HMGCR Antibody
- Known as:
- HMGCR Antibody
- Catalog number:
- csb-pa010565la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- HMGCR Antibody
Related genes to: HMGCR Antibody
- Gene:
- HMGCR NIH gene
- Name:
- 3-hydroxy-3-methylglutaryl-CoA reductase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: HMGCR Antibody
Related articles to: HMGCR Antibody
- Immune-mediated necrotizing myopathy (IMNM) are rare muscular inflammatory muscle diseases that bear poor prognosis. Description of their clinical evolution remains limited in the literature. This study aimed to describe the clinical, biological, and serological features of patients with anti-HMGCR or anti-SRP IMNM presenting with muscle involvement at diagnosis and to identify factors associated with relapse during follow-up. - Source: PubMed
Publication date: 2026/08/06
Batton RomainRoullée LéopoldCarrette MarionLanglois VincentMembrey BenjaminLe Besnerais MaëllePerrin ShonaJouen FabienneSilva MurielBenhamou YgalBoyer OlivierLeclercq Mathilde - Sea cucumber is a high-value marine food that contains characteristic bioactive components, notably saponins and polysaccharides. Strategies promoting their biosynthesis to improve sea cucumber quality are vital for the industry. The impacts of three dietary yeast β-glucans (native β-glucan, ultrasonic-degraded low-molecular-weight β-glucan, and carboxymethylated β-glucan) on the biosynthesis of saponin and fucosylated chondroitin sulfate (FCS) in A. japonicus and the underlying mechanism were investigated. A 28-day feeding trial showed that modified β-glucans improved growth performance and immune responses, as well as elevated the body wall accumulation of saponin and FCS. Mechanistically, modified β-glucans up-regulated the genes involved in the saponin and FCS biosynthesis, including the core mevalonate pathway (hmgcr, mvk, mvd), downstream post-squalene modifications (sqle), and chondroitin backbone biosynthesis (xylt1, chsy1, chpf). Moreover, these β-glucans up-regulated the TLR-MAPK signaling axis genes (tlr, myd88, irak4, traf6, tak1, mkk1, erk, p38) and increased p38/ERK protein abundance and phosphorylation levels. In vivo MAPK inhibition attenuated β-glucan-induced saponin and FCS accumulation and the expression of hmgcr, sqle, xylt1, and chsy1. Our findings reveal that modified β-glucans enhance A. japonicus quality by promoting saponin and FCS biosynthesis in association with the TLR-MAPK signaling axis-mediated immune-metabolic crosstalk. - Source: PubMed
Publication date: 2026/08/06
Qi ZezhengZhang ZeyuDai WenyueMa HongmeiGe JunpengYu YutongCheng MenglingZhao WenjianPan ShihuiGu MinBai Nan - Hantavirus infection triggers life-threatening hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), driven by severe endothelial barrier breakdown and systemic capillary leakage. Clinical severity varies widely with undefined host regulators, and no targeted endothelial-protective treatments exist. Recent data link hantaviruses to gut microbiome remodeling, while bile acid (BA) receptors FXR and TGR5 potently inhibit NF-κB-mediated endothelial inflammation. We synthesize four core lines of evidence. First, metagenomic reports confirm hantavirus reshapes gut/lung microbiota in rodent reservoirs. Second, we re-analyzed three public GEO datasets via standardized RNA-seq/microarray pipelines: (i) GSE245916: SEOV-infected human/rat lung ECs show conserved VCAM1/ICAM1 upregulation (human VCAM1 logFC=+1.17, P = 0.023; rat Icam1 logFC=+0.32, padj=0.016) with unaltered FXR; (ii) GSE7271: SEOV-infected rat lung displays sustained Nfkb1 suppression (all timepoints, P<0.05) and day-15 Slc10a2 downregulation (P = 0.028); (iii) GSE270172: PUUV 3D vessel chips feature robust IL6 elevation (logFC=+1.22, P = 3.1×10) and disrupted BA transporters (ABCC3 logFC=-1.44, P = 7.4×10¹²). TGR5 (GPBAR1) was undetectable in endothelial cells across all datasets. Third, FXR/TGR5 agonists repress NF-κB inflammation and mitigate lung vascular injury. Fourth, HTNV upregulates CH25H to block HMGCR-dependent cholesterol synthesis, depleting BA precursor substrates. We propose a unified pathogenic model: hantavirus-triggered gut dysbiosis plus virus-impaired cholesterol metabolism deplete circulating FXR/TGR5 agonistic BAs, relieving constitutive inhibition of endothelial NF-κB and monocyte NLRP3 inflammasomes to exacerbate capillary leakage. We define tiered testable predictions covering clinical multi-omics cohorts, receptor modulation assays and pharmacological interventions. This gut microbiota-BA-FXR/TGR5 axis represents a repurposable therapeutic target for hantavirus diseases, though direct causal evidence connecting BA signaling to viral vascular damage remains absent; our framework offers a rigorous testable roadmap for subsequent validation. - Source: PubMed
Publication date: 2026/07/22
Liu LeiLin JiyongSang KaiLai JianpingHuang NaZhong PeilingLiu YuxiangChen Sheng - Diabetes mellitus, especially type 2 diabetes mellitus (T2DM), represents a significant global health challenge. Growing evidence indicates that Akkermansia muciniphila, a promising next-generation beneficial microorganism, could help alleviate metabolic disorders. Nevertheless, its strain-specific effects and associated mechanisms require further investigation. Here, we investigated the potential effects of pasteurized A. muciniphila AKK PROBIO in T2DM using db/db mice. - Source: PubMed
Publication date: 2026/08/04
Chen MenglingLi RaoXiang YanglingMa XinYu XuepingZhao JingqiRen Dayong - This study aims to elucidate the material basis and mechanism of action of the Aconitum pendulum Busch product processed with highland barley wine against rheumatoid arthritis(RA). UPLC-Q-TOF-MS/MS was employed to preliminarily identify 55 compounds from the product. Through network pharmacology, 19 potential active ingredients and 140 corresponding targets were screened out. The drug targets were intersected with 89 RA targets collected from the OMIM database to yield a set of potential intervention targets. The protein-protein interaction(PPI) network was constructed via STRING and topological analysis was conducted via Cytoscape, which identified eight core targets: PPARG, EGFR, SLC6A3, OPRM1, PRKCA, CYP2D6, HTR1A, and HMGCR. Gene Ontology(GO) functional and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses performed in the Metascape database revealed that these targets were significantly enriched in processes such as TRP channels, the phosphatidylinositol 3 kinase(PI3K)-protein kinase B(Akt) signaling pathway, and neutrophil extracellular traps(NETs) formation. An integrated "drug-ingredient-disease-target-pathway" network was constructed, which selected seven core ingredients(dehydrolucidusculine, linoleic acid, pyraconitine, 16-epipyroaconitine, delphinine, 1-monopalmitin, and songorine) for molecular docking with the eight core targets. The results demonstrated favorable binding activity between each ingredient and the targets. Animal experiments showed that the A. pendulum product processed with highland barley wine alleviated joint swelling and inflammatory pathological changes of synovial tissue in the rat model of adjuvant-induced arthritis(AA) in a dose-dependent manner. In terms of the serum inflammatory cytokine levels, it downregulated the expression of pro-inflammatory cytokines tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), interleukin-17A(IL-17A), and interleukin-6(IL-6). Furthermore, the product significantly reduced the phosphorylation levels of PI3K and its downstream signaling molecule Akt of knee synovial tissue in the rat model of AA. In conclusion, this study preliminarily reveals that the A. pendulum product processed with highland barley wine may exert anti-RA effects through multi-ingredient, multi-target, and multi-pathway mechanisms, particularly by regulating the PI3K-Akt signaling pathway and inflammatory responses. - Source: PubMed
Yu HaoDong DanChen Si-QiJiang NuanJiang Si-SiWencheng Dang-ZhiMa MinJia Wa