Anti-Human GC1q R (C1QBP) [Clone 60.11] – Purifiedin vivoGOLD™ Functional Grade,Leinco,G234

Host

Mouse

Reactivity

Human

Application

FC,IHC,WB

Platform ID

BAB635291448

Leinco

Headquarters

410 Axminister Drive St. Louis, Missouri 63026

Contact

Tel: +1 (800) 538-1145,+1 (636) 230-9477
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Product Specifications
Scientific Background

Specifications

NameAnti-Human GC1q R (C1QBP) [Clone 60.11] – Purifiedin vivoGOLD™ Functional Grade
Cat. No.G234
HostMouse
ReactivityHuman
ApplicationFC,IHC,WB
Clone Number60.11
Concentration≥ 5.0 mg/ml
ImmunogenRecombinant human gC1qR (C1QBP) fusion protein
Purity≥95% monomer by analytical SEC ⋅ >95% by SDS Page
Endotoxin Level< 1.0 EU/mg as determined by the LAL method
Shipping2 – 8° C Wet Ice
FormulationThis monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
StorageFunctional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.

Scientific Background

The globular C1q Receptor (gC1qR), encoded by the C1QBP gene, is a highly acidic, doughnut-shaped homotrimer that serves as a central hub for complement activation and inflammatory signaling. While predominantly mitochondrial (where it regulates oxidative phosphorylation), surface-translocated gC1qR acts as a receptor for the globular heads of C1q, the recognition molecule of the classical complement pathway 1 . Beyond complement, gC1qR interacts with the kinin-kallikrein system (Factor XII, High-Molecular-Weight Kininogen) to drive the production of bradykinin, a potent vasoactive peptide that promotes vascular permeability and inflammation 4 . In the context of cancer, surface gC1qR facilitates tumor cell proliferation and migration by activating the PI3K/Akt and ERK signaling pathways. It also suppresses the oxidative burst in phagocytes, thereby aiding tumor immune evasion 3,5 . Clone 60.11 is a functional blocking antibody widely utilized to dissect these pathogenic axes. By binding specifically to the C1q-binding site, 60.11 prevents the interaction between gC1qR and C1q, effectively neutralizing downstream inflammatory signals 1 . In preclinical models of triple-negative breast cancer (TNBC), treatment with 60.11 significantly inhibited tumor growth and reduced angiogenesis (CD31+ vessel density) by blocking gC1qR-dependent mitogenic signaling 5 . Additionally, 60.11 has been shown to reduce tissue colonization by Staphylococcus aureus in models of infective endocarditis, as the bacteria exploit host gC1qR to adhere to endothelial cells 6 .

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