SMCC, CROSS-LINKING REAGENTS FOR BIOCONJUGATION
- Known as:
- SMCC, CROSS-LINKING REAGENTS BIOCONJUGATION
- Catalog number:
- E030W0025
- Category:
- -
- Supplier:
- Cyanagen
- Gene target:
- SMCC CROSS-LINKING REAGENTS FOR BIOCONJUGATION
Related genes to: SMCC, CROSS-LINKING REAGENTS FOR BIOCONJUGATION
- Gene:
- CNN1 NIH gene
- Name:
- calponin 1
- Previous symbol:
- -
- Synonyms:
- SMCC, Sm-Calp
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-16
- Date modifiied:
- 2016-01-19
- Gene:
- TAGLN NIH gene
- Name:
- transgelin
- Previous symbol:
- -
- Synonyms:
- SM22, WS3-10, TAGLN1, SMCC, DKFZp686P11128
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2014-11-19
Related products to: SMCC, CROSS-LINKING REAGENTS FOR BIOCONJUGATION
"CROSS PTFE 1_4""_28 " Prod. Code K(Z-Cys-OH)2, peptide reagents(Z-Cys-OH)2, peptide reagents10X DPBS, with Ca, Mg, cell culture reagents10X DPBS, without Ca, Mg, cell culture reagents10X HBSS, with Ca, Mg, cell culture reagents10X HBSS, without Ca, Mg, cell culture reagents10X PBS, cell culture reagents17 alpha Hydroxyprogestrone antibody (Prediluted for IHC), IHC Reagents, Host Rabbit, Isotype IgG17 alpha Hydroxyprogestrone antibody (Prediluted for IHC), IHC Reagents, Host Rabbit, Isotype IgG1M HEPES solution, cell culture reagents1X DPBS, with Ca, Mg, cell culture reagents1X DPBS, with Ca, Mg, cell culture reagents1X DPBS, without Ca, Mg, cell culture reagents1X DPBS, without Ca, Mg, cell culture reagents Related articles to: SMCC, CROSS-LINKING REAGENTS FOR BIOCONJUGATION
- The litter size of goats is a key factor affecting their reproductive performance. The ovary plays a central role in the reproductive process of goats. However, the relationship between the dynamic changes in the ovarian proteome and the prolific traits of goats remains unclear. The Jining Grey Goat, an excellent dual-purpose meat and skin breed in China, is famous for its distinctive coat color characteristics and high reproductive performance. - Source: PubMed
Publication date: 2026/06/19
Li RuiZhang WenhaoRen YifanHe JunminMao JingyiLi XueZhang GuopingMa KailunWang MingNie FumeiTian KechuanHuang Xixia - Vascular smooth muscle cells (VSMCs) are critical players in atherosclerotic plaque development and progression, but existing isolation methods often yield low cell viability, making them suboptimal for several downstream applications. As such, we aimed to optimize an enzymatic digestion protocol for isolating viable VSMCs from human carotid plaques suitable for cell culture analysis. Carotid plaques were obtained following endarterectomy and subjected to a streamlined enzymatic digestion protocol using a simplified cocktail optimized to minimize cell damage. After brief culture to passage 1, single-cell suspensions were processed using the 10X Genomics Chromium platform. Single-cell RNA sequencing (scRNA-seq) data underwent rigorous quality filtering, Harmony-based integration, clustering, gene ontology (GO) enrichment analysis, and pseudotime trajectory inference to validate cell identity and assess phenotypic transitions. The protocol yielded high-viability single-cell suspensions, with approximately 23,661 cells sequenced after quality filtering from four carotid plaques: two classified as stable and two as unstable, obtained from both male and female patients. scRNA-seq revealed that the majority of isolated cells were VSMCs, confirmed through positive module scores for canonical VSMC markers (TAGLN, ACTA2, MYH11, CNN1, MYL9) and GO enrichment of VSMC-related biological processes. Label transfer analysis using the Tabula Sapiens vasculature reference further confirmed VSMCs as the predominant population. Subcluster analysis identified four transcriptionally distinct VSMC phenotypes. Pseudotime analysis demonstrated a trajectory originating from contractile VSMCs, progressing through intermediate foam cell-like and inflammatory synthetic states, and ultimately transitioning into fibroblast-like phenotypes. This confirms that the entire isolated population was VSMC-derived and undergoing phenotypic switching. In conclusion, this optimized protocol enables the reliable isolation of highly viable VSMCs from human carotid plaques, as validated by single-cell transcriptomic profiling. These findings lay the groundwork for future applications of isolated VSMCs in single-cell studies, disease modeling, and mechanistic investigations of VSMC phenotypic switching and plaque instability. - Source: PubMed
Publication date: 2026/01/10
Byun Jae HyunQuintanilla Helena PapacostasEngin IremAladeeb RachelHo JuliaHe YingRios Francisco JMontezano Augusto CTouyz Rhian MRagoussis JiannisDaskalopoulou Stella S - This study aimed to explore the common differentially expressed genes (DEGs) between atherosclerosis (AS) and nonalcoholic fatty liver disease (NAFLD) through bioinformatics. The GSE89632 and GSE100927 datasets from the open-source GEO database were selected for analysis in this study. DEGs between the control and disease groups were identified from the datasets of NAFLD and AS, leading to the identification of genes that are commonly dysregulated in both conditions. Gene set enrichment analysis (GSEA) was performed on 2 datasets, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses to investigate the potential biological functions and signaling pathways associated with the common DEGs. A protein-protein interaction network was constructed using the STRING database to identify hub genes. The diagnostic efficacy of these hub genes was evaluated through receiver operating characteristic curve analysis of the GSE63067 and GSE57691 datasets. A total of 45 common DEGs were identified. GSEA indicated that there were common pathways in the GSE89632 and GSE100927 datasets. The GO and KEGG pathway enrichment analyses revealed that the co-expressed genes were mainly enriched in regulating cytokine production, increasing responsiveness to external stimuli, and macrophage activation. The identified signaling pathways primarily included cytokine-cytokine receptor interaction, the toll-like receptor signaling pathway, and the interleukin-17 signaling pathway. Ten hub genes were OSM, IL1B, CCL3, CSF3, IL1RN, TAGLN, CNN1, RGCC, MYH11, and ACTG2. Common DEGs were identified between AS and NAFLD, indicating that these diseases may mutually influence and exacerbate each other during their progression. Exploring their shared pathogenic mechanisms may provide insights into potential therapeutic targets and contribute to the prevention of AS development in patients with NAFLD. - Source: PubMed
Yan RuiLi PingSong JiahuiQiang YuweiZhai Guangyao - Pathologically activated vascular smooth muscle cells (VSMCs) upregulate proprotein convertase subtilisin/kexin type 9 (PCSK9), contributing to vascular inflammation and remodeling. Although both PCSK9 and 25-hydroxyvitamin D (25OHD), the active form of Vitamin D, are linked to inflammatory regulation, their interaction in modulating VSMC phenotype remains unclear. Here, we investigated the effect of 25OHD on PCSK9 expression in human aortic SMCs (HASMCs) under lipopolysaccharide (LPS)-induced inflammatory stress. LPS stimulation increased PCSK9 mRNA >2-fold, while 25OHD pre-treatment significantly reduced this induction and restored expression of contractile markers (Acta2, Cnn1, Myocd, Tagln). Functional assays revealed that both 25OHD and PCSK9 knockdown attenuated LPS-induced proliferation and migration in HASMCs. In vivo, 25OHD supplementation in C57BL/6 mice for six weeks prior to partial carotid artery ligation suppressed injury-induced PCSK9 expression in SMCs and reduced neointimal hyperplasia. Supporting these findings, reanalysis of RNA-seq data revealed that airway SMCs (ASMCs) derived from asthma patients and treated with Vitamin D exhibited lower PCSK9 expression and concomitantly elevated sirtuin expression relative to untreated asthmatic controls. Mechanistically, 25OHD enhanced SIRT6 activation, and inhibition of SIRT6 with nicotinamide reversed 25OHD-mediated PCSK9 downregulation, identifying SIRT6 as a key regulator. Together, these findings reveal a novel SIRT6-dependent mechanism by which Vitamin D suppresses PCSK9-driven VSMC phenotypic switching, exerting protective effects against vascular inflammation and remodeling. News and Noteworthy: This study highlights the crucial role of PCSK9 in the inflammation and phenotypic modulation of VSMCs. The active Vitamin D metabolite, 25OHD, suppresses inflammation-induced PCSK9 expression and restores contractile gene markers in HASMCs. In vivo, Vitamin D supplementation reduces PCSK9 levels and neointimal hyperplasia following flow-mediated vascular injury. Mechanistically, 25OHD activates SIRT6, establishing a novel 25OHD-SIRT6-PCSK9 regulatory axis with promising therapeutic implications for vascular inflammation and remodeling. - Source: PubMed
Publication date: 2025/12/12
Duddu SushmithaKatakia Yash TSuresh NivedhaChakrabarti RituparnaMajumder SyamantakShukla Praphulla Chandra - The role of peripheral vascular smooth muscle cells (VSMCs) in vascular calcification has been overlooked compared with that of the major VSMCs. This study aimed to investigate the differentially expressed genes (DEGs) of peripheral VSMCs in patients with critical limb ischemia (CLI) results from peripheral arterial disease and Chronic Kidney disease (CKD). - Source: PubMed
Publication date: 2025/10/22
Lee DongohKim Ji HyeLee Dong Yeon