ImmunoCult?-SF Macrophage Medium
Serum-free medium for differentiation of human monocytes to macrophages
Request Pricing
Thank you for your interest in this product. Please provide us with your contact information and your local representative will contact you with a customized quote. Where appropriate, they can also assist you with a(n):
Estimated delivery time for your area
Product sample or exclusive offer
In-lab demonstration
By submitting this form, you are providing your consent to 海角破解版 Technologies Canada Inc. and its subsidiaries and affiliates (“海角破解版”) to collect and use your information, and send you newsletters and emails in accordance with our privacy policy. Please contact us with any questions that you may have. You can unsubscribe or change your email preferences at any time.
This site is protected by reCAPTCHA and the ?and??apply.
This site is protected by reCAPTCHA and the ?and??apply.
Overview
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (12)
Publications (6)
Lipoprotein(a)/CD36 Interaction Drives IL-6/RhoA-GTP Signaling and miRNA Epigenetic Regulation in Coronary Artery Spasm
Pharmaceuticals 2025 Sep
Abstract
Background: Lipoprotein(a) [Lp(a)]-induced inflammation contributes to coronary artery spasm (CAS) by the contraction of vascular smooth muscle cells. However, the interaction between Lp(a) and soluble CD36 (sCD36)/interleukin (IL)-6/RAS Homolog Family Member A (RhoA)-GTP signaling pathway has not been evaluated. Methods: We investigated the relevance of Lp(a)/CD36 signaling in CAS patient monocyte-derived macrophages (PMDMs) and a human coronary artery smooth muscle cell (HCASMC) line using expression profile correlation analyses, molecular docking, RNA sequencing, flow cytometry, immunoblotting, and quantitative reverse transcription polymerase chain reaction. Results: Plasma Lp(a) and sCD36 levels in 41 CAS patients were significantly higher ( p = 0.001) and positively correlated (r 2 = 0.3145, p < 0.001), a trend not observed in 36 non-CAS controls. RNA sequencing indicated a significant co-overexpression of CD36 and RhoA in Lp(a)-treated CAS PMDMs and HCASMCs, of which the mRNA and protein expression of CD36 and RhoA were significantly enhanced ( p < 0.001) dose-dependently. Lp(a) rather than LDL preferentially induced CD80+ PMDM (M1) polarization. In HCASMCs, the CD36 knockdown using either short hairpin RNA or natural biflavonoid amentoflavone suppressed Lp(a)-upregulated protein expression of CD36, RhoA-GTP, IL-6, tumor necrosis factor (TNF)-α, nuclear factor (NF)-κB, and CD80; however, overexpressed CD36 increased their levels. Lp(a) decreased and amentoflavone increased the epigenetic expression of CD36 inhibitors, miR-335-5p, and miR-448, respectively. Reciprocally, an miRNA inhibitor or mimic could magnify or diminish Lp(a)-induced CD36, TNF-α, NF-κB and IL-6 expressions in HCASMCs, respectively. Conclusions: Elevated Lp(a) levels upregulate the CD36-dependent TNF-α/NF-κB/IL-6/RhoA-GTP signaling pathway in CAS PMDMs and HCASMCs, indicating that Lp(a)/CD36 inflammatory signaling, HCASMC activation, and macrophage M1 polarization mediate CAS development.
Targeting CD37 promotes macrophage-dependent phagocytosis of multiple cancer cell types and facilitates tumor clearance in mice
Nature Communications 2025 Jul
Abstract
Macrophages play vital roles in innate and adaptive immunity, and their functions are mediated via phagocytosis and antigen presentation. Despite the effort to identify phagocytic checkpoints and explore their mechanism of action, current checkpoint-scanning strategies cannot provide a complete and systematic list of such immune checkpoints. Here, we perform in vitro phagocytosis assays using primary healthy donor macrophages co-cultured with breast cancer cells followed by ribosome profiling of sorted macrophages, to identify immune system-specific checkpoints. We observe a downregulation of CD37 in phagocytic macrophages and demonstrate that targeting CD37 with a specific antibody promotes the phagocytosis of multiple cancer cells in vitro. Mechanistically, tumorous macrophage migration inhibitory factor (MIF) directly binds to CD37, promoting the phosphorylation of CD37Y13 and activating a transduction cascade that involves the recruitment of SHP1 and inhibition of AKT signaling, ultimately impairing phagocytosis. In vivo, targeting CD37 promotes tumor clearance in multiple preclinical mouse models and synergizes with anti-CD47 therapy. Thus, our study identifies a previously unidentified phagocytic checkpoint and provides new potential for precise therapy. Cancer cells evade the immune system by disrupting phagocytic clearance. Here, the authors identify CD37 as a potential checkpoint molecule expressed on non-phagocytes and propose that binding to tumor-derived MIF reduces the phagocytic ability via inhibiting the AKT pathway. In preclinical mouse models, anti-CD37-based therapy enhances phagocytosis by macrophages, facilitating tumor clearance.
Interaction of chikungunya virus glycoproteins with macrophage factors controls virion production
The EMBO Journal 2024 Sep
Abstract
Despite their role as innate sentinels, macrophages can serve as cellular reservoirs of chikungunya virus (CHIKV), a highly-pathogenic arthropod-borne alphavirus that has caused large outbreaks among human populations. Here, with the use of viral chimeras and evolutionary selection analysis, we define CHIKV glycoproteins E1 and E2 as critical for virion production in THP-1 derived human macrophages. Through proteomic analysis and functional validation, we further identify signal peptidase complex subunit 3 (SPCS3) and eukaryotic translation initiation factor 3?subunit K (eIF3k) as E1-binding host proteins with anti-CHIKV activities. We find that E1 residue V220, which has undergone positive selection, is indispensable for CHIKV production in macrophages, as its mutation attenuates E1 interaction with the host restriction factors SPCS3 and eIF3k. Finally, we show that the antiviral activity of eIF3k is translation-independent, and that CHIKV infection promotes eIF3k translocation from the nucleus to the cytoplasm, where it associates with SPCS3. These functions of CHIKV glycoproteins late in the viral life cycle provide a new example of an intracellular evolutionary arms race with host restriction factors, as well as potential targets for therapeutic intervention.
Related Products
Related Products
Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
