CDK2 polyclonal antibody
- Known as:
- CDK2 pab (anti-)
- Catalog number:
- PAB9940
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CDK2 polyclonal antibody
Related genes to: CDK2 polyclonal 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 polyclonal antibody
Related articles to: CDK2 polyclonal antibody
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Publication date: 2026/07/11
Jiang RuiqiCao MingnanLiu DanShang MeiyuMei ShenghuiYang ShuxianZhang LuofeiJi NanZhao Zhigang - This study explored the therapeutic effect and mechanism of Rubia cordifolia stem on Escherichia coli-induced diarrhea in chickens. A total of 180 one-day-old white-feathered broilers were adaptively reared for 7 days and randomly assigned into six groups: blank control group, Escherichia coli model group, enrofloxacin group, 1000 mg/kg Rubia cordifolia stem group, 2000 mg/kg Rubia cordifolia stem group, and 4000 mg/kg Rubia cordifolia stem group, with 30 birds per group, six replicates and five broilers per replicate. The influences of different doses of the extract on growth performance, diarrhea severity, intestinal morphology, antioxidant status, immune-inflammatory response and intestinal microbiota were evaluated, and its mechanism was analyzed via network pharmacology and molecular docking. Results indicated that Rubia cordifolia stem improved growth performance, alleviated diarrhea, attenuated intestinal mucosal injury, significantly enhanced serum antioxidant enzyme activities, downregulated ileal pro-inflammatory gene expression, and upregulated immunoglobulin and anti-inflammatory factor levels. It also reshaped intestinal flora and restored microecological balance (P < 0.05). Network pharmacology analysis identified 25 intersecting targets between Rubia cordifolia L. and Escherichia coli infection. Among them, CASP3, ESR1, BCL2, CDK2, and PTGS2 were recognized as core targets primarily involved in inflammatory regulation and immune response pathways. Molecular docking verification confirmed that the main active ingredients of Rubia cordifolia L. stably bound to these core targets, and β-sitosterol exhibited the optimal binding activity. In summary, Rubia cordifolia stem treated broiler colibacillosis by enhancing antioxidant capacity, inhibiting inflammation, regulating immune function, and maintaining intestinal microecological balance. This study provided experimental and theoretical evidence for the application of Rubia cordifolia stem as an antibiotic substitute in poultry production. - Source: PubMed
Publication date: 2026/06/26
Cheng XuWang XuejingWang ZijuanWu YujiaMu YixuanWang Xiaodan - Generative artificial intelligence (AI) has rapidly advanced over the past decade in the field of drug discovery, particularly for the de novo design of small molecules based on target protein structures. While generative AI has the potential to complement traditional structure-based drug design (SBDD) to discover novel hits, their performance is often assessed using non-standardized evaluation criteria. As the number of generative AI models continue to grow, it becomes increasingly important to determine whether these tools are sufficiently robust and reliable for integration into medicinal chemistry workflow. Here, we propose ScrambleBench, a benchmarking workflow designed to evaluate structure-based generative AI models that align with medicinal chemists' practical objectives to identify chemically diverse, drug-like hit candidates that adopt plausible binding conformations and exhibit favourable docking affinities. Using six representative models (Pocket2Mol, PocketFlow, Lingo3DMol, DiffSBDD, PMDM, and Chemistry42), we systematically assessed performance across diverse target classes, including two GPCRs, two kinases, and two hydrolases. While some generative models show superior performance for particular evaluation endpoints, none demonstrates overall dominance across all evaluated criteria. Notably, despite benchmarked proteins (e.g., CDK2, GSK3β) being present in the training datasets, the models still show limited generalization to target binding sites, which resulted in high redocking RMSD values and low virtual hit rates. Our results highlight the importance of evaluating chemical diversity explicitly and using the recently proposed metrics such as Hamiltonian Diversity (HamDiv) which assess both quantity and dissimilarity of a molecular set. Furthermore, as many generated ligands fail to meaningfully engage the target active site, we propose that future generative frameworks incorporate improved loss functions that place greater emphasis on drug-like physicochemical properties and correct pharmacophore recognition.Scientific contributionWhile numerous de novo generative models have been proposed for structure-based molecular design, objective comparison between methods remains challenging due to inconsistent benchmarking practices and heterogeneous evaluation criteria. ScrambleBench introduces a unified and reproducible benchmarking workflow that integrates diversity analysis, conformational validity assessment, docking reproducibility, pharmacophore matching, and virtual hit rate evaluation within a single framework. By systematically comparing representative generative models using common datasets and standardized assessment criteria, this work advances the field by enabling transparent evaluation model performance and practical applicability. Overall, ScrambleBench provides a holistic medicinal chemistry-oriented framework that identifies methodological strengths, limitations, and opportunities for future model development. - Source: PubMed
Publication date: 2026/07/06
Yap VeincentXu PanMak Frankie SFoo KlementKang CongbaoAnbazhagan PadmanabhanXu Weijun - Thyroid cancer, a prevalent endocrine malignancy, has shown a significant global rise in incidence over the past 15 years and currently ranks as the sixth most common cancer worldwide, with higher prevalence among women. Dysregulation of the TIMP-1-induced FAK/PI3K/AKT signaling pathway plays a pivotal role in disease progression, highlighting its potential as a therapeutic target. This study investigated the anticancer effects of zeylenone in thyroid carcinogenesis, based on its reported inhibition of TIMP-1-mediated FAK/PI3K/AKT signaling in tumor cells. The ability of zeylenone to suppress proliferation of TPC-1 thyroid cancer cells and the underlying molecular mechanisms were evaluated through analyses of cell viability, oxidative stress, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), apoptosis, and cell proliferation, with an emphasis on the TIMP-1/FAK/PI3K/AKT pathway. Zeylenone significantly suppressed cell proliferation, induced apoptosis, increased ROS and TBARS levels, reduced MMP, decreased antioxidant status, and inhibited TIMP-1-induced FAK/PI3K/AKT signaling. In silico docking analyses demonstrated interactions between zeylenone and key apoptotic and cell-cycle regulators, including Bax, Cyclin E1, and CDK2, while molecular dynamics simulations using Schrödinger's Desmond module confirmed the stability of the zeylenone-CDK2 complex. However, limitations include the use of a single cell line (TPC-1) and a lack of in vivo validation. Future perspectives involve testing in additional thyroid cancer models, animal studies, and clinical translation to assess efficacy and safety. Collectively, these findings demonstrate that zeylenone suppresses proliferation and promotes apoptosis in TPC-1 cells primarily through suppression of the TIMP-1-mediated FAK/PI3K/AKT signaling pathway, highlighting its potential as a therapeutic candidate for thyroid carcinoma. - Source: PubMed
Publication date: 2026/07/04
Qin ShichenZhou JieWu XuemeiJiang Liangxing - Triple-negative breast cancer (TNBC) is a highly aggressive subtype with limited therapeutic options. An urgent need thus exists to develop novel therapeutic strategies to treat TNBC. We previously demonstrated that 1‑palmitoyl‑4‑piperidinopiperidine (PPI), a derivative of palmitic acid, exerts anticancer effects against human colon carcinoma cells and human pancreatic ductal adenocarcinoma cells by inhibiting signal transducer and activator of transcription 3 (STAT3) phosphorylation. To date, no studies have assessed PPI potency in murine TNBC EO771 cells. We examined cell viability after treatment with PPI for 48 h, and evaluated the expression levels of apoptosis- and cell cycle-related proteins using immunocytochemistry and western blotting. PPI inhibited cell proliferation in a dose-dependent manner, with an IC of 3.06 µM. PPI treatment was found to induce apoptosis. We also observed G1 cell cycle arrest as indicated by cyclin D1 and Cdk2 downregulation. Phosphorylated STAT3 levels and those of downstream proteins including CXCR4, MMP2, MMP9, TWIST, VEGF, and Vimentin, decreased following PPI treatment. STAT3 knockdown modestly reduced the sensitivity of EO771 cells to PPI, supporting partial involvement of STAT3 signaling in the anticancer effects of PPI. These results suggest that PPI exerts anticancer effects on EO771 cells that are associated with suppression of STAT3 signaling. - Source: PubMed
Publication date: 2026/07/04
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