HNRNPA2B1 Antibody
- Known as:
- HNRNPA2B1 Antibody
- Catalog number:
- 32193
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- HNRNPA2B1 Antibody
Related genes to: HNRNPA2B1 Antibody
- Gene:
- HNRNPA2B1 NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein A2/B1
- Previous symbol:
- HNRPA2B1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-29
- Date modifiied:
- 2016-10-05
Related products to: HNRNPA2B1 Antibody
Related articles to: HNRNPA2B1 Antibody
- Genomic instability contributes to tumor progression and limits the effectiveness of anticancer therapy. In this study, we investigated whether the citrus flavonoid hesperidin influences cytogenetic damage and epitranscriptomic markers in tumor cells exposed to ionizing radiation or maintained under long-term culture conditions. In human glioblastoma cell lines U87MG and LN229, hesperidin reduced radiation-induced micronucleus formation and decreased the spontaneous micronucleus frequency during prolonged passaging with repeated supplementation. Immunocytochemical analysis demonstrated that long-term hesperidin treatment was accompanied by reduced HNRNPA2B1 protein expression and lower global mA RNA levels. In a primary culture of collecting duct renal carcinoma cells, hesperidin altered cell morphology and growth dynamics during long-term cultivation. Together, these findings indicate that hesperidin reduces markers of genomic instability in tumor cell models and is accompanied by changes in HNRNPA2B1 expression and global mA RNA methylation. The mechanistic relationship between these observations requires further investigation. - Source: PubMed
Publication date: 2026/09/08
Sazonova ViktoriiaZun PavelTonkji IliaOnikienko SergeyErofeeva TatyanaBasharin VadimZhigalova NadezhdaIlyushkina AlexandraSkorb EkaterinaRuzov AlexeyShityakov SergeyKravtsov Viacheslav
- Source: PubMed
- Chordoma is a rare malignant bone tumor characterized by aggressive local invasion and high recurrence, yet its molecular regulatory mechanisms remain poorly understood. Circular RNAs (circRNAs) have emerged as important regulators of gene expression, but how circRNA epigenetic modifications contribute to oncogenic signaling is largely unknown. Here, we identify circPSMB1 as a significantly downregulated circRNA in chordoma tissues through high-throughput circRNA sequencing. Functionally, circPSMB1 suppresses chordoma cell proliferation, migration, and invasion in vitro and inhibits tumor growth in vivo. Mechanistically, METTL3-dependent m6A modification facilitates the association of circPSMB1 with the m6A reader HNRNPA2B1. CircPSMB1 competitively reduces the association of HNRNPA2B1 with c-MYC mRNA, thereby decreasing c-MYC protein expression without altering c-MYC transcript abundance. Beyond mechanistic insight, we develop an injectable circPSMB1-loaded HMnO-based nanohydrogel that enables sustained circRNA delivery and tumor microenvironment-responsive therapy, effectively suppressing chordoma progression in vivo. - Source: PubMed
Publication date: 2026/08/29
Tang YingchuangQiu LiangRuan XingbangShi YihanWang YeLi HanwenZhang KaiChen Kangwu - Type 2 diabetes mellitus (T2D) is a major global health challenge associated with a high burden of cardiovascular and microvascular complications. Endothelial dysfunction is a hallmark of T2D and represents a critical link between metabolic abnormalities and vascular disease. Chronic hyperglycemia, insulin resistance, obesity-associated inflammation, oxidative stress, and mitochondrial dysfunction disrupt endothelial homeostasis, resulting in impaired nitric oxide bioavailability, vascular inflammation, endothelial senescence, barrier dysfunction, and defective vascular repair. However, the molecular mechanisms integrating metabolic stress with endothelial injury in T2D remain incompletely understood. Neddylation is a reversible ubiquitin-like post-translational modification mediated by neural precursor cell expressed, developmentally downregulated 8 (NEDD8). Through activation of Cullin-RING E3 ubiquitin ligases and modification of non-cullin substrates, neddylation regulates protein turnover, signal transduction, metabolism, inflammation, oxidative stress responses, and mitochondrial homeostasis. Emerging evidence suggests that dysregulated neddylation contributes to several metabolic abnormalities implicated in endothelial dysfunction, including insulin resistance, obesity-associated metabolic dysfunction, oxidative stress, and mitochondrial dysfunction. In diabetic retinopathy, excessive cullin neddylation promotes degradation of protective factors such as nuclear factor erythroid 2-related factor 2 (NRF2) and heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1), thereby enhancing oxidative stress, inflammation, vascular leakage, and pathological angiogenesis. Conversely, physiological neddylation appears necessary for endothelial homeostasis through regulation of endothelial barrier integrity, angiogenesis, and stabilization of vascular endothelial growth factor receptor 2 (VEGFR2). Although direct evidence remains largely limited to retinal endothelial cells and diabetic retinopathy models, current findings support the hypothesis that dysregulated neddylation may act as an important molecular link between metabolic dysfunction and endothelial injury in diabetes. Pharmacological modulation of the neddylation pathway, including inhibition of the NEDD8-activating enzyme with MLN4924 (pevonedistat), improves metabolic homeostasis, suppresses inflammatory signaling, enhances antioxidant defenses, and attenuates vascular injury in preclinical studies. In this review, we summarize current advances in neddylation biology, discuss emerging evidence linking dysregulated neddylation to diabetes-associated endothelial dysfunction, highlight critical knowledge gaps, and evaluate the opportunities and challenges of targeting the neddylation pathway for the prevention and treatment of diabetic vascular complications. - Source: PubMed
Publication date: 2026/08/24
Cheng ZhongjianWittmann ChrisKishore Raj - Maltreatment in adolescence poses a major public health crisis as a primary factor for the development of adult psychiatric disorders. The anterior insula (AI) has been implicated as a hub in adult psychiatric disorders but the gene expression profile of AI in psychiatric disease in either humans or animal models is unknown. RNA sequencing of AI in adult male mice exposed to maltreatment in adolescence revealed altered expression of multiple ribosomal proteins and genes related to neurodegeneration. AI-specific neuronal rescue of a top RNA binding protein target, Hnrnpa2b1, in adulthood after adolescent maltreatment, significantly restored normative social behavior in defeated male mice. Together these preclinical findings reveal a regionally specific molecular pathway in male mice that should be further investigated as a possible target to reduce fear-based symptoms of adolescent maltreatment. - Source: PubMed
Publication date: 2026/08/17
Hisey Erin EBeatty Zoe GOtten JoyKlengel ClaudiaDillmann Larissa JMayeaux MirandaKearney Matthew GHartmann JakobCarlezon William AKlengel TorstenRessler Kerry J