p53R2 Antibody
- Known as:
- p53R2 Antibody
- Catalog number:
- 2383
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- p53R2 Antibody
Related genes to: p53R2 Antibody
- Gene:
- RRM2B NIH gene
- Name:
- ribonucleotide reductase regulatory TP53 inducible subunit M2B
- Previous symbol:
- -
- Synonyms:
- p53R2
- Chromosome:
- 8q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-14
- Date modifiied:
- 2019-04-23
Related products to: p53R2 Antibody
Related articles to: p53R2 Antibody
- The dedifferentiation of chondrocytes significantly restricts their functional performance and practical applications. In our previous research, an easily preparable microcavitary alginate hydrogel (MCG) was shown to effectively promote the redifferentiation of dedifferentiated chondrocytes. Building on this, the present study further investigates the transcriptomic changes during chondrocyte dedifferentiation, utilizing high-throughput RNA sequencing to explore how MCG regulates passage-four dedifferentiated porcine chondrocytes over a 28-day period. Integrated analysis of transcriptomic profiling data across multiple time points identified the p53 signaling pathway as a potentially central regulatory node. Key findings validated by quantitative real-time polymerase chain reaction, Western blot, and Cell Counting Kit-8 assays demonstrated the following: (1) MCG arrested the progression of dedifferentiation, downregulated fibrosis/degeneration markers (COL1A1, WNT5A/B), and partially restored chondrogenic gene expression relative to P4; (2) Time-series analysis revealed MCG's influence on cell cycle regulation, extracellular matrix organization, DNA repair, and differentiation processes; (3) Crucially, MCG dynamically regulated the p53 pathway: early activation (TP53, p-p53 Ser15, MDM2) promoted DNA repair (RRM2B) and suppressed excessive inflammation/apoptosis (IL6/8, PMAIP1/CASP3), while subsequent attenuation of the pathway correlated with enhanced late-stage proliferation. In conclusion, the growth factor-free MCG microenvironment alleviates chondrocyte dedifferentiation and facilitates partial redifferentiation by orchestrating cellular behaviors through dynamic regulation of the p53 pathway-particularly via enhanced DNA repair-thereby offering a promising strategy for cell-based therapeutic approaches. - Source: PubMed
Publication date: 2026/05/07
Yao YongchangSu WeixianNie YupengSun HaoyangWang RuiLiu RixuDong Weiqiang - Differentiation therapy offers a promising approach in acute myeloid leukemia (AML) by overcoming the developmental block that maintains leukemic blasts. Increasing evidence indicates that DNA replication stress can promote differentiation rather than cytotoxicity; however, the metabolic mechanisms linking replication stress to differentiation remain poorly defined. Here, we investigated how perturbations in nucleotide metabolism regulate replication stress-driven differentiation. Using metabolomic and functional analyses in AML cell lines, we show that agents inducing differentiation through replication stress, including 5-aminoimidazole-4-carboxamide ribonucleoside (AICAr), dihydroorotate dehydrogenase (DHODH) inhibition, and low-dose cytarabine, converge on disruption of nucleotide pool balance. Low-dose AICAr induced a pyrimidine-purine imbalance, S phase arrest, and enhanced differentiation, whereas high-dose reduced these effects. Although brequinar and cytarabine altered nucleotide metabolism through distinct mechanisms, differentiation induced by all agents was abolished by supplementation with high levels of ribo- and deoxyribonucleosides, confirming that nucleotide imbalance is a central driver. We further identify ribonucleotide reductase (RNR) as a critical modulator of this process. Replication stress induced context-dependent regulation of RNR subunits, with RRM2 upregulated in p53-mutant U937 cells and the p53-responsive RRM2B isoform predominating in p53-wild-type MOLM-13 cells. Consistent with these differences, RRM2 depletion enhanced differentiation in U937 cells without affecting viability but impaired differentiation and survival in MOLM-13 cells. These findings position nucleotide metabolism as a key regulator of AML differentiation and suggest that combining RNR-targeted and checkpoint-modulating strategies could optimize therapeutic responses. - Source: PubMed
Publication date: 2026/04/24
Brcic AlojzijaLalic HrvojeSmoljo TomislavBardač KlaraDembitz VilmaPenker RomanaRodriguez Blanco GiovannyBedalov AntonioVisnjic Dora - Maintaining sustained deoxyribonucleotide triphosphate (dNTP) pools is essential for DNA replication fidelity and genome stability. In EGFR-mutant non-small cell lung carcinoma (NSCLC), we found that disruption of dNTP homeostasis plays a critical role in determining sensitivity to the EGFR inhibitor osimertinib and in shaping mechanisms of acquired resistance. Transcriptomic and biochemical analyses revealed that osimertinib suppresses RRM2 expression, a key regulator of dNTP synthesis, through downregulation of the transcription factor MYBL2. In response to osimertinib-mediated replication stress and dNTP depletion, cells activated a compensatory pathway involving the stress-inducible ribonucleotide reductase subunit RRM2B via a transcriptional regulator, TNNT3. CHK2 signaling was essential for TNNT3 nuclear translocation and RRM2B transcriptional activation. Inhibition of CHK2 or combined CHK1/2 blockade impaired RRM2B induction, exacerbated replication stress, and delayed the development of osimertinib resistance both in cell lines and in xenograft models. Collectively, these findings reveal that EGFR-mutant NSCLC cells rely on dynamic signaling through EGFR-MYBL2-RRM2 and CHK2-TNNT3-RRM2B regulatory pathways to maintain dNTP pool balance under therapeutic pressure. Disruption of this signaling network sensitizes tumors to osimertinib and impairs the acquisition of resistance, linking metabolic regulation to therapeutic resistance and disease progression. - Source: PubMed
Publication date: 2026/04/06
Xie QianWang YingyingFernandez AnthonyLei YiGong YuanhangHess Jessica DYang LinXin DiWilliams Terence MZheng LiShen BinghuiLi Min - Post-stroke depression (PSD), a prevalent neuropsychiatric complication of stroke, manifests as persistent low mood and depressive symptoms secondary to cerebrovascular injury, contributing to increased morbidity and mortality. Although the modified Jie-Yu-He-Huan (MJYHH) capsule has demonstrated clinical efficacy in alleviating PSD symptoms, its pharmacological targets and mechanisms of action remain unclear. - Source: PubMed
Publication date: 2026/02/04
Wang XinyuGao QianLiu ChaoHu MinghuiLiu ZhiyaoLi ZifaZhang HaoWu LidanChen KaiXu KaiyongGeng XiwenLiu WeiWei Sheng - To report a family with autosomal-dominant chronic progressive external ophthalmoplegia due to a novel truncating pathogenic variant in RRM2B and to show the challenges facing clinicians in diagnosing rare neuromuscular diseases. - Source: PubMed
Publication date: 2026/03/03
Mayer DemianKartsonaki EmmanouelaWilder-Smith EinarSchaller AndréFrank StefanBohlhalter StephanMihaylova Violeta