Ask about this productRelated genes to: HMGB2 antibody
- Gene:
- HMGB2 NIH gene
- Name:
- high mobility group box 2
- Previous symbol:
- HMG2
- Synonyms:
- -
- Chromosome:
- 4q34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-13
- Date modifiied:
- 2016-10-05
Related products to: HMGB2 antibody
Related articles to: HMGB2 antibody
- Increasing evidence supports important roles of post-transcriptional regulation in brain development; however, the precise mechanism remains unclear. Here, we show that Fragile X autosomal homolog 1 (FXR1), a brain-enriched RNA-binding protein (RBP), is essential for human neurogenesis. FXR1-deficient human cortical neural progenitor cells (NPCs) have reduced proliferation and impaired cell cycle exit during differentiation, leading to impaired neuronal differentiation. Transcriptomic and co-expression network analyses revealed FXR1 as an orchestrator of stage-specific gene programs driving neural differentiation. High-mobility group protein B2 (HMGB2), a master transcriptional regulator in stem cells, is a direct target of FXR1. FXR1 and HuR co-regulate HMGB2 mRNA, and their opposing actions on mRNA stability maintain the levels of HMGB2 in human NPCs. Reducing HMGB2 levels in FXR1-deficient NPCs rescues NPC proliferation and neuronal differentiation. Together, these findings establish post-transcriptional regulation as a key mechanism that maintains neurogenic potency of human NPCs. - Source: PubMed
Publication date: 2026/09/17
Méndez-Albelo Natasha MZhang YajieSandoval Soraya OGuo YuGao YuPeters Lily ASirois Carissa LWidicus Anna BYang PaofueTrygstad Drew NEckholm Magnus TXu ZhiyanSmith Riley VDisher Rachel MJohnston Christian JZhao Xinyu - Acute traumatic brain injury (TBI) is accompanied by systemic immune responses, but their whole-blood transcriptomic features at hospital arrival remain incompletely characterized. We aimed to characterize these features in patients with acute TBI compared with healthy controls. - Source: PubMed
Publication date: 2026/09/14
Nishida TakeshiNakamura YouheiMatsumoto HisatakeMitsuyama YumiEbihara TakeshiNakao ShunichiroOnishi ShinyaMuratsu ArisaYoneda KazuhiroNukiwa RyotaOkuzaki DaisukeOgura HiroshiOda Jun - Delayed cervical lymph node metastasis is strongly associated with poor prognosis in early-stage tongue squamous cell carcinoma, but useful biomarkers remain limited. This study evaluated cyclin B1, high-mobility group box protein 1 and 2, and proliferating cell nuclear antigen for stratifying the risk of delayed cervical lymph node metastasis. - Source: PubMed
Publication date: 2026/09/08
Kakuguchi WataruYanagawa-Matsuda AyaMaishi NakoChida TakehiroTakahashi KentaKirikoshi ShokoHida KyokoAshikaga YuichiOhiro Yoichi - Cisplatin is used in the treatment of ovarian cancer; however, the development of resistance, often due to the efficient repair of cisplatin-induced DNA damage, remains a major barrier to effective therapy. Among these lesions, DNA interstrand crosslinks (ICLs) are particularly cytotoxic because they prevent DNA replication and transcription. HMGB2, a member of the high-mobility group box (HMGB) protein family, can bind DNA lesions and has been implicated in genome maintenance and DNA repair. This study investigated whether HMGB2 contributes to the processing of cisplatin-induced DNA damage and modulates cisplatin sensitivity in human ovarian cancer cells. HMGB2 expression was suppressed by siRNA in cisplatin-sensitive A2780 and cisplatin-resistant CP70 human ovarian cancer cells. Cellular responses to cisplatin were assessed using clonogenic survival assays, cell cycle analysis, Western blotting, slot blot analysis, and modified alkaline comet assays. HMGB2 depletion reduced clonogenic survival in cisplatin-resistant CP70 cells and increased the sub-G1 population, indicating enhanced apoptotic DNA fragmentation following cisplatin treatment in both cell lines. Depletion of HMGB2 resulted in increased persistence of cisplatin-DNA adducts and impaired ICL processing, as demonstrated by persistent DNA damage over time and reduced ICL unhooking efficiency. DNA damage response signaling following cisplatin treatment was also altered by HMGB2 depletion in both cell lines, whereas the expression levels of key DNA repair proteins were unchanged. Our findings demonstrate that HMGB2 is involved in the cellular response to cisplatin treatment by promoting the efficient processing of cisplatin DNA adducts, particularly ICLs, thereby modulating cisplatin sensitivity in human ovarian cancer cells. These findings suggest that targeting HMGB2 may serve as a potential therapeutic strategy for overcoming cisplatin resistance in ovarian cancer. - Source: PubMed
Publication date: 2026/08/02
Huynh VanWang GuliangVasquez Karen M - Moyamoya disease (MMD) is a progressive cerebrovascular disorder characterized by intracranial arterial stenosis and abnormal collateral vessel formation. The molecular mechanisms by which extracellular vesicle (EV)-derived microRNAs contribute to endothelial dysfunction remain poorly understood. We investigated whether circulating extracellular vesicle-derived microRNAs (EV-miRNAs) contribute to endothelial dysfunction and serve as functional mediators of MMD pathogenesis. Plasma EV-miRNA profiles were compared among patients with MMD, intracranial atherosclerosis (ICAS), and healthy controls, and differentially expressed EV-miRNAs were validated in an independent cohort. Functional studies were performed in human umbilical vein endothelial cells and patient-derived induced pluripotent stem cell-derived endothelial cells. Three EV-miRNAs were significantly upregulated in MMD, among which miR-558 showed the strongest diagnostic performance. miR-558 overexpression impaired endothelial tube formation and proliferation, whereas its inhibition enhanced angiogenic activity. Mechanistically, HMGB2 was identified as a direct target of miR-558, and miR-558 overexpression reduced HMGB2 protein expression. Patient-derived endothelial cells recapitulated increased miR-558 expression, reduced HMGB2 levels, and impaired angiogenic capacity. These findings identify circulating EV-miR-558 a potential biomarker and show that miR-558 suppresses HMGB2 and impairs endothelial angiogenesis in adult MMD, suggesting that the EV-miR-558/HMGB2 pathway represents a potential mechanism underlying endothelial dysfunction and therapeutic target for MMD. - Source: PubMed
Publication date: 2026/08/13
Kim Eun HeeBang Oh YoungOh Gyun SikOh Mi JeongLee Woo JooSung Jin JeaChung Jong-WonSeo Woo-KeunKim Gyeong-MoonJee Tae KeunYeon Je YoungKim Jong-SooJang Jiho