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
- Spermatogonial differentiation is a key step in spermatogenesis, yet the transcriptional programs that control this process are not fully defined. E4f1 has been reported to be essential for embryonic development, mitochondrial function and spermatogonial stem cell (SSC) maintenance in mice. However, its function in spermatogonial differentiation and meiosis progression is unknown. - Source: PubMed
Publication date: 2026/04/14
Wang Fei-ChenHe ZhenYan Rong-GeWang Yu-JunWu Jia-LuYang Qi-En - Robust liver regeneration counteracts and facilitates recovery from liver injuries. The underlying epigenetic mechanisms, however, are not fully understood. Here we investigated the role of suppressor of variegation 3-9 homolog 1 (Suv39h1), a histone H3K9 methyltransferase, in liver regeneration. Suv39h1 expression was repressed by DNMT1 during liver regeneration. Systemic or hepatocyte-specific deletion of Suv39h1 in mice enhanced liver regeneration and post-surgery survival following partial hepatectomy. RNA sequencing revealed high-mobility group protein B2 (HMGB2) as a target for Suv39h1. Suv39h1 downregulation in proliferating hepatocytes allowed E2F1 to activate HMGB2 transcription. Consistently, HMGB2 knockdown attenuated proliferation of hepatocytes in response to HGF treatment and suppressed liver regeneration in mice. Integrated transcriptomic analysis indicated that HMGB2 may contribute to proliferation of hepatocytes by regulating a panel of proregenerative genes. Importantly, Suv39h1 inhibition by chaetocin boosted liver regeneration in mice. Finally, a significant correlation between Suv39h1, HMGB2 and proliferative markers was identified in patients with acute liver failure. In conclusion, our data uncover an unrecognized role for Suv39h1 in liver regeneration. Therefore, targeting Suv39h1 may be considered as a viable strategy to boost liver regeneration after injury. - Source: PubMed
Publication date: 2026/04/10
Lu YunjieZhou JiawenMiao XiulianZeng ShengQin LeiXu YongWang ShuaiLi Zilong - Intestinal epithelium relies on intestinal stem cells (ISCs) for rapid and precise tissue replenishment to maintain gut normal function. The self-renewal maintenance of ISCs is finely regulated by multiple stemness factors and signaling pathways. However, the transcription mechanisms of some key stemness factors remain poorly understood. Here, we identify that small nucleolar RNA Snora61 is highly expressed in ISCs. Snora61 is mainly distributed in the nucleoplasm. Snora61 knockout impairs ISC self-renewal and intestinal regeneration. Mechanistically, Snora61 binds to the promoter region of Lgr5 gene and engages with RNA-binding protein RBMX to recruit HMGB2 onto Lgr5 promoter, leading to Lgr5 transcription and expression. Snora61 promotes the self-renewal of small intestinal stem cells, which in turn enhances the proliferation of differentiated epithelial cells, thereby contributing to the maintenance of intestinal homeostasis. Conversely, Snora61 knockout causes reduced LGR5 expression. Deletion of Lgr5 with Snora61 displays more severely impaired ISC self-renewal and intestinal regeneration. Our findings reveal a regulatory mechanism of Lgr5 transcription underlying ISC self-renewal maintenance. - Source: PubMed
Publication date: 2026/04/07
He JiachengLan YufeiXu YuweiXiong ZhenYi ZhibinGuo HuiZhang JiahangZhou ZihengDu YingPan FanFan Zusen - Although distant metastasis is uncommon in differentiated thyroid carcinoma (DTC), it remains the leading cause of thyroid cancer-related mortality. The genetic landscape of distantly metastatic DTC (DMDTC) has not been well characterized in large cohorts. This study aimed to identify functional genetic alterations in DMDTC and validate their biological significance. We included 78 patients with DMDTC and performed DNA-based next-generation sequencing (NGS) in all cases, followed by RNA-based NGS for fusion gene detection, along with a review of previously reported isolated cases. Plasmids harbouring novel variants, including SPON1::ALK and RFTN1::BRAF fusions, and mutations in PTEN (c.322_345del, c.740del, c.968dup), STK11 (c.842C>T, c.1225C>T), and DNMT3A (c.891G>A, c.2312G>A, c.2595A>T, c.2606G>A) were constructed and transfected into TPC-1 and HEK293T cells to investigate downstream signalling. The methylation status of differentially methylated genes (DMGs) associated with DNMT3A mutations was analysed using the Infinium MethylationEPIC v2.0 BeadChip, with several DMGs validated by real-time quantitative PCR. The cohort consisted of 25 males and 53 females, with a mean age of 60.3 years at the diagnosis of metastasis. Histological types included papillary carcinoma (31 cases), follicular carcinoma (44 cases), and oncocytic carcinoma (3 cases). The lung and bone were the most common metastatic sites. Multiple metastases and older age were associated with metastasis-free and overall survival. Genetic alterations involving phosphorylation signalling pathways were identified in 61 cases, among which pathological alterations of DNA damage repair (DDR)-related genes were detected in ten cases. Novel RFTN1::BRAF and SPON1::ALK fusions, along with PTEN (c.740del, c.968dup) and STK11 (c.842C>T) mutations, could enhance downstream phosphorylation levels. DNMT3A mutations (c.891G>A, c.2312G>A, c.2595A>T, c.2606G>A) induced genome-wide methylation dysregulation, with altered expression of SLC12A7, FLNC, HMGB2, BNC2, and DAPK1. This study shows that DMDTCs are characterized by dysregulated phosphorylation signalling, accompanied by chromosomal instability and aberrant methylation, thus underscoring DDR gene-targeted therapy as a promising strategy. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/03/25
Kong WeimaoBao LongnvHu JianxiaLi GuangqiLiu YixuanRan WenwenZhang TinglingGu HaiyanZhang XinyiWang MeiliJi HongZong XuzhangZhang YongshengDang ShouqinLi DongFa LianglingYu XunzongPan XingzhuLi XueqingWang Jigang - The influenza virus polymerase mediates both transcription and replication, but the host factors involved were unclear. In this issue of Cell Chemical Biology, Rasmussen et al. identify RPAP2 as a transcription cofactor and HMGB2 as a replication cofactor, demonstrating HMGB2 inhibition enhances antiviral effects when combined with existing antivirals. - Source: PubMed
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