CDK2 ELISA kit
- Known as:
- CDK2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CDK2-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CDK2 ELISA kit
Related genes to: CDK2 ELISA kit
- 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
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- This study aimed to assess the effects of simulated microgravity (SMG) on bovine muscle satellite cells (bSCs). The results demonstrated that bSCs maintained a fibroblast-like morphology throughout SMG exposure from day 3 to day 7. However, cells in the SMG group exhibited reduced proliferation compared to the control group, as indicated by lower cell density at both time points. In contrast, cell viability was higher in the SMG group than in the control group. Cell cycle analysis revealed a higher proportion of SMG-treated bSCs in the G0/G1 phase and a lower proportion in the S phase at day 3, suggesting cell cycle arrest at an early stage. Interestingly, by day 7, the percentage of cells in the S phase increased in the SMG group and exceeded that of the control group, indicating a partial recovery of proliferative activity. Western blot analysis showed decreased expression of key cell cycle-related proteins, including cyclin A1/A2, cyclin D1, and CDK2, in SMG-treated cells compared to controls at the early stage. Notably, cyclin D1 and CDK2 expression levels were upregulated at the later stage under SMG conditions. Additionally, nuclear morphology in SMG-treated bSCs displayed enlargement and irregularity. Overall, these findings suggest that SMG initially suppresses bSC proliferation by inducing cell cycle arrest, but cells can partially retrieve their proliferative capacity at later stages, potentially through upregulation of cell cycle regulatory proteins. - Source: PubMed
Ho Nguyen Quynh ChiNguyen Thai MinhDoan Minh ThuyNguyen Bao KhoiPham Minh AnhPhan Minh Cuong LePhan Lu Chinh NhanDang Thi Tung LoanLee Huu TrinhDoan Chinh ChungHoang Nghia SonNguyen Thai Minh HanVu Quang ManhLe Thanh Long - Neuromyelitis optica spectrum disorders (NMOSD) are autoimmune demyelinating diseases of the central nervous system. The role of microRNA-34b (miR-34b) in NMOSD pathogenesis remains unclear. This study investigates the expression and functional mechanism of miR-34b in NMOSD, specifically its regulation of the TIA-1-stress granule pathway. - Source: PubMed
Dai YanDai AnlangLiu Yuhuan - Cancer remains a major cause of mortality worldwide; therefore, research continues to focus on the development of more effective therapeutic agents. - Source: PubMed
Publication date: 2026/09/02
Moradimehrabadi MahkamehSadeghian SaraPoustforoosh AlirezaEmami LeilaKhabnadideh Soghra - To investigate the effects of astragaloside Ⅰ (AS-Ⅰ) on full-thickness skin defects in diabetic rats and its underlying mechanism. This study was an experimental study with grouped design and repeated measures design. Twenty-four male Sprague-Dawley rats aged 6-8 weeks were divided into control group (=6) and modeling group (=18) using a random number table method (the same grouping method was used throughout). After successful induction of diabetes mellitus, the modeling group was further divided into model group, low-dose AS-Ⅰ group, and high-dose AS-Ⅰ group, with 6 rats in each group. A full-thickness skin defect wound of 10 mm in diameter was created on the back of each rat. Wounds in control group and model group were treated with normal saline, while wounds in low-dose AS-Ⅰ group and high-dose AS-Ⅰ group were treated with 1.15 and 11.50 mmol/L AS-Ⅰ, respectively, for 3 consecutive days. Wound healing rates of rats were calculated at 3, 5, 7, 9, 13, and 15 days after injury. At 15 days after injury, Masson's trichrome staining was used to assess the deposition of collagen fibers in wound tissue; immunohistochemical staining was performed to detect Ki-67 positive expression in wound tissue, and the expression level was quantified. Network pharmacology analysis was applied to screen for potential core targets of AS-Ⅰ in treatment of diabetic wounds; molecular docking simulation was utilized to validate the binding affinity of AS-Ⅰ to the core targets, and molecular dynamics simulation was performed to verify the dynamic stability of the interaction between AS-Ⅰ and forkhead box O1 (FOXO1). At 15 days after injury, Western blotting was used to determine the protein expression levels of epidermal growth factor receptor (EGFR), cyclin-dependent kinase 2 (CDK2), growth factor receptor-bound protein 2 (GRB2), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), signal transducer and activator of transcription 3 (STAT3), and FOXO1 in wound tissue of rats in four groups. Compared with those in control group, the wound healing rates of rats in model group at 3 and 15 days after injury were significantly decreased (<0.05); whereas the wound healing rates of rats in low-dose AS-Ⅰ group at 7 and 13 days after injury, and in high-dose AS-Ⅰ group at 5, 7, 9, 13, and 15 days after injury were significantly increased (<0.05). Compared with those in model group, the wound healing rates of rats in both low-dose AS-Ⅰ group and high-dose AS-Ⅰ group at 3, 9, 13, and 15 days after injury were significantly increased (<0.05). At 15 days after injury, collagen fibers in the wound tissue of rats in control group were arranged in an orderly and dense manner; whereas those in the wound tissue of model group were sparse and disorganized; the deposition of collagen fibers in the wound tissue of rats in low-dose AS-Ⅰ group was improved compared with model group; collagen fibers in the wound tissue of rats in high-dose AS-Ⅰ group exhibited dense and orderly arrangement with a high degree of maturity. At 15 days after injury, the expression level of Ki-67 in wound tissue of rats in model group was significantly lower than that in control group (<0.05); compared with that in model group, the Ki-67 expression level in wound tissue of rats in low-dose AS-Ⅰ group was significantly higher (<0.05); compared with those in control group, model group, and low-dose AS-Ⅰ group, the Ki-67 expression level in wound tissue of rats in high-dose AS-Ⅰ group was significantly higher (with values all <0.05). The results of network pharmacology analysis identified 63 overlapping targets between AS-Ⅰ-associated targets and diabetic wound-related targets, involving the FOXO signaling pathway (with target protein FOXO1) and target proteins including EGFR, CDK2, GRB2, PIK3CA, and STAT3. The results of molecular docking simulation showed that AS-Ⅰ exhibited strong binding affinity to the target proteins. The results of molecular dynamics simulation demonstrated that the conformation of the complex formed by AS-Ⅰ and FOXO1 protein could maintain dynamic stability. At 15 days after injury, compared with those in control group, the protein expression levels of STAT3, GRB2, and FOXO1 in wound tissue of rats in model group were significantly upregulated (with values all <0.05), while the protein expression levels of PIK3CA, EGFR, and CDK2 were significantly downregulated (with values all <0.05). Compared with those in model group, the protein expression levels of STAT3, GRB2, and FOXO1 in wound tissue of rats in low-dose AS-Ⅰ group and high-dose AS-Ⅰ group were significantly downregulated (with values all <0.05), while the protein expression levels of PIK3CA, EGFR, and CDK2 were significantly upregulated (with values all <0.05). Compared with those in low-dose AS-Ⅰ group, the protein expression levels of STAT3, GRB2, and FOXO1 in wound tissue of rats in high-dose AS-Ⅰ group were significantly downregulated (with values all <0.05), while the protein expression levels of PIK3CA, EGFR, and CDK2 were significantly upregulated (with values all <0.05). AS-Ⅰ may promote wound healing of full-thickness skin defects and improve collagen fiber arrangement in diabetic rats by downregulating the protein expression of STAT3, GRB2, and FOXO1 and upregulating that of PIK3CA, EGFR, and CDK2. - Source: PubMed
Li YZheng Y YWang Y HZhang Z YLiu J PLuo Z H - Cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6 inhibitors) combined with endocrine therapy have become a therapeutic backbone for hormone receptor-positive, human epidermal growth factor receptor 2-negative breast cancer, yet durable disease control is frequently limited by intrinsic and acquired resistance. Canonical tumor-cell mechanisms, including retinoblastoma-pathway escape, cyclin E-cyclin-dependent kinase 2 (CDK2) activation, endocrine adaptation, and phosphoinositide 3-kinase (PI3K)-AKT-mechanistic target of rapamycin (mTOR) signaling, explain only part of this failure because they do not fully capture dynamic immune and stromal remodeling. Preclinical and translational studies indicate that early CDK4/6 inhibition can enhance antigen presentation, activate interferon-related programs, restrain regulatory T cells, and promote a T-cell-inflamed state. These effects are conditional and may not persist during prolonged treatment. Sustained therapy can instead drive heterogeneous resistant niches characterized by stromal remodeling, myeloid recruitment, checkpoint adaptation, and T-cell dysfunction. This immune-state dependence provides a rationale for immune checkpoint blockade, although clinical combinations have shown mixed efficacy and clinically relevant hepatic, pulmonary, and hematologic toxicities. Sequential or lead-in strategies therefore warrant prospective evaluation. Oxidative phosphorylation (OXPHOS) and redox adaptation may sustain selected resistant states and expose context-dependent ferroptotic vulnerabilities. Ferroptosis may connect tumor-cell killing with immune regulation, whereas nanomedicine may improve tumor-selective delivery. Both strategies remain largely preclinical and require further evaluation of pharmacokinetics, biodistribution, toxicity, manufacturability, and immune-cell safety. This Review distinguishes intrinsic from acquired resistance across interpatient, intratumoral, spatial, and temporal dimensions. It integrates tumor-cell escape with cytokine, immune, stromal, vascular, and metabolic remodeling and summarizes emerging therapeutic strategies. We further propose a candidate biomarker-informed framework that integrates genomic profiling, spatial immune architecture, circulating biomarkers, T-cell receptor (TCR) dynamics, transcriptomic and single-cell analyses, artificial intelligence (AI)-assisted multimodal integration, and longitudinal sampling. This framework is intended to support biomarker development and prospective trial design rather than current clinical decision-making, providing a translational basis for testing state-informed and sequence-aware therapeutic strategies. - Source: PubMed
Publication date: 2026/08/21
Tang YuhanZhu YingzeLiu ShaochunHan XiaoxiZhang HaoluZhao Wenhui