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
- Periodontitis is a chronic inflammatory disease characterized by progressive alveolar bone loss. Although spheroid culture enhances the osteogenic and regenerative potential of human periodontal ligament-derived multipotent mesenchymal stromal cells (hPDLMSCs), the underlying molecular mechanisms remain unclear. This study aimed to investigate the transcriptional features of spheroid-cultured hPDLMSCs, with a particular focus on cell cycle regulation and Forkhead Box O (FOXO) transcription factors. - Source: PubMed
Publication date: 2026/04/30
Hironaka ShoOnizuka SatoruSano KotaroOka YuichiroSuga TakenoriKokabu ShoichiroAriyoshi WataruNakazawa KohjiMochizuki ShinichiUsui Michihiko - The clinical behavior and molecular underpinnings of rare cases of poorly differentiated thyroid carcinoma (PDTC) diagnosed in young adults are not established. We evaluated 13 cases of PDTC in adult patients ≤ 45 years of age. The median age at diagnosis was 40 years (range 27 - 45 years). The median tumor size was 3.7 cm. The median mitotic count was 6 per 2 mm. Necrosis was present in 7 (54%) cases. Eleven (85%) cases were either encapsulated with extensive (≥ 4 foci) angioinvasion or widely invasive. Molecular analysis was available for nine (69%) cases and revealed two (22%) with PAX8::PPARG fusions, two (22%) with NRAS alterations, one (11%) with a DICER1 variant, one (11%) with alterations in ATM, CDKN1A and TERT, one (11%) with a TSC2 deletion and TERT copy number gain, and two (22%) with variants of uncertain significance only. Of the 12 (92%) patients with follow-up data available (median 6.2 years, range 1.5-16.4 years), the only patient who died of disease had distant metastases at diagnosis. Of the remaining patients with initial M0 disease, only one had disease recurrence, developing local recurrence and distant metastasis with persistent disease at last follow up. Our findings suggest that PDTC in adults ≤ 45 years of age at diagnosis, may have a better prognosis than is typically associated with PDTC despite high-grade features and invasive growth. Additionally, we found a higher rate of PAX8::PPARG fusions and a lower rate of TERT alterations, suggesting that the molecular profile might explain the improved survival. - Source: PubMed
Publication date: 2026/05/07
Riascos Maria CristinaMarqusee EllenAhmadi SaraPappa TheodoraFisch Adam SBarletta Justine A - Tamoxifen-inducible gene targeting in mice with estrogen receptor-dependent Cre (CreER) recombinase has enormously advanced vascular biology research. However, CreER activation under the control of vascular endothelial promoters causes off-target effects that impair the vascularization of the retina, a widely used model to study the molecular and cellular mechanisms of angiogenesis. Although ubiquitously expressed CreER is also used to study retinal angiogenesis, it remains unknown whether it causes similar or more severe off-target effects compared to endothelial-selective CreER activation. Moreover, the molecular and cellular processes disrupted by CreER activation in endothelial cells remain to be identified. Here, we demonstrate that ubiquitous CreER activation in postnatal mice decreases body growth and impairs retinal angiogenesis. We further show that CreER activation slows endothelial cell proliferation and promotes apoptosis concomitant with p21/CDKN1A upregulation in the angiogenic retina, although retinal vasculature progressively normalizes. By contrast, CreER activation in quiescent adult retinal vasculature did not induce endothelial cell apoptosis or p21 activation. Altogether, our findings indicate that ubiquitous promoters should be avoided to drive CreER expression when studying gene function during retinal angiogenesis, and that CreER activation controls, although essential to account for endothelial apoptosis and proliferation defects in short-term studies, may be less critical for adult vascular studies. - Source: PubMed
Publication date: 2026/05/05
Ioannou ElenaDong MengmengRashbrook Victoria SRuhrberg ChristianaRudnicki Martina - The aggregation of alpha-synuclein (αSN) is a key pathological feature of Parkinson's disease (PD), leading to neural cell death via reactive oxygen species (ROS) overload and activation of downstream neurotoxic pathways. Betanin, a beetroot-derived small molecule, has exhibited antioxidant and neuroprotective properties. In this study, three betaxanthins-Bxn-A, Bxn-B, and Bxn-C-were chemically synthesized from betanin to enhance its therapeutic properties. Betaxanthin Bxn-A effectively reduced intracellular ROS levels without cytotoxicity, even at 500 µM. Additionally, betanin and its derivatives revealed neuroprotective effects, including significant reductions in apoptosis, preservation of mitochondrial membrane potential, modulated autophagy, and enhanced cell viability in PD-model cells. In terms of aggregation inhibition, betaxanthins Bxn-A and Bxn-B significantly reduced αSN aggregation compared to the control after 48 h of incubation. Betaxanthin Bxn-A also triggered disaggregation of existing aggregates and inhibited formation of large, insoluble species. Moreover, αSN aggregation and disaggregation products formed in the presence of betanin or its derivatives exhibited significantly lower cytotoxicity than those formed in their absence. Specifically, cells treated with aggregates formed in the presence of 50 µM betaxanthin Bxn-B showed 100% viability, while those treated with disaggregation products formed in the presence of 100 µM betaxanthin Bxn-A showed 20% greater viability than those treated with untreated disaggregates. Molecular docking revealed interactions between betaxanthins and key αSN residues, suggesting destabilization mechanisms. Docking analyses with five ROS-PPI network key proteins-C5, CDC42, BCL2, CDKN1A, and CDKN1B-indicated potential roles in inhibiting oxidative stress-related pathways. Drug-likeness predictions indicated that the derivatives enhanced pharmacological potential, making them promising candidates for PD treatment. - Source: PubMed
Publication date: 2026/05/04
Ghahari AydaAlikhanian AlirezaSolaei Fatemeh AkhondFattahi ArghavanHourfar HamdamSchallmey AnettMohammadi MehdiMorshedi Dina - : Retinoblastoma represents the most common intraocular malignancy in childhood; however, the clinical applicability of mitomycin C (MMC) is restricted by dose-dependent ocular toxicity. Consequently, the development of pharmacological strategies that sensitize tumor cells to MMC while allowing dose reduction remains an unmet therapeutic objective. In this context, quercetin, a bioactive flavonoid with pleiotropic anticancer properties, has emerged as a potential chemosensitizing agent. : Human retinoblastoma cell lines Y79 and WERI-Rb1 were exposed to MMC and quercetin, administered either individually or in fixed-ratio combinations. Cytotoxic responses were quantified through dose-response modeling and IC determination following 24 and 48 h of treatment. Drug-drug interactions were quantitatively characterized using the Chou-Talalay combination index (CI) approach and isobologram analysis. Cell cycle distribution was assessed by propidium iodide (PI)-based flow cytometric analysis to evaluate treatment-associated alterations in cell cycle progression. Apoptotic cell death was assessed by Annexin V-FITC/PI flow cytometry, while transcriptional modulation of genes associated with apoptosis, cell cycle regulation, and oxidative stress (BAX, BCL-2, TP53, CASP3, CDKN1A, and HMOX1) was evaluated by qRT-PCR. Modulation of tumor-supportive signaling was examined by measuring VEGF and IL-6 secretion. Translational relevance was further investigated using a three-dimensional (3D) tumor spheroid model, and the functional contribution of reactive oxygen species (ROS) was interrogated through N-acetyl-L-cysteine (NAC) rescue experiments. : Quercetin significantly enhanced the cytotoxic activity of MMC in both retinoblastoma cell lines, with CI values below 1 across IC-IC effect levels, indicating a synergistic pharmacological interaction. PI-FACS analysis revealed that combined MMC and quercetin treatment induced a pronounced accumulation of cells in the G2/M phase, consistent with cell cycle arrest, with a more marked effect observed in Y79 cells compared with WERI-Rb1 cells. Combination treatment resulted in a pronounced increase in apoptotic cell populations compared with single-agent exposure and triggered a coordinated pro-apoptotic transcriptional response, characterized by increased expression of BAX, TP53, CASP3, CDKN1A, and HMOX1, alongside suppression of BCL-2 and a marked shift in the BAX/BCL-2 ratio. Concurrently, VEGF and IL-6 secretion were significantly reduced, reflecting attenuation of pro-angiogenic and pro-inflammatory signaling. Notably, synergistic cytotoxicity was maintained in 3D tumor spheroids, where combined treatment induced spheroid shrinkage, architectural disruption, and reduced viability. NAC pretreatment diminished ROS accumulation and partially restored cell viability, indicating that oxidative stress contributes to, but does not solely account for, the observed synergistic cytotoxic effect. : Collectively, these findings indicate that quercetin appears to function as an effective chemosensitizing adjuvant to MMC in retinoblastoma models, through transcriptional changes consistent with p53-associated apoptotic signaling at the transcriptional level, G2/M cell cycle arrest, and partial involvement of ROS-related cellular stress responses, along with suppression of tumor-supportive signaling pathways. The preservation of synergistic activity in 3D tumor spheroids supports the potential preclinical relevance of this combination. However, these findings are based on transcriptional and phenotypic analyses and should be interpreted as hypothesis-generating, requiring further validation through protein-level and in vivo studies before translational application. - Source: PubMed
Publication date: 2026/03/28
Duman ErkanMaçin AydınÖzdemir İlhanÖztürk ŞamilTuncer Mehmet Cudi