CDKN1A Antibody - N-terminal region (ARP30198_P050)
- Known as:
- CDKN1A Antibody - N-terminal region (ARP30198_P050)
- Catalog number:
- arp30198_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CDKN1A Antibody - N-terminal region (ARP30198_P050)
Related genes to: CDKN1A Antibody - N-terminal region (ARP30198_P050)
- 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 - N-terminal region (ARP30198_P050)
Related articles to: CDKN1A Antibody - N-terminal region (ARP30198_P050)
- Gulf War Illness (GWI) is a chronic neuroimmune condition affecting veterans of the 1990-91 Gulf War. Current treatments primarily target symptom relief, and the biological mechanisms underlying GWI remain poorly understood. Using a validated mouse model of Gulf War Illness (GWI) combining corticosterone (CORT) and diisopropyl fluorophosphate (DFP) exposure to induce stress- and toxicant-related neuroimmune priming, we examined how prior exposure alters molecular responses to a subsequent immune challenge. Male mice were exposed to CORT and DFP with repeated intermittent CORT, followed by lipopolysaccharide (LPS) or saline to assess transcriptional and epigenetic changes in brain and blood. We analysed transcript abundance, chromatin accessibility, and DNA methylation in the hippocampus, frontal cortex, and blood at 6 h, 12 h and 24hrs after LPS challenge (3-4 mice per group). We identified widespread transcriptional changes and dynamic chromatin accessibility following LPS exposure, with DNA methylation modifications that persisted in the hippocampus and blood. Thirty-three genes, including , , , and , were differentially expressed and methylated in both hippocampus and blood across all time points. These genes clustered in immune- and glial-related pathways. Transcription factor analysis revealed enrichment of NF-κB, CREB1, EGR1, JUN, and MYC binding motifs in regions with differential methylation. Our findings identify novel candidate biomarkers in peripheral blood that reflect brain molecular changes, providing a new framework for elucidating the long-term epigenetic impacts of stress and toxicant exposure in GWI. - Source: PubMed
Publication date: 2026/03/11
Sasaki AKelly K AMichalovicz L TAshbrook D GWijenayake SO'Callaghan J PMcGowan P O - During cancer metastasis, tumor cells survive in circulation by acquiring resistance to anoikis. Restoring vulnerability of cancer cells to anoikis can impair metastatic colonization, minimize treatment resistance and tumor recurrence in patients. A compelling body of evidence has identified strategies for the development of effective inhibitors that can block survival pathways such as FAK, PI3 K/AKT, MAPK and integrin signaling to prevent prostate cancer cells from leaving the primary tumor/site and/or to impair their colonization at secondary sites. Transcriptomic profiling recently identified anoikis-centered genes, including CDKN1A, NEDD9, CFL1, and JAM2, that may have potential prognostic value in prostate cancer progression and may also contribute to the emergence of therapeutic resistance to antiandrogens and taxane chemotherapy. Direct cytoskeletal remodeling by cofilin, a transforming growth factor-β (TGF-β) effector is linked to phenotypic plasticity changes. NEDD9 causes cytoskeletal dynamics through signaling pathways and it is correlated with tumor aggressiveness. CDKN1A affects cell cycle regulation, and JAM2 influences cell adhesion. This review interrogates the current evidence in the literature on the cellular drivers of anoikis resistance, intersecting with phenotypic plasticity in the prostate tumor microenvironment (TME), towards determination of the underlying molecular mechanisms that can be exploited at the translational level for therapeutic applications. The identification and subsequent validation of novel anoikis-resistance based signatures can be of potential value as predictive markers of therapy resistance and tumor recurrence in patients with advanced prostate cancer. - Source: PubMed
Publication date: 2026/04/17
Kouspou MariaZhu AlecMartires LaurenTewari Ashutosh KMehrazin RezaKyprianou Natasha - Current clinical tools for predicting relapse and guiding adjuvant therapy in clear cell renal cell carcinoma (ccRCC) lack precision, especially in intermediate-risk disease. This study evaluated whether a non-proliferative tumour cell phenotype, P21 (CDKN1A inhibitor) positive and MCM2 (DNA replication protein) negative (P21⁺/MCM2⁻), could serve as a robust biomarker to improve prognostic stratification and guide post-nephrectomy treatment decisions. We used multiplex immunofluorescence and AI-based image analysis on nephrectomy specimens from three independent ccRCC cohorts: UK arm of the SORCE trial (n=382), Korean (n=71), and Scottish (n=88). An optimal 2% cut-off for P21⁺/MCM2⁻ cells was determined using X-tile software. Additional analyses assessed endoglin/CD105 co-expression, paired primary-metastatic samples (n=41), and associations with adjuvant sorafenib therapy. In two intermediate-risk ccRCC cohorts (SORCE, n=63; Korean, n=71), patients with >2% P21⁺/MCM2⁻ cells had significantly longer time to relapse (HR=0.17, 95% CI: 0.06-0.54; HR=0.27, 95% CI: 0.10-0.72). Prognostic value was confirmed in high-risk (SORCE, HR=0.43, 95% CI: 0.19-0.99) and all-risk (Scottish, HR=0.37, 95% CI: 0.14-0.98) cohorts. Notably, patients with high P21⁺/MCM2⁻ levels on placebo fared better than those receiving adjuvant TKI therapy (HR=0.29, 95% CI: 0.16-0.50). In 41 paired samples, 85% showed higher P21⁺/MCM2⁻ abundance in metastases than in primary tumours. As a conclusion, P21⁺/MCM2⁻ cell count is a robust biomarker that refines relapse risk stratification in ccRCC and identifies patients who may not benefit from adjuvant tyrosine kinase inhibitor therapy. High levels of these non-proliferative, senescent-like cells suggest tumour dormancy and a more favourable outcome without treatment. - Source: PubMed
Publication date: 2026/04/16
Abdullah HazemUm In HwaStewart Grant DJeong Chang WookKwak CheolMoon Kyung ChulLaird AlexanderFrangou ElenaEisen TimMeade AngelaHarrison David J - To investigate the regulatory role and molecular mechanisms of TSPAN9-mediated mitocytosis in an interleukin-1β (IL-1β)-induced rat chondrocyte senescence model, and to identify novel therapeutic targets for osteoarthritis (OA). - Source: PubMed
Chen QuanDa WaciliLuo NaijiaShen Bin - The senescence-associated secretory phenotype (SASP) is a hallmark of senescent cells and plays a critical role in the development and progression of various age-related diseases, including cancer, cardiovascular disorders, and neurodegenerative diseases. In this study, we characterize SASP heterogeneity using single-cell RNA sequencing (scRNA-seq) data, focusing on the transcriptional signatures associated with elevated expression of individual SASP genes in mature senescent cells, as well as time-dependent variation in SASP expression across the early and mature senescent states in the WI-38 human lung fibroblast cell line. We generated multiple gene sets, each representing the transcriptional landscape linked to high expression of a specific SASP gene, and integrated them into an ensemble that reflects the temporal dynamics of SASP gene expression. Applying SASP scores derived from this ensemble of gene sets (SASP scores/EGS) to publicly available scRNA-seq datasets from human lung, skin, and eye tissues enabled the identification of senescent fibroblasts and revealed as a consistently upregulated marker in p21 or p16 fibroblasts across diverse human tissues. Our framework supports improved detection of both early and mature fibroblast replicative senescent cells, offering valuable insights into aging and age-related disease research. - Source: PubMed
Publication date: 2026/03/26
Kim HyunsooKummerfeld ErichNiedernhofer Laura JAliferis ConstantinRobbins Paul DWang Jinhua