Ask about this productRelated genes to: Cip1 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: Cip1 antibody
Related articles to: Cip1 antibody
- Alzheimer's disease (AD) is strongly associated with aging, yet the interactions remain unclear. This study modeled replicative senescence in patient-derived fibroblasts to compare gene expression between AD dementia and controls across senescence stages and to evaluate whether stage-specific alterations reflect disease characteristics with diagnostic implications. - Source: PubMed
Publication date: 2025/12/16
Cho Young JoonYoon SunwooKim YeojinSong Ho MinNam You JinLee Sang HyukLee SeheeShin DonghyukLee Sun MinMoon So YoungKim Eun-JooCho Soo HyunKim Byeong CChoi Seong HyeSeo Sang WonKim Jin CheolPark Young JoonKang Hee YoungLee Sang-RaeHong SunhwaSon Sang JoonHong Chang HyungRoh Hyun Woong - Penile squamous cell carcinomas (SCC) develop via a transforming human papillomavirus (HPV) infection or independent of HPV. We assessed the role of copy-number alterations (CNA) affecting chromosome arms, oncogenes and tumor suppressor genes (TSG) in 121 penile SCC (52% HPV-associated and 48% HPV-independent) using shallow whole-genome sequencing. CNA were common and complex, with frequent co-occurrences. Neither etiology had exclusive CNA. Arm-level changes included gains of 3q and 8q (48% each), 1q (36%), 1p (26%), 9q (36%) and 9p (31%) and losses of 19p (48%), 8p (44%), 1q (36%), and 3p (33%) of SCC. Oncogene amplifications included broad 3q alterations affecting TP63, SOX2, PIK3CA (43%) and 8q including MYC, HEY, RAD21 (40%). Homozygous deletions affected WRN, NRG1 (8p;29%), BAP1, FANCD2, VHL (3p) and ARHGEF12, BCL9L, ATM (11q22/23) in 19% each. CNA affecting TP53, CDKN2A/B, CDKN1A/B, and RB1 occurred in similar numbers in HPV-induced (16%) and HPV-independent SCC (24%) quite in contrast to TSG somatic mutations exclusive to HPV-independent SCC associated with lichenoid dermatoses. HPV-induced SCC had more 1p amplifications (adj. p=.003), while HPV-independent SCC carried more 8q full-arm gains (adj. p=.00003), amplifications of oncogenes on 8q (adj. p=.006) including MYC and homozygous deletions of 8p (adj. p=.03). MYC amplifications coincided with an increased fraction of genome altered indicative for genomic instability (p=.00001). EGFR amplifications dominated in HPV-negative wild-type TP53/CDKN2A SCC without dermatoses. Together with mutations in PIK3CA, HRAS and FGFR3 they represent an alternative RTK/Ras/PI3K-mediated carcinogenesis pathway. More than half of advanced SCC irrespective of etiology harbored targetable CNA such as EGFR, MTAP, ATM. - Source: PubMed
Publication date: 2026/04/22
Ermakov Mikhail SRegauer SigridKashofer Karl - We present a reproducible in vitro protocol for harvesting and culturing murine bone marrow-derived macrophages, with the added capability of freezing bone marrow cells at -80°C for scalability and long-term storage. To induce macrophage senescence, we developed a genotoxic stress-based method using either 10 Gy ionizing radiation or 500 nM doxorubicin treatment. The resulting senescent macrophages exhibit key hallmarks of cellular senescence, including irreversible cell cycle arrest, upregulation of senescence-associated markers (e.g., Cdkn1a), secretion of senescence-associated secretory phenotype (SASP) factors, morphological changes, and SA-β-galactosidase activity. This model serves as a valuable tool for investigating macrophage senescence, a relatively understudied senescent cell type, and provides mechanistic insights into the contribution of the innate immune system to aging and age-related diseases. © 2026 The Author(s). Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: Mouse dissection and bone marrow harvest Basic Protocol 2: Thawing and plating cryopreserved murine bone marrow for macrophage differentiation Support Protocol 1: Flow cytometry validation of macrophage surface markers Support Protocol 2: Gene expression analysis via RT-qPCR Basic Protocol 3: Inducing senescence in macrophages using doxorubicin or irradiation Alternate Protocol: Maintenance and expansion of control macrophages Support Protocol 3: Brightfield microscopy and SA-β-galactosidase staining to assess senescence-associated morphology Support Protocol 4: Quantifying senescence and SASP marker expression by qPCR and/or western blot Support Protocol 5: Assessment of cell cycle arrest using EdU labeling with optional DNA content staining. - Source: PubMed
Torres GrasielaTripathi UtkarshSalladay-Perez IvanAvila ItzetlCovarrubias Anthony J - Focal articular cartilage defects lack intrinsic regenerative capacity and can progress to osteoarthritis as no effective treatment exists to slow, stop or reverse cartilage degeneration. Cellular senescence, characterized by elevated p21 (CDKN1A) expression, impairs chondrocyte proliferation and cartilage repair. We hypothesized that targeted p21 suppression via lentiviral delivery would enhance cartilage regeneration. Lentiviral shRNA vectors targeting p21 or non-sense controls with a tdTomato reporter were constructed. In vitro, murine synovial progenitor cells and MC3T3E1 preosteoblasts were transduced and p21 mRNA was quantified by qRT-PCR. Cell cycle analysis was performed using flow cytometry. In vivo, immunocompromised (B6.Cg-Prkdc/SzJ) and immunocompetent (C57BL6) mice received full-thickness cartilage defects followed by intraarticular p21 shRNA or nonsense control injection. Cartilage repair was assessed by Safranin O staining and tissue cytometry quantified lentiviral transduction and p21 knockdown in chondrocytes. In vitro, p21 shRNA achieved ~80% reduction in p21 mRNA and increased G2M phase cells. In vivo, p21 shRNA treatment significantly improved cartilage repair in both strains. Tissue cytometry revealed 90% transduction efficiency with p21 cells reduced from ~90% to ~30%. Spearman correlation showed significant negative correlation between p21 expression and repair outcomes. Hepatic off-target transduction was minimal in uninjured animals but increased in injured animals, yet morphological hepatotoxicity was not observed. p21 knockdown via lentiviral shRNA effectively promotes cartilage regeneration, supporting the concept of targeting p21 and/or the p21 pathway as a therapeutic strategy for cartilage repair. - Source: PubMed
Larijani LeilaAhadzadeh Ardebili AriaOrtiz Vales NiniStürmer Andreas TKrawetz Roman J - Meox1 is aberrantly expressed in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate the effects of Meox1 on HCC cells and explore the underlying molecular mechanisms. Cell proliferation, colony formation, migration, invasion, and cell cycle distribution were assessed by CCK-8, clonogenic, Transwell, and flow cytometry assays, respectively. Protein expression was examined by Western blotting. Meox1 silencing significantly inhibited proliferation, clonogenic capacity, migration and invasion of HCC cells. Cell cycle analysis showed a reduction in G1-phase cells with a marked accumulation in the G2 phase following Meox1 knockdown. Western blot analysis revealed that suppression of Meox1 reduced p21CIP1/WAF1 expression. Meox1 contributest to HCC progression and may represent a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/19
Ruan JieXie YingZhang ChaoqunSun Dianxing