CDKN1A Antibody
- Known as:
- CDKN1A Antibody
- Catalog number:
- XW-7422
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CDKN1A Antibody
Related genes to: CDKN1A Antibody
- Gene:
- CDKN1A NIH gene
- Name:
- cyclin dependent kinase inhibitor 1A
- Previous symbol:
- CDKN1
- Synonyms:
- P21, CIP1, WAF1, SDI1, CAP20, p21CIP1, p21Cip1/Waf1, p21
- Chromosome:
- 6p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2018-06-06
Related products to: CDKN1A Antibody
Related articles to: CDKN1A Antibody
- This study comprehensively employed network toxicology and experimental validation to systematically investigate the potential mechanisms by which triclosan (TCS) exacerbates rheumatoid arthritis (RA). Through multi-database screening, 173 common targets between TCS and RA were obtained. Combined with protein-protein interaction (PPI) network analysis and five machine learning algorithms, eight core hub genes (AR, CDKN1A, IGF1R, JAK2, JUN, MAPK8, MYC, and PARP1) were identified. Enrichment analysis indicated that TCS primarily interferes with signalling pathways, such as JAK-STAT, cellular senescence, and mitophagy. In vitro experiments demonstrated that TCS induces macrophage senescence and polarisation toward the M1 phenotype, promotes the expression of inflammatory cytokines, and inhibits mitophagy, leading to the accumulation of mitochondrial reactive oxygen species (ROS), loss of mitochondrial membrane potential, and impaired mitochondrial function, thereby exacerbating the inflammatory response. This study reveals that TCS may disrupt immune-metabolic homeostasis through multi-target, multi-pathway mechanisms to promote the onset and progression of RA, providing a new theoretical basis for understanding its environmental toxicity and for the prevention and treatment of RA. - Source: PubMed
Publication date: 2026/09/10
Zhang JingChen TongMa YingJieWang WenguangChen BocenJian ShaoqinXiao Man - One of the most common prevalent forms of cancer in the world is oral squamous cell carcinoma (OSCC). In the present study, we explore the chemotherapeutic effect of Sclareol on human oral carcinoma KB cells in scientifically found that cellular and molecular alterations. The human oral carcinoma KB cell and African green monkey kidney normal cell line (Vero) were evaluated for a several types of investigations following they had been various concentrations of Sclareol (5-50 µM) and cisplatin (0-10 µM) for 24 h. Additionally, we exhibited that sclareol induces cytotoxicity effect by MTT assay, Reactive oxidative stress (ROS) was measured by DCFH-DA staining assay, loss of mitochondrial membrane potential (Δψm) was assessed by Rho123 staining method, nuclear condensation, and apoptotic morphological changes was investigated by DAPI and AO/EtBr staining in KB cells. Sclareol promoted oxidative stress via an imbalance in redox status and increased DNA damage in human oral carcinoma KB cells. Besides, Sclareol induces apoptosis by activating dependent p21, thereby down-regulating the expression levels of phosphorylation of Rb (ser 780), cyclin D1, and cyclin-E. Furthermore, it is associated with mitochondrial-mediated apoptotic and proapoptotic markers, as evidenced by the downregulated Bcl-2 protein and the upregulation of (Bax, Cytochrome C, Cleaved PARP, Cleaved Caspase and Caspase-9 &-3) induced apoptosis signaling through p53 independent pathways. Therefore, our present study findings suggest that Sclareol could be the productive new chemotherapeutic agent for against oral squamous cell carcinoma. - Source: PubMed
Nallu AnandhiKathiresan SureshAzhamuthu TheerthuRamadoss HemavardhaniAsath Nihal Ahamed AbulkalamRavichandran PugazhendhiVasu Rajeswari - Therapy resistance remains the primary cause of treatment failure in rhabdomyosarcoma (RMS), the most common pediatric soft tissue sarcoma, yet underlying mechanisms are poorly understood. Using vincristine-resistant fusion-negative RMS models, RNA sequencing, genetic perturbations, and a syngeneic zebrafish tumor model, we demonstrate that resistance is driven by enhanced MAPK signaling, validated in post-chemotherapy patient specimens. MEK inhibition induced senescence through an MYC-p21 axis; MYC represses CDKN1A transcription, and its overexpression bypasses senescence. Resistant cells exhibited BCL-XL dependence, and combined MEK/BCL-XL inhibition eradicated resistant tumors and . These findings reveal that enhanced MAPK signaling and MYC-mediated senescence bypass are candidate resistance-associated mechanisms in fusion-negative RMS with implications across cancer types, and identify targetable vulnerabilities (MEK and BCL-XL), providing preclinical rationale for treatment-refractory RMS. - Source: PubMed
Publication date: 2026/08/25
Wang YadongLargent Andrea DLee DorothyModi PaulomiWang LongBandhlish AnshuIgnatius MyronChen Eleanor Y - The role of neutrophil extracellular traps (NETs) in cervical cancer (CC) progression, particularly their association with human papillomavirus (HPV) infection, remains unclear. - Source: PubMed
Publication date: 2026/08/20
Wang XinJulaiti AlimireAisikaer AikelimuWei HongjianJie RundaLiu XinyanShi Yonghua - Glutamic-Pyruvic Transaminase 2 (GPT2) significantly contributes to the advancement of colorectal cancer (CRC). This study aimed to elucidate the expression patterns, functional significance, and underlying mechanisms of GPT2 in CRC. Data from the TCGA repository, supplemented by immunohistochemical analysis, showed that GPT2 is substantially overexpressed in CRC specimens relative to adjacent non-cancerous tissues. This elevated expression level was further correlated with poorer clinical prognosis in patients. Cellular investigations using qPCR and Western blotting revealed differential GPT2 expression across CRC cell lines, with notably high levels in SW620 cells and minimal expression in SW1417 cells. Functional assays revealed that GPT2 overexpression in SW1417 cells notably increased their proliferation, migration, and invasion, while extending the G0/G1 cell cycle phase. Conversely, knocking down GPT2 in SW620 cells suppressed these malignant phenotypes and induced G2/M phase arrest. To investigate the molecular basis, RNA sequencing was performed on GPT2-knockdown SW620 cells, identifying 1020 differentially expressed genes. Enrichment analyses based on GO and the KEGG indicated that the identified genes are predominantly associated with biological processes related to the regulation of blood coagulation and functions localized within the endoplasmic reticulum lumen. Analysis of the PPI network for differentially expressed genes identified five core candidate genes: SERPINE1, CDKN1A, GADD45A, EPHA2, and ASNS. qPCR confirmed the expression levels of these genes, demonstrating a positive correlation with GPT2 expression. In conclusion, GPT2 acts as an oncogenic driver in colorectal cancer, enhancing tumor cell proliferation, migration, and invasive capabilities. This effect is likely mediated through the regulation of downstream targets, including SERPINE1 and CDKN1A. These findings suggest that GPT2 holds potential as both a prognostic indicator and a therapeutic target in colorectal cancer. - Source: PubMed
Publication date: 2026/08/28
Xu XiulianXie PingGan HailinHuang YimingLiu ZhihengLv Qijun