InVivoMAb polyclonal mouse IgG
Product Description
Specifications
| Isotype | Mouse IgG |
|---|---|
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤1EU/mg (≤0.001EU/μg) Determined by LAL assay |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from mouse serum |
| Purification | Protein G |
| RRID | AB_1107789 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Liao, Y., et al (2020). "Inflammation mobilizes copper metabolism to promote colon tumorigenesis via an IL-17-STEAP4-XIAP axis" Nat Commun 11(1): 900.
PubMed
Copper levels are known to be elevated in inflamed and malignant tissues. But the mechanism underlying this selective enrichment has been elusive. In this study, we report a axis by which inflammatory cytokines, such as IL-17, drive cellular copper uptake via the induction of a metalloreductase, STEAP4. IL-17-induced elevated intracellular copper level leads to the activation of an E3-ligase, XIAP, which potentiates IL-17-induced NFκB activation and suppresses the caspase 3 activity. Importantly, this IL-17-induced STEAP4-dependent cellular copper uptake is critical for colon tumor formation in a murine model of colitis-associated tumorigenesis and STEAP4 expression correlates with IL-17 level and XIAP activation in human colon cancer. In summary, this study reveals a IL-17-STEAP4-XIAP axis through which the inflammatory response induces copper uptake, promoting colon tumorigenesis.
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Mostafa, H. H., et al (2016). "Non-invasive Imaging of Sendai Virus Infection in Pharmacologically Immunocompromised Mice: NK and T Cells, but not Neutrophils, Promote Viral Clearance after Therapy with Cyclophosphamide and Dexamethasone" PLoS Pathog
PubMed
In immunocompromised patients, parainfluenza virus (PIV) infections have an increased potential to spread to the lower respiratory tract (LRT), resulting in increased morbidity and mortality. Understanding the immunologic defects that facilitate viral spread to the LRT will help in developing better management protocols. In this study, we immunosuppressed mice with dexamethasone and/or cyclophosphamide then monitored the spread of viral infection into the LRT by using a noninvasive bioluminescence imaging system and a reporter Sendai virus (murine PIV type 1). Our results show that immunosuppression led to delayed viral clearance and increased viral loads in the lungs. After cessation of cyclophosphamide treatment, viral clearance occurred before the generation of Sendai-specific antibody responses and coincided with rebounds in neutrophils, T lymphocytes, and natural killer (NK) cells. Neutrophil suppression using anti-Ly6G antibody had no effect on infection clearance, NK-cell suppression using anti-NK antibody delayed clearance, and T-cell suppression using anti-CD3 antibody resulted in no clearance (chronic infection). Therapeutic use of hematopoietic growth factors G-CSF and GM-CSF had no effect on clearance of infection. In contrast, treatment with Sendai virus-specific polysera or a monoclonal antibody limited viral spread into the lungs and accelerated clearance. Overall, noninvasive bioluminescence was shown to be a useful tool to study respiratory viral progression, revealing roles for NK and T cells, but not neutrophils, in Sendai virus clearance after treatment with dexamethasone and cyclophosphamide. Virus-specific antibodies appear to have therapeutic potential.
Product Citations
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Regulatory B cells contribute to allergen-encapsulating nanoparticle immunotherapy efficacy for food allergy.
In JCI Insight on 10 August 2026 by Rad, L. M., Saunders, M. N., et al.
PubMed
B cells contribute to the pathogenesis of food allergies as they induce allergen-specific antibody production. Clinically used allergen-specific immunotherapies have been shown to induce regulatory B cell subsets as well as target and reduce allergy-driving B cell functions. This report aims to elucidate the contribution of regulatory B cells to an allergen-encapsulating nanoparticle (aeNP) immunotherapy in a murine model of food allergy. In this model, B cells directly associated with aeNPs. CD20+ B cell depletion after aeNP treatment increased the number of mice with severe allergic reactions during oral food challenges and reduced the expansion of regulatory immune cells including CD103+ DCs and CCR9+ gut-homing Tregs, indicating that B cells are a component of aeNP immunomodulation. B cell communication in the gastrointestinal tract of aeNP-treated mice identified CD23 signaling as a potential inducer of regulatory CD103+ DC functions and disrupter of allergy-driving B cell-T cell communication. These tolerogenic signaling patterns were also identified in IL-10+ B cells, which are known to impart regulatory immune effects in both murine and human disease. Ultimately, B cells are a component of the complex immunomodulation leading to aeNP efficacy at reducing allergic reactivity.
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IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.
In Nat Commun on 17 June 2026 by Panagioti, E., Kelley, H. J., et al.
PubMed
Oncolytic virotherapy represents a promising yet under-explored approach for precision cancer treatment, particularly when tailored to tumor-specific molecular profiles. Patients with high-grade isocitrate dehydrogenase (IDH) mutant astrocytomas have limited treatment options and poor prognoses. Here, we investigate the therapeutic efficacy of rQNestin34.5 v.2 (CAN-3110), an engineered oncolytic herpes simplex virus 1 (oHSV-1), in IDH1-R132H-mutant diffuse gliomas. We demonstrate that the IDH1-R132H mutation enhances glioma susceptibility to viral infection through upregulation of Nectin-1, the main HSV-1 entry receptor. Concurrently, IDH1-R132H-driven DNA hypermethylation suppresses interferon (IFN) signaling, creating a permissive microenvironment that facilitates viral replication and tumor cell apoptosis. In immunocompetent murine glioma models, intratumoral administration of rQNestin34.5 v.2 induces robust antitumor immune activation, including increased immune infiltration and systemic IFN-γ release. However, elevated expression of poliovirus receptor (PVR) and the immune checkpoint T-cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT) on tumor-infiltrating leukocytes suggests a potential resistance mechanism to virotherapy. Combining rQNestin34.5 v.2 with TIGIT blockade enhances therapeutic efficacy compared to monotherapy, identifying IDH1-R132H as a potential predictive biomarker for oncolytic virotherapy response.
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The protective role of TIGIT+ B cells in attenuating type 1 diabetes progression.
In Diabetes Obes Metab on 1 December 2025 by Peng, Y., Li, J., et al.
PubMed
Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing pancreatic β-cells. While T cells are well-known critical, growing evidence shows that B cells also play a key role in T1D development. T cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT), as an inhibitory immune checkpoint, is important in maintaining immune homeostasis and has become a therapeutic target for several autoimmune diseases. Our recent study identified a protective role of TIGIT+ regulatory T cells (Tregs) in T1D. However, the involvement of TIGIT+ B cells in T1D progression remains unclear.
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USP52 inhibits cell ferroptosis via Hippo-YAP pathway and blocks immunotherapy in colorectal cancer.
In J Biol Chem on 1 November 2025 by Zhou, J., Nie, H., et al.
PubMed
Colorectal cancer (CRC) is one of the most prevalent malignancies in humans. Understanding its molecular mechanisms to guide clinical management is crucial. Ferroptosis represents a novel form of regulated cell death that is characterized by highly iron-dependent lipid peroxidation. Despite growing interest, the roles and vulnerabilities determining ferroptosis sensitivity in CRC remain unclear. In this study, we identified ubiquitin-specific peptidase 52 (USP52) as a specific deubiquitinating enzyme of Yes-associated protein (YAP) in CRC, which could stabilize YAP by removing the K11-linked ubiquitin chains. USP52 knockdown decreased the expression of YAP protein and its target gene (CTGF, CYR61). Through a series of comprehensive in vivo and in vitro experiments, we proved that USP52 promoted CRC cell proliferation, migration, and invasion and attenuated the sensitivity of CRC cells to ferroptosis. Notably, USP52 inhibition retarded tumor growth and enhanced CD8+ T-cell infiltration, which potentiated tumor response to anti-programmed death-ligand-1 immunotherapy in vivo. In general, our research uncovered that USP52 suppressed ferroptosis through the Hippo-YAP signaling and highlighted targeting USP52 as a potential therapeutic strategy to boost ferroptosis for enhancing cancer immunotherapy.