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
- Acute exercise markedly alters blood glucose levels and the secretion of glucose-regulating hormones. However, as a central organ involved in glucose homeostasis, the molecular mechanisms underlying pancreatic responses to acute exercise remain poorly understood. Therefore, this study aimed to investigate the molecular adaptations of pancreatic tissue to acute exercise using a mouse treadmill exercise model combined with integrated multi-omics analyses. C57BL/6 mice were randomly assigned to either an exercise group or a control group, and pancreatic tissues were collected immediately after exercise intervention for transcriptomic and metabolomic analyses. Acute exercise significantly increased blood glucose and glucagon levels while reducing circulating insulin levels. Metabolomic analysis revealed significant elevations in several metabolites related to amino acid metabolism, including tryptophan, kynurenic acid, leucine, isoleucine, and valine. Transcriptomic analysis further identified significant upregulation of multiple genes, including Ins1, Ins2, Cdkn1a, Dusp1, Fkbp5, and Pdk4. These findings suggest that acute exercise induces rapid transcriptional and metabolic remodeling in pancreatic tissue and that these differential metabolites and genes may contribute to the pancreatic adaptive response to acute exercise. - Source: PubMed
Publication date: 2026/08/19
Sun ZilinFan JingjingQiao ZhixianChai XiaocuiWang YanLiu Renyi - Clinical and animal experiments have shown that Gui-qi-yi-shen (GQYS) granules, a traditional Chinese medicine formula, exhibited considerable therapeutic efficacy in the treatment of diabetic nephropathy (DN). However, the underlying pharmacological mechanisms remain unknown. To address this, we investigated the potential mechanisms of GQYS against DN using an integrated strategy combining network pharmacology and transcriptomics, followed by molecular docking and validation in db/db mice. A total of 64 unique active compounds and 670 potential targets of GQYS were identified. 213 candidate targets for GQYS-DN were further defined at the intersection of active compound targets of GQYS and disease targets of DN. 53 core targets were identified through network analysis. Integration of network pharmacology with transcriptomics identified 11 hub targets. The enriched signaling pathways mainly focus on inflammatory signaling pathways, including the TNF signaling pathway, IL-17 signaling pathway, and toll-like receptor signaling pathway. Molecular docking and molecular dynamics simulations suggested stable complexes of IL1β-quercetin, Cdkn1a-quercetin, Jun-quercetin, and Jun-β-sitosterol. The docking results, along with experiments supported the main targets and relevant signaling pathways, thereby demonstrating the reliability of the integrative strategy. Collectively, our results indicate that GQYS treats DN mainly through the anti-inflammatory effects, providing a potential theoretical basis for its clinical application. - Source: PubMed
Publication date: 2026/08/18
Cao JiaweiLu MengdanBi PengTang YuewenWan Feng - Ankylosing spondylitis (AS) is a chronic inflammatory condition primarily impacting the spine and sacroiliac joints, driven by immune dysregulation. While T cells are known contributors to AS, the specific cellular and molecular changes within affected tissues, especially in the spine, remain to be fully elucidated. We conducted single-cell RNA (scRNA-seq) and T cell receptor (TCR) sequencing on synovial fluids and spinal ligament samples from AS patients, supplemented by public AS and healthy control data. The analysis identified nine T cell clusters, with CD8 + memory T cells enriched in spine ligaments (SL), while mucosal-associated invariant T lymphocytes (MAIT) cells and regulatory T lymphocytes (Tregs) were enriched in synovial fluids. Differential expression and pathway analyses revealed that senescence-related genes, such as calmodulin 1 () and cyclin-dependent kinase inhibitor 1A (), were enriched in SL, suggesting the presence of senescent T cells, and cytotoxic genes, including natural killer cell granule protein 7 (), were enriched in synovial fluids. Furthermore, TCR repertoire analysis uncovered biased usage of T cell receptor gamma variable () genes in SL and T cell receptor beta variable 9 () in synovial fluid, indicating tissue-specific clonal expansion. Lastly, peptide prediction identified potential human leukocyte antigen-B27 (HLA-B27)-presented peptides, highlighting their contribution to inflammation. Our study demonstrates a unique immune landscape in AS, characterized by differential clonal expansion in peripheral and axial joints. These findings underscore T cell-mediated immune responses in AS pathology, contributing to the understanding of the immunological mechanisms of AS and potential immune-focused therapies. - Source: PubMed
Publication date: 2026/03/25
Zhu HongziTang YulongYu YuexinZhu QiJin LiWang JiucunHwang MarkLiu Jing - Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and excessive immune activation, for which curative therapies remain limited. This study aimed to investigate the role of small proline-rich protein 2B (SPRR2B) in psoriasis pathogenesis. In this study, gene Expression Omnibus (GEO) dataset GSE13355 was analyzed using R Language. Cell proliferation, gene and protein expression were measured with CCK8, RT-qPCR and immunofluorescence staining, respectively. Bioinformatics analysis of the GSE13355 dataset revealed that SPRR2B was significantly overexpressed in psoriatic lesions and was positively correlated with immune cell infiltration and multiple inflammatory pathways. In an M5-induced HaCaT keratinocyte psoriatic model, SPRR2B knockdown markedly suppressed cell proliferation and promoted apoptosis via regulation of the MDM2/p53/CDKN1A axis. Furthermore, SPRR2B knockdown reduced the secretion of IL-6, IFN-γ, TNF-α, and IL-1β, and inhibited JAK1 phosphorylation. These findings demonstrated that SPRR2B promotes keratinocyte proliferation and inflammatory response in psoriasis, suggesting it may serve as a promising diagnostic biomarker and therapeutic target for the disease. - Source: PubMed
Publication date: 2026/08/06
Ding ZhenzhenWang ChengchiLv Mingfeng - Asthma remains a prevalent global health challenge, necessitating novel therapeutic targets. This study hypothesized that pear polysaccharide alleviates asthma by modulating ferroptosis-related biomarkers. We integrated transcriptomic data (GSE143303, GSE147878) with database mining (CTD, OMIM, GeneCards, HERB, and FerrDb) to identify genes shared among asthma, pear, and ferroptosis. Machine learning screened core biomarkers, validated in independent datasets (GSE43696 and GSE63142). An ovalbumin-induced asthma mouse model was used to test the effect of Korla fragrant pear polysaccharide (10 and 40 mg/kg). Bioinformatics analysis identified 146 asthma-pear shared genes enriched in oxidative stress. Seven biomarkers (AR, CDKN1A, HMOX1, IL1B, IL6, PARP1, and TP53) were screened. In vivo, pear polysaccharide significantly attenuated cytokine release, and reversed the expression of the seven biomarkers in lung tissue and BALF of murine asthma model.Our study demonstrates that pear polysaccharide alleviates asthma pathology, potentially by targeting a hub gene network centered on ferroptosis-related biomarkers. - Source: PubMed
Yang FeiMao QionglingLiu JinlongTaoerdahong Hailiqian