Ask about this productRelated genes to: CDK2 antibody
- 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: CDK2 antibody
Related articles to: CDK2 antibody
- Herpes simplex virus type-1 (HSV-1) affects over 60% of the human population and increasingly develops resistance to antiviral therapies. Efficient HSV-1 replication requires host-derived deoxynucleotide triphosphates and the manipulation of cellular DNA replication and repair. This work positions the protein phosphatase 2A (PP2A) regulatory subunit PR130 (PPP2R3A) as cellular factor that suppresses the replication of laboratory strains and clinical isolates of HSV-1 in epithelial and neuronal cells. HSV-1 infection in turn decreases PR130 levels. Global proteome and phosphoproteome profiling combined with functional assays demonstrate that PR130 modulates key regulators of the cell cycle and DNA repair. PR130 controls the expression and phosphorylation of the cyclin-dependent kinase (CDK) inhibitor p21 (CDKN1A) at serine 130 (S130) which CDK2 catalyzes. The levels and activities of p21, which HSV-1 infection attenuates, and CDK2 are decisive factors for HSV-1 replication. Inhibition of the ubiquitin-specific protease USP7 stabilizes the p53-p21 axis and reduces HSV-1 viral titers. Additionally, PR130 depletion enhances signaling of the DNA damage-responsive checkpoint kinase ataxia-telangiectasia mutated (ATM) upon HSV-1 infection and creates a dependency of HSV-1 replication on ATM activity. These findings uncover host-intrinsic mechanisms regulating HSV-1 replication and highlight PR130 as central hub regulator of HSV-1 infection. - Source: PubMed
Publication date: 2026/05/15
Jungwirth JohannesJacob Christoph FNguyen AlexandraBeyer MandyMieland Andreas ODejung MarioChen Jia-XuanBrenner WalburgisEhrhardt ChristinaHenke AndreasKrämer Oliver H - Lactucin, a sesquiterpene lactone isolated from chicory (Cichorium intybus L.), demonstrates broad-spectrum anticancer activity across multiple malignancies, yet its mechanistic role in gastric cancer (GC) remains unexplored. This study aimed to elucidate the potential mechanism by which lactucin modulates GC cell proliferation and apoptosis. - Source: PubMed
Publication date: 2026/05/15
Wei DanWang Peng-LiJiang Jing - The present study investigates temperature stress-induced production of a salicylic acid derivative from endophytic isolated from (rosemary), with a focus on the potential of controlled temperature variations to enhance fungal-derived salicylic acid biosynthesis. Following morphological and microscopic identification, was cultured in modified Czapek broth at temperatures ranging from 25°C to 42°C with 3°C stepwise increases in a shaking incubator at 150 rpm. Salicylic acid was extracted using ethyl acetate and purified through column chromatography, preparative high-performance liquid chromatography (HPLC), and gas chromatography-mass spectrometry (GC-MS), yielding 7.27 mg of pure compound from 81.39 g of crude extract in a 1000 ml culture volume. Structural confirmation was performed using Fourier-transform infrared spectroscopy (FTIR) and proton nuclear magnetic resonance (H NMR) spectroscopy. Molecular docking studies demonstrated the highest binding affinity with cyclin-dependent kinase 2 (CDK2) (-6.1), followed by cyclooxygenase-1 (COX-1) (-6.0), cyclooxygenase-2 (COX-2) (-5.5), and high-mobility group protein B1 (HMGB1) (-4.9), indicating CDK2 as a potential primary target. anti-inflammatory activity, assessed using the egg albumin denaturation assay, showed that ibuprofen exhibited greater inhibition than salicylic acid alone; however, their combination resulted in the highest inhibition rate (29.56% at 300 μg mL), with a dose-dependent increase observed. These findings suggest that fungal-derived salicylic acid enhances the anti-inflammatory potential of ibuprofen and may serve as a promising natural adjunct to conventional nonsteroidal anti-inflammatory drug therapy. - Source: PubMed
Publication date: 2026/04/29
Saleem AyeshaAhmad SajjadKhattak Saeed UllahJalil HumaAbdel-Maksoud Mostafa AAlsabih Ahmed OthmanAl-Qahtani Wahidah HHussein Ahmed M - Tubo-ovarian, high-grade serous carcinoma (HGSC) is the most lethal gynecological malignancy, with limited targeted therapies and poor outcomes. Heterozygous loss of occurs in approximately 81% of HGSCs and drives chromosome instability and cellular transformation. Here, we identify as a novel synthetic lethal (SL) interactor of in clinically relevant fallopian tube secretory epithelial cell models. Genetic silencing or pharmacologic inhibition of CDK2 with siRNA duplexes or SNS-032, respectively, selectively reduced viability and induced cytotoxicity in cells, with significantly lower EC values compared to controls. Importantly, in two malignant HGSC cell lines (COV362 and OVCAR-3), we further observed that silencing or SNS-032 treatment in combination with silencing induced significant reductions in cell numbers, thereby extending the SL interaction to established HGSC models. Mechanistically, SNS-032 treatment led to increased DNA double-strand breaks and apoptosis, as evidenced by increased numbers of γ-H2AX foci and cleaved Caspase-3 signal intensities. To our knowledge, this is the first demonstration of a SL interaction that exploits a heterozygous disease state in HGSC. These findings highlight CDK2 inhibition as a promising precision medicine strategy for -deficient tumors, broaden the applicability of SL approaches beyond homozygous gene loss, and provide strong preclinical rationale for further therapeutic development. - Source: PubMed
Publication date: 2026/04/28
Farrell Ally CLam Lukas AChen HelenNeudorf Nicole MSajesh Babu VLepage Chloe CLichtensztejn ZeldaMcManus Kirk J - Hepatocellular carcinoma (HCC) is characterized by high recurrence rates and limited targeted therapies. Centromere protein I (CENPI), a core kinetochore component linked to chromosomal instability, is dysregulated in multiple malignancies, yet its role and mechanism in HCC progression remain incompletely elucidated. - Source: PubMed
Publication date: 2026/05/12
Liu DemengYang PeihaoWang JiyaoLi JunleWang XinGu XiaohuiLiu ChaoFang Yan