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 |
| Murine Pathogen Tests |
Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theiler’s Murine Encephalomyelitis: Negative |
| 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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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.
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CBD promotes antitumor activity by modulating tumor immune microenvironment in HPV associated head and neck squamous cell carcinoma.
In Front Immunol on 6 June 2025 by Sen, P., Sadat, S., et al.
PubMed
Marijuana use is associated with HPV-positive head and neck squamous cell carcinoma (HNSCC). However, cannabinoid use continues to increase in the US general population for recreational purposes as well as in cancer patients for palliative care. In this study, we explored the role of cannabidiol (CBD) in promoting anti-tumor activity by modulating immune response in HPV-positive HNSCC by using pre-clinical models.
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LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.
In Theranostics on 14 April 2025 by Lim, S. T., Zhao, X., et al.
PubMed
Rationale: Acute pancreatitis (AP) is a common gastrointestinal disease affecting nearly 3 million people annually worldwide. Although AP is typically self-limiting, up to 20% of patients may develop life-threatening complications. Individuals who suffer from AP also have an increased likelihood of developing other exocrine and endocrine pancreatic disorders. However, to date, there are no specific, targeted treatment modalities that can effectively improve the clinical outcomes of AP. Leucine-rich alpha-2 glycoprotein 1 (LRG1) is a multifunctional protein with established roles in inflammation and cell mitosis. This study aims to investigate the functional role of LRG1 in AP progression and develop LRG1-targeted AP therapeutics. Methods: Levels of circulating and tissue LRG1 were determined in human patient samples and mouse models of caerulein-induced AP and pancreatic duct ligation-induced AP. Histopathological grading, amylase assay, real-time polymerase chain reaction analysis and Western blotting were used to evaluate the extent of pancreatic damage and recovery following caerulein-induced AP in both wild-type and Lrg1-/- mice. Primary acinar cells were also isolated from mice for in-vitro mechanistic studies. LRG1 neutralizing antibody was administered post-AP induction to evaluate its therapeutic potential in improving AP outcomes. Results: LRG1 is markedly increased in serum and acinar cells of AP patients and C57BL/6 mice subjected to caerulein-induced AP or pancreatic duct ligation-induced AP. Despite demonstrating no obvious pancreatic dysfunction, Lrg1-/- mice exhibited more severe pancreatic damage and inflammation during the early stages of caerulein-induced AP. However, the resolution of AP was accelerated in the absence of Lrg1, which is at least partially due to LRG1's role in regulating the expression of trophic cholecystokinin (CCK) Type 1 receptor (CCK1R) via the TGFβ/ALK5/AKT pathway in acinar cells. Importantly, the administration of an LRG1-blocking antibody promoted AP recovery, evidenced by reduced overall inflammation and increased acinar cell proliferation. Conclusions: Our data provide compelling evidence for targeting LRG1 as a potential innovative therapy for promoting AP recovery.