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
- Chondrosarcoma is a common bone sarcoma in adults with limited therapeutic options due to frequent chemoresistance. Cisplatin (CDDP) is a key chemotherapeutic agent, but resistance often develops. This study investigated the role and mechanism of circular RNA HMGB2 (circHMGB2) in cisplatin resistance of chondrosarcoma. Clinically, circHMGB2 was upregulated in chondrosarcoma tumors and associated with cisplatin resistance and poor patient survival. Functionally, exogenous overexpression of circHMGB2 elevated cisplatin resistance in chondrosarcoma cells (SW1353, OUMS-27) in vitro, while its silencing re-sensitized resistant cells. Mechanistically, circHMGB2 did not function as a miRNA sponge but acted as a competitive molecular decoy for the RNA-binding protein IGF2BP1. We demonstrated that circHMGB2 directly binds IGF2BP1, competitively impairing IGF2BP1's binding to and stabilization of Grb10 mRNA, leading to its destabilization and subsequent downregulation of Grb10 protein. This suppression of Grb10, a known negative regulator of the PI3K/Akt pathway, resulted in constitutive Akt phosphorylation, driving resistance. Crucially, co-overexpression of IGF2BP1 rescued circHMGB2-induced Grb10 downregulation, Akt activation, and cisplatin resistance, validating the decoy mechanism. Furthermore, in a cisplatin-resistant xenograft model, silencing circHMGB2 synergized with cisplatin to significantly inhibit tumor growth, improve host survival, and upregulate intratumoral Grb10 while suppressing Akt phosphorylation. Our results delineate a novel circHMGB2/IGF2BP1/Grb10/Akt axis that drives cisplatin resistance in chondrosarcoma. Targeting circHMGB2 could therefore serve as a promising therapeutic strategy to overcome chemoresistance and enhance treatment efficacy. - Source: PubMed
Publication date: 2026/08/05
Zhu Y ISong HuiDU ShengyangZhang WeijunCao Lei - Sepsis is a life-threatening syndrome characterized by dysregulated immune responses, while the molecular basis of immune dysfunction remains unclear. Increasing evidence suggests that R-loop accumulation and DNA damage may contribute to immune disorders, but their roles in sepsis have not been systematically investigated. - Source: PubMed
Publication date: 2026/08/06
Chen MinKang Jie-XiangHe Shi-LingHu Hui-RongWeng Hai-JunZhang Xiao-QiWeng Pei-Qing - Sepsis, characterized by a rapid transition to systemic immune dysregulation and multiorgan failure, poses a formidable clinical challenge. The lack of spatiotemporally stable biomarkers severely impedes early diagnosis and risk stratification. By integrating large-scale transcriptomic profiling with machine learning algorithms, this study identified a robust three-gene diagnostic signature (TLR5, HMGB2, and C19orf59). Single-cell RNA sequencing precisely localized the sepsis-induced specific upregulation of these targets to the myeloid immune compartment, notably monocytes and neutrophils. Crucially, disease severity stratification analysis (based on SOFA scores) revealed that while TLR5 and HMGB2 excel in identifying high-risk sepsis, C19orf59 maintains highly consistent diagnostic efficacy across all clinical severity strata. To definitively validate these findings while rigorously eliminating confounding effects from surgical or environmental stress, strictly time-matched sham-controlled cecal ligation and puncture (CLP) murine models and vehicle-controlled in vitro models were utilized. In vivo results corroborated the persistent in situ upregulation of this signature across vital target organs (lung, heart, liver) and systemic circulation. Parallel in vitro lipopolysaccharide (LPS)-stimulated cellular models further characterized their dynamic expression, with HMGB2 exhibiting a distinct biphasic kinetic profile mechanistically characteristic of danger-associated molecular patterns (DAMPs). Finally, independent clinical validation using sepsis patient serum corroborated the translational relevance of these targets. Collectively, this systematic multidimensional evaluation establishes TLR5, HMGB2, and C19orf59 as a highly reliable diagnostic and severity-stratification panel, providing novel molecular insights into the septic pathological cascade. - Source: PubMed
Zhang XinGuo XiaoqingJiang ShuaiCao YantingWang ShuyaXie WentaoTian JiayinZhou YazheWang ManChang HuiYang Yang - Administration of recombinant tissue plasminogen activator (rtPA) beyond 4.5 h after ischemic stroke exacerbates blood-brain barrier (BBB) disruption, leading to vasogenic cerebral edema and hemorrhage. However, current therapies remain ineffective. - Source: PubMed
Publication date: 2026/07/27
Zhang YiChen Fan-KaiYue Shan-ShanPan Chun-ShuiLi QuanYan LiHuo Xin-MeiSun KaiLu Xiao-QingLiang Hong-BiaoYao Shu-QiLiu Bo-TongLiu JianHan Jing-Yan - Recessive dystrophic epidermolysis bullosa is an inherited skin disorder characterized by fragile skin, blistering, and chronic wounds. Keratinocytes, the primary cells in the epidermis, are directly affected by persistent injury in recessive dystrophic epidermolysis bullosa, contributing to chronic inflammation. HMGB1 (high mobility group box 1) is elevated in the serum of individuals with recessive dystrophic epidermolysis bullosa. However, its role in keratinocyte inflammation remains unclear. In this study, we report an increase in expression in keratinocytes at chronic wound sites compared with that on matched nonwounded skin from an individual with recessive dystrophic epidermolysis bullosa, suggesting a potential link to the upregulation of local proinflammatory stimuli. Pharmacologic inhibition of HMGB1 using inflachromene reduced lipopolysaccharide-induced secretion of proinflammatory cytokines in keratinocytes, supporting a role for keratinocyte-specific HMGB1 in inflammatory response. Surprisingly, deletion of alone or together with its paralog did not suppress the release of proinflammatory cytokines in response to lipopolysaccharide. Furthermore, inflachromene still reduced the secretion of proinflammatory cytokines in - and -knockout cells. This unexpected discrepancy between genetic deletion and pharmacologic inhibition points to a more complex role for HMGB1 or off-target effects of the compound. These findings suggest that HMGB1 may contribute to proinflammatory signaling in keratinocytes; however, its exact function needs further investigation. - Source: PubMed
Publication date: 2026/05/12
Bui Kacey GuentherChang Ya-ChuChiraphapphaiboon WannasiriWang JianfengEbens Christen LTolar JakubBielinsky Anja-KatrinNguyen Hai Dang