C1QC Antibody (OASA09135)
- Known as:
- C1QC Antibody (OASA09135)
- Catalog number:
- oasa09135
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- C1QC Antibody (OASA09135)
Related genes to: C1QC Antibody (OASA09135)
- Gene:
- C1QC NIH gene
- Name:
- complement C1q C chain
- Previous symbol:
- C1QG
- Synonyms:
- -
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2019-04-23
Related products to: C1QC Antibody (OASA09135)
Related articles to: C1QC Antibody (OASA09135)
- Metastatic breast cancer remains incurable, underscoring the need for novel therapeutic strategies. Epidemiological and preclinical evidence suggests statins suppress metastatic outgrowth, however the underlying mechanisms remain unclear. We employed high-resolution spatial transcriptomics (ST) to explore the cellular composition and differentially expressed genes (DEGs) in the metastatic microenvironment following atorvastatin treatment. Formalin-fixed, paraffin-embedded breast cancer liver metastases from control and atorvastatin-treated mice were analyzed by Nanostring CosMx Spatial Molecular Imager (SMI)/Bruker using a 973-gene panel, profiling 212 and 207 tumor-adjacent field of views (FOVs) (TAFs) respectively, which identified eight cell clusters, while non-tumor FOVs (NTFs) were sparse. Preferential depletion of LRRC15⁺ myofibroblastic cancer associated fibroblasts (CAFs), CXCL8⁺ inflammatory CAFs, and C1QC⁺/SPP1⁺ tumor associated macrophages (TAMs) subsets were revealed by harmony-assisted cell annotation and Seurat label transfer, which further separated CAFs and TAMs into discrete functional subpopulations. Immunohistochemistry (IHC) was also performed to validate cell types in both the tissues. Wilcoxon-based DEG analysis identified metastasis-associated gene expression changes between groups. Atorvastatin treatment reduced CAFs, Hepatic stellate cells (HSCs) (significantly), and macrophages (trending) in TAFs, with no changes in NTFs. These findings were supported by IHC (n = 4), which confirmed prominent reductions in these cell types while hepatocyte and endothelial markers remained unchanged. DEG analysis revealed coordinated downregulation of metastasis and extracellular matrix- associated transcripts in atorvastatin-treated TAFs. Our findings suggest that atorvastatin alters the cellular milieu in the disseminated microenvironment towards one in which pro-tumorigenic CAF and HSC populations are reduced, to create a microenvironmental niche favorable for maintaining metastatic dormancy and preventing relapse. - Source: PubMed
Publication date: 2026/09/12
Atale NehaChen JieIsett Brian RBao RiyueMeyer Ernest MWells Alan - Kikuchi-Fujimoto disease (KFD) is a rare disorder involving necrotizing lymphadenitis which was first described in Japan. The presentations include lymphadenopathy, fever, and leukopenia of unknown cause. - Source: PubMed
Publication date: 2026/09/06
Tan Cheryl WeiqiRaveentheran GayatiriRafi'ee KhadijahDas LenaKoh Mark Jean-AanTan Ene-Choo - Still disease (SD) is an autoinflammatory syndrome characterized by innate immune dysregulation. While complement can drive inflammation, its involvement in SD remains to be defined. Thus, we aimed to assess complement activation in SD. - Source: PubMed
Publication date: 2026/08/25
Huijsmans Freya M C HThalheim TabeaBodelón AlejandraRogani GretaSijbers Lyanne J P MErkens Remco G Ade Ligt AafkeScholman RianneBrinker AronBeretta Gisella BTer Haar Nienke MVogl ThomasRoth JohannesDuong Trang Tde Roock SytzeSwart Joost FMarshall Deborah ABenseler Susanne MYeung Rae S MKessel ChristophVastert Sebastiaan JVerweyen Emely Lvan Loosdregt Jorg - Bovine trypanosomiasis, caused by Trypanosoma vivax, presents a major threat to livestock health, primarily due to the lack of efficient field diagnostic tools. This study aimed to identify potential parasite and host-derived biomarkers through a longitudinal proteomic analysis of serum from sheep experimentally infected with a T. vivax isolate. Utilizing LC-MS/MS and bioinformatics, 154 proteins were identified, comprising 150 host (Ovis aries) and four pathogen proteins. Principal Component Analysis (PCA) demonstrated a clear separation of samples according to infection stages: Control, Infection (15 parasites/field), and Peak Infection (30-60 parasites/field) Among the parasite proteins, TvY486_0014340, TvY486_0040500, and TvY486_0042480 were identified as candidate antigens for future evaluation. In silico analysis revealed these proteins contain multiple B-cell epitopes with no cross-reactivity to related Trypanosoma species, supporting their potential for immunodiagnostic development. Additionally, three host proteins-folate receptor 3 (FOLR3) and complement components C1QA and C1QC-were significantly modulated across all infection phases. The upregulation of FOLR3 likely reflects a compensatory response to parasite-induced anemia, while the downregulation of C1Q components suggests immune evasion strategies. These findings highlight specific parasite antigens and host regulatory patterns that may serve as candidate biomarkers for the diagnosis and monitoring of T. vivax infection, facilitating the development of improved point-of-care assays. - Source: PubMed
Publication date: 2026/08/22
Marques JúliaBassi das Neves GabriellaScheffer Eduarda KarolyneRibeiro Brenda GuedesMaso Erika SensoloBorges Gabriela KaiserFranco Cintia de SouzaRussi Bruna CarolineMoreira Renato SimõesMiletti Luiz Claudio - Multiple myeloma (MM) persists within a specialized bone marrow niche in which malignant plasma cells, immune dysfunction, inflammatory signaling, and metabolic stress reinforce one another. To resolve this ecosystem at compartment-level resolution, we integrated public single-cell RNA sequencing data with pathway scoring, cell-cell communication inference, independent clinical validation, multiplex immunofluorescence, and metabolic perturbation experiments. Analysis of 95,940 bone marrow cells identified 32 annotated populations and revealed broad microenvironmental remodeling in MM, including plasma-cell expansion, altered cytotoxic and dendritic-cell compartments, TAM-associated inflammatory programs, and lineage-specific hematopoietic perturbations. Hallmark pathway analysis identified recurrent immunometabolic programs, including IL6-JAK-STAT3, TNFα-NFκB, mTORC1 signaling, oxidative phosphorylation, unfolded protein response, hypoxia, and checkpoint/exhaustion-associated pathways. CellChat analysis showed disease-associated rewiring of ligand-receptor networks involving malignant plasma cells, TAMs, dendritic cells, and T/NK subsets, with checkpoint-enriched communication and clinically relevant plasma-cell and CD274 survival associations. Serum IL-6 was elevated in an independent clinical validation cohort. Multiplex immunofluorescence confirmed PD-L1-positive plasma cells, C1QA/C1QB/C1QC-positive TAMs expressing LAG3, and CD8-positive/LAG3-positive cytotoxic T cells. Mechanistically, malignant plasma cells showed transcriptional activation of LDH-associated glycolytic/lactate programs and ASCT2/SLC1A5-GLS-linked glutamine-metabolic programs, nominating these pathways as functional vulnerabilities. Accordingly, the LDH inhibitor galloflavin and the ASCT2/SLC1A5 glutamine-transport inhibitor V-9302 suppressed RPMI-8226 viability in dose- and time-dependent manners; their combination produced synergistic anti-myeloma activity supported by Bliss synergy, combination-index analysis, observed-versus-expected inhibition, and apoptosis-related validation. Together, these findings support an IL6-centered immunometabolic communication circuit linking malignant plasma cells, TAMs, and dysfunctional T cells, and identify cooperative glycolytic/lactate and glutamine-dependent metabolic vulnerabilities with therapeutic relevance in MM. - Source: PubMed
Publication date: 2026/07/27
Lang DelongWu JingZhang JiayouFeng Yuhu