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
- Sunitinib is associated with a higher incidence of thrombocytopenia than other molecularly targeted drugs. However, the underlying mechanism remains unclear. Because platelets are derived from megakaryocytes originating from hematopoietic progenitor cells in the bone marrow, sunitinib is presumed to interfere with megakaryocyte proliferation, maturation, or platelet production. Therefore, megakaryocytes play a crucial role in elucidating the mechanism of sunitinib-induced thrombocytopenia. However, in vivo sampling of megakaryocytes is challenging due to the invasiveness of bone marrow collection and the limited cell yield. Accordingly, we investigated the mechanism of thrombocytopenia induced by sunitinib and its active metabolite, N-desethyl sunitinib, using human induced pluripotent stem cell-derived immortalized megakaryocyte cell lines (imMKCLs). Both sunitinib and N-desethyl sunitinib suppressed the proliferation and cell division of imMKCLs. Furthermore, RNA sequencing revealed downregulation of cell cycle-related genes. Although the expression of cyclin-dependent kinase inhibitors, CDKN1A and CDKN1B, was significantly increased, polyploidization in imMKCLs remained unaffected. In conclusion, sunitinib and N-desethyl sunitinib induce thrombocytopenia by inhibiting the proliferation of immature megakaryocytes through suppression of cell cycle progression. - Source: PubMed
Publication date: 2026/07/14
Iwasaki MoemiHashita TadahiroHori EiseiNakamura SouEto KojiHashimoto YutakaMatsunaga TamihideIwao Takahiro - Physical exercise is a potent modifier of CNS aging, but its relationship with the cyclin-dependent kinase inhibitor p21 (CDKN1A) is neither uniformly suppressive nor equivalent to cellular senescence. Direct evidence remains sparse and preclinical. Sustained physiological exercise reduced hippocampal or cortical p21-associated signatures in models of metabolic distress, natural aging, and amyloid pathology. Conversely, acute treadmill exercise transiently increased hippocampal Cdkn1a, while spatial transcriptomics identified increased endothelial Cdkn1a during broader exercise-associated vascular rejuvenation. At the maladaptive extreme, excessive swimming produced sustained hippocampal p53-p21 activation accompanied by oxidative injury, apoptosis, senescence-associated β-galactosidase activity, and cognitive impairment. Genetic studies further indicate that endogenous p21 restrains exercise-responsive neural stem-cell activation, but they do not demonstrate that exercise itself reduces p21. To reconcile these findings, this review applies a four-axis interpretive matrix based on signal persistence, cellular and subcellular compartment, corroborating senescence-associated features, and functional consequence. The evidence is integrated into three states: physiological exercise associated with attenuation of persistent p21-related stress, transient or cell-specific adaptive p21 induction, and maladaptive exercise overload characterized by sustained p53-p21 signaling and tissue injury. Current findings therefore support exercise more strongly as a stress-preventive or senomorphic intervention than as a proven CNS senolytic or p21-targeted therapy. The central question is not simply whether exercise increases or decreases p21, but when, where, for how long, and within which cellular and molecular context the response reflects repair, quiescence, persistent senescence-like dysfunction, or progression toward cell death. - Source: PubMed
Publication date: 2026/08/22
Sun ChenMuthusamy ParamasivamPattanimuthu AnanthiLiu Muyuan - The clinical utility of doxorubicin (DOX) is severely limited by dose-dependent cardiotoxicity, for which effective interventions remain scarce. Huangqi Guizhi Wuwu Decoction (HGWD) shows promising cardioprotective potential, but its mechanisms against DOX-induced cardiotoxicity (DIC) remain unexplored. This study explored the molecular mechanisms using an integrated metabolomics and transcriptomics approach. We identified 57 compounds in HGWD by liquid chromatography ion trap time-of-flight mass spectrometry (LC-IT-TOF/MS), and quantified five representative compounds for standardization. Mice were randomized into six groups: control, DOX (10 mg/kg × 2), DOX + low-dose HGWD (7 g/kg/d), DOX + high-dose HGWD (14 g/kg/d), DOX + dexrazoxane (100 mg/kg × 2), and HGWD (14 g/kg/d) alone. HGWD effectively alleviated cardiac dysfunction and reduced serum injury markers, with the high-dose group demonstrating efficacy comparable to the positive control drug, dexrazoxane. Subsequently, multi-omics profiling was performed on heart tissues from the control, DOX, and DOX + high-dose HGWD groups. Metabolomics identified 31 differential metabolites, highlighting energy metabolism restoration (e.g., acylcarnitines, citric acid) and inflammatory mediator modulation (e.g., arachidonic acid). Transcriptomics uncovered 37 genes enriched in innate immunity (e.g., Irf7, Isg15) and apoptosis (e.g., Bax, Cdkn1a). Network analysis constructed a core regulatory module, pinpointing CDKN1A as a potential mediator. Validation experiments confirmed that HGWD suppressed DOX-induced CDKN1A upregulation in mouse hearts. Furthermore, in H9c2 cells, HGWD mitigated DOX-induced apoptosis and inflammation, exhibiting cytoprotection comparable to pifithrin-α, a specific p53 inhibitor. In summary, HGWD protects against DIC by modulating a multi-target network and the suppression of CDKN1A represents a key underlying mechanism. - Source: PubMed
Publication date: 2026/08/21
Hou QianYu XinyueWu KeChen SilingMao XinQian XinyingLi ChangjinSheng LidanWang RuipingHuang Yin - Resistance to immunotherapy in colorectal cancer (CRC) is closely linked to an immunosuppressive tumour microenvironment (TME), in which cancer-associated fibroblasts (CAFs) are key regulators. Cellular senescence and the senescence-associated secretory phenotype (SASP) are increasingly recognised as drivers of CAF activity, yet their systematic prognostic and immunomodulatory value in CRC remains poorly defined METHODS: Using transcriptomic and clinical data from the TCGA-COADREAD cohort, we screened differentially expressed cellular senescence-related genes (DE-CSRGs) and constructed a prognostic signature, externally validated in independent GEO cohorts (GSE39582). Multi-omics analyses-functional enrichment, immune-infiltration estimation, single-cell and spatial transcriptomics, and ligand-receptor inference-were integrated to characterise the associated biology, and findings were validated at the protein level by multiplex immunofluorescence and immunohistochemistry in an independent pMMR CRC cohort. - Source: PubMed
Publication date: 2026/08/20
Chen YingyingZhang YingLv Chi - 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