Ask about this productRelated genes to: HMG20B antibody
- Gene:
- HMG20B NIH gene
- Name:
- high mobility group 20B
- Previous symbol:
- -
- Synonyms:
- SOXL, HMGX2, BRAF35, SMARCE1r, BRAF25, HMGXB2
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2014-11-19
Related products to: HMG20B antibody
Related articles to: HMG20B antibody
- Insulin resistance (IR) is a central pathological feature of type 2 diabetes mellitus and metabolic syndrome, with dysregulated glycolytic metabolism in adipose tissue playing a critical role. Coptisine (Cop), a natural alkaloid, has been shown to exhibit anti-inflammatory and glucose-lowering properties; however, its mechanism in IR remains unclear.c Using both high-fat diet (HFD)-induced IR mice and tumor necrosis factor-α (TNF-α)-stimulated adipocytes, this study systematically evaluated the effects of Cop on insulin sensitivity and glycolytic metabolism. Techniques including glucose tolerance tests (GTTs), insulin tolerance tests (ITTs), Seahorse metabolic analysis, quantitative polymerase chain reaction (qPCR), Western blotting, and immunohistochemistry were employed to investigate the underlying mechanisms and the involvement of the key molecular target SMARCE1. Cop markedly improved IR in HFD-fed mice, reducing serum insulin levels, enhancing insulin sensitivity, and ameliorating adipose tissue architecture. In adipocyte models, Cop decreased levels of glycolytic metabolites lactate and pyruvate, expression of key glycolytic enzymes, includinng hexokinase 2 (HK2), lactate dehydrogenase A (LDHA), and pyruvate kinase M2 (PKM2), as well as extracellular acidification rate (ECAR). Further experiments revealed that Cop significantly inhibited SMARCE1 expression under IR conditions, while SMARCE1 overexpression reversed its inhibitory effects on glycolysis. In vivo studies confirmed that SMARCE1 overexpression exacerbated IR and up-regulated glycolytic enzyme expression in mice. Cop ameliorates IR by targeting SMARCE1-mediated suppression of glycolytic flux. These findings elucidate both the mechanistic basis and therapeutic potential of Cop for the treatment of metabolic disorders. - Source: PubMed
Publication date: 2026/02/06
Zhang YiWang WanqiuJin YixuanWu WeimingHan JianiQian LinglingZhang XiaomengJin Chao - In response to the urgent unmet needs of heterogeneity, unpredictability, and diagnostic delay in systemic lupus erythematosus (SLE), we aimed to identify and validate new immunoglobulin (Ig)G and IgA autoantibody specificities. - Source: PubMed
Publication date: 2025/05/14
Parodis IoannisLagutkin DenisLindblom JuliusIdborg HelenaBeretta LorenzoBorghi Maria Orietta Peyper Janique MBarturen GuillermoJakobsson Per-JohanAlarcón-Riquelme Marta ESherina NataliaNikolopoulos Dionysis - The genomic landscape of esophageal squamous cell carcinoma (ESCC) has been characterized extensively, but there remains a significant need for actionable targets and effective therapies. - Source: PubMed
Publication date: 2025/01/09
Lin Zhi-RuiXia Tian-LiangWang Meng-YaoZhang Lan-JunLiu Yan-MinYuan Bo-YuZhou Ai-JunYuan LiZheng JianBei Jin-XinLin Dong-XinZeng Mu-ShengZhong Qian - Aberrant alternative splicing (AS) contributes to tumor progression. A crucial component of AS is cleavage and polyadenylation specificity factor 4 (CPSF4). It remains unclear whether CPSF4 plays a role in triple-negative breast cancer (TNBC) progression through AS regulation. In this study, our objective is to investigate the prognostic value of CPSF4 and pinpoint pivotal AS events governed by CPSF4 specifically in TNBC. - Source: PubMed
Publication date: 2024/12/27
Zhong GuanshengShen QinyanZheng XinliYu KunLu HongjiangWei BajinCui HaidongDai ZhijunLou Weiyang - Skin color is highly variable in Africans, yet little is known about the underlying molecular mechanism. Here we applied massively parallel reporter assays to screen 1,157 candidate variants influencing skin pigmentation in Africans and identified 165 single-nucleotide polymorphisms showing differential regulatory activities between alleles. We combine Hi-C, genome editing and melanin assays to identify regulatory elements for MFSD12, HMG20B, OCA2, MITF, LEF1, TRPS1, BLOC1S6 and CYB561A3 that impact melanin levels in vitro and modulate human skin color. We found that independent mutations in an OCA2 enhancer contribute to the evolution of human skin color diversity and detect signals of local adaptation at enhancers of MITF, LEF1 and TRPS1, which may contribute to the light skin color of Khoesan-speaking populations from Southern Africa. Additionally, we identified CYB561A3 as a novel pigmentation regulator that impacts genes involved in oxidative phosphorylation and melanogenesis. These results provide insights into the mechanisms underlying human skin color diversity and adaptive evolution. - Source: PubMed
Publication date: 2024/01/10
Feng YuanqingXie NingInoue FumitakaFan ShaohuaSaskin JoshuaZhang ChaoZhang FangHansen Matthew E BNyambo ThomasMpoloka Sununguko WataMokone Gaonyadiwe GeorgeFokunang CharlesBelay GurjaNjamnshi Alfred KMarks Michael SOancea ElenaAhituv NadavTishkoff Sarah A