Ask about this productRelated genes to: SMARCE1 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
- Gene:
- SMARCE1 NIH gene
- Name:
- SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily e, member 1
- Previous symbol:
- -
- Synonyms:
- BAF57
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2014-11-19
Related products to: SMARCE1 antibody
Related articles to: SMARCE1 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 - Proteins containing high-mobility group (HMG) domains are segregated into two major groups. Members of one group are identified by the presence of more than one HMG domain that binds to DNA without sequence specificity, and they are usually ubiquitously expressed. In contrast, members of the other group possess a single HMG domain with high affinity to specific DNA sequences. Generally, members of the second group resemble classic tissue-specific transcriptional regulators. In contrast, Smarce1/BAF-57 is a ubiquitously expressed, novel protein with a single HMG domain that displays nonspecific DNA-binding characteristics. Additionally, as a core subunit of the mammalian SWI/SNF-like transcriptional activator complex, Smarce1/BAF-57 is also the first member of the HMG protein family that was reported to contain a kinesin-like coiled-coil (KLCC) domain. Here we report the cloning, as well as the chromosomal and phylogenetic analysis, of a novel mammalian protein that is structurally related to Smarce1, termed Smarce1-related (Smarce1r). The unique arrangement of an HMG with a KLCC domain shared with Smarce1/BAF-57 suggests a similar, albeit still unknown, function in chromatin assembly as part of a mammalian SWI/SNF-like complex. The linkage of a single nonspecific DNA-binding HMG domain with a KLCC domain makes both proteins the founding members of a third group of HMG proteins. - Source: PubMed
Wattler FWattler SKelly MSkinner H BNehls M