatability across model organisms. Molecular docking showed RA binds robustly to GSK3β's ATP-binding pocket (estimated affinity: 58.11 nM in SeeSAR scoring), compared to previously validated inhibitors such as Tideglusib (4077.20 nM in SeeSAR scoring) and Laduviglusib (93.26 nM in SeeSAR scoring). Independent Glide docking reproduced the binding orientation (GlideScore: - 7.548 kcal/mol), and MM-GBSA refinement indicated favorable binding free energy (ΔG = - 42.37 kcal/mol). A 100 ns molecular dynamics simulation demonstrated stable ligand retention and sustained catalytic pocket interactions with the engagement of catalytic amino acid residues including Lys85 and Asp200. Off-target docking against CDK2, CDK5, and GSK3α suggested preferential binding toward GSK3β. Structure-activity exploration of RA analogs identified aromatic balance and moderated polarity as determinants of predicted affinity. Together, these findings provide convergent computational evidence that RA may directly interact with GSK3β, supporting further biochemical and cellular validation studies to assess its potential as a modulator of GSK3β-associated pathways relevant to ASD pathophysiology. - Source: PubMed
Publication date: 2026/04/28
Joon PriyaBansal SaumyaAranjani Jesil MathewKumar AnilDeepak Deepak - Thyroid-stimulating hormone beta subunit () gene, a member of the glycoprotein hormone beta subunit family, has been detected in ovarian tissues and granulosa cells (GCs) of several species, suggesting a potential involvement in ovarian function. However, its molecular regulatory mechanisms and functional roles in Duolang sheep remain unclear. - Source: PubMed
Publication date: 2026/05/01
Sun HuiPingZhu LeXiaoShahbaz GulMuhammadGu RuoHuaiHe ChengLongChen ShuXinWang ChaoFanXing FengYan XiangLin - Euchromatic histone-lysine N-methyltransferase 2 (EHMT2) has been implicated in cardiovascular diseases, yet its role in vascular remodeling remains incompletely understood. Here we investigated the contribution of EHMT2 to vascular smooth muscle cell (VSMC) proliferation, migration and neointima formation following vascular injury using carotid artery injury models and in vitro VSMC studies. Transcriptomic (RNA sequencing) and epigenomic (CUT&Tag) profiling revealed that EHMT2 levels were elevated in injured arteries and growth-stimulated VSMCs, whereas EHMT2 deletion attenuated injury-induced neointima formation. Mechanistically, EHMT2 methyltransferase activity promoted VSMC proliferation and migration, with pathway analyses implicating cell cycle and growth programs as major downstream targets. We further identified GADD45G as a critical EHMT2-regulated gene characterized by H3K9me2 enrichment, and demonstrated that GADD45G enforced G1-phase arrest by suppressing cyclinB1, cyclinD1, CDK2 and CDK4. Importantly, both genetic and pharmacological inhibition of EHMT2, through GADD45G knockdown or administration of the EHMT2 inhibitor BIX-01294, significantly reduced neointimal lesion formation in injury models. These findings collectively establish EHMT2 as a key epigenetic driver of vascular remodeling by repressing GADD45G and facilitating cell cycle progression, highlighting EHMT2 as a potential therapeutic target for vascular proliferative diseases. - Source: PubMed
Publication date: 2026/05/01
Wang ZelanZhao JunyongLuo WenjianSun NingMa XingyuZhong FangyuanWu BojiTang HengNing KeHe JingyuWang XuhongZhang KunZhang JihangLiu ChuanRen JunZhao YanQin Zhexue - Despite the initial clinical success of CDK4/6 inhibitors in combination with endocrine therapy, the development of resistance (intrinsic and acquired) remains a significant challenge in the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative (HR+/HER2-) metastatic breast cancer (mBC). Recent advances have shed light on resistance mechanisms that primarily affect the cell cycle machinery, including loss of Rb function, cyclin E1 overexpression leading to CDK2 activation, and CDK6 or CDK4 upregulation. These alterations disrupt the G1/S checkpoint and drive proliferation independently of CDK4/6 inhibition. In contrast, non-cell cycle-related pathways, such as PI3K/AKT/mTOR and FGFR signaling, may also contribute but appear less central in many resistant tumors. These findings have highlighted the need for next-generation therapeutic approaches aimed at overcoming resistance. Selective inhibition of CDK2 and/or CDK4 is among the most promising strategies, potentially offering a more favorable therapeutic index while maintaining anti-proliferative efficacy. Early-phase trials of selective CDK2/CDK4 inhibitors, alone or combined, have shown encouraging activity, particularly in tumors resistant to prior CDK4/6 inhibition. However, most available data are limited to small, selected cohorts, underscoring the need for larger, randomized studies. Another emerging approach targets lysine acetyltransferases (KAT), key epigenetic regulators of transcription and cancer progression. KAT inhibition has shown potential to modulate oncogenic signaling and sensitize tumor cells to existing therapies, offering a complementary avenue for overcoming resistance. This review focuses on emerging cell cycle-centric mechanisms of resistance to CDK4/6 inhibitors and highlights innovative therapeutic strategies aimed at improving outcomes in HR+/HER2- mBC. - Source: PubMed
Publication date: 2026/04/27
Stachyra PaulinaHernando Meliá CristinaLópez-Guerrero José AntonioGavilá Gregori JoaquínGuerrero-Zotano Ángel Luis