InVivoPlus polyclonal Armenian hamster IgG
Product Description
Specifications
| Isotype | Armenian hamster 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* |
≤0.5EU/mg (≤0.0005EU/μg) Determined by LAL assay |
| Aggregation* |
<5% Determined by DLS |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from Armenian hamster serum |
| Purification | Protein G |
| RRID | AB_1107773 |
| 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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Khmaladze, I., et al (2014). "Mannan induces ROS-regulated, IL-17A-dependent psoriasis arthritis-like disease in mice" Proc Natl Acad Sci U S A 111(35): E3669-3678.
PubMed
Psoriasis (Ps) and psoriasis arthritis (PsA) are poorly understood common diseases, induced by unknown environmental factors, affecting skin and articular joints. A single i.p. exposure to mannan from Saccharomyces cerevisiae induced an acute inflammation in inbred mouse strains resembling human Ps and PsA-like disease, whereas multiple injections induced a relapsing disease. Exacerbation of disease severity was observed in mice deficient for generation of reactive oxygen species (ROS). Interestingly, restoration of ROS production, specifically in macrophages, ameliorated both skin and joint disease. Neutralization of IL-17A, mainly produced by gammadelta T cells, completely blocked disease symptoms. Furthermore, mice depleted of granulocytes were resistant to disease development. In contrast, certain acute inflammatory mediators (C5, Fcgamma receptor III, mast cells, and histamine) and adaptive immune players (alphabeta T and B cells) were redundant in disease induction. Hence, we propose that mannan-induced activation of macrophages leads to TNF-alpha secretion and stimulation of local gammadelta T cells secreting IL-17A. The combined action of activated macrophages and IL-17A produced in situ drives neutrophil infiltration in the epidermis and dermis of the skin, leading to disease manifestations. Thus, our finding suggests a new mechanism triggered by exposure to exogenous microbial components, such as mannan, that can induce and exacerbate Ps and PsA.
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Awe, O., et al (2015). "PU.1 Expression in T Follicular Helper Cells Limits CD40L-Dependent Germinal Center B Cell Development" J Immunol .
PubMed
PU.1 is an ETS family transcription factor that is important for the development of multiple hematopoietic cell lineages. Previous work demonstrated a critical role for PU.1 in promoting Th9 development and in limiting Th2 cytokine production. Whether PU.1 has functions in other Th lineages is not clear. In this study, we examined the effects of ectopic expression of PU.1 in CD4+ T cells and observed decreased expression of genes involved with the function of T follicular helper (Tfh) cells, including Il21 and Tnfsf5 (encoding CD40L). T cells from conditional mutant mice that lack expression of PU.1 in T cells (Sfpi1lck-/-) demonstrated increased production of CD40L and IL-21 in vitro. Following adjuvant-dependent or adjuvant-independent immunization, we observed that Sfpi1lck-/- mice had increased numbers of Tfh cells, increased germinal center B cells (GCB cells), and increased Ab production in vivo. This correlated with increased expression of IL-21 and CD40L in Tfh cells from Sfpi1lck-/- mice compared with control mice. Finally, although blockade of IL-21 did not affect GCB cells in Sfpi1lck-/- mice, anti-CD40L treatment of immunized Sfpi1lck-/- mice decreased GCB cell numbers and Ag-specific Ig concentrations. Together, these data indicate an inhibitory role for PU.1 in the function of Tfh cells, germinal centers, and Tfh-dependent humoral immunity.
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Ballesteros-Tato, A., et al (2014). "Epitope-specific regulation of memory programming by differential duration of antigen presentation to influenza-specific CD8(+) T cells" Immunity 41(1): 127-140.
PubMed
Memory CD8(+) T cells are programmed during the primary response for robust secondary responsiveness. Here we show that CD8(+) T cells responding to different epitopes of influenza virus received qualitatively different signals during the primary response that altered their secondary responsiveness. Nucleoprotein (NP)-specific CD8(+) T cells encountered antigen on CD40-licensed, CD70-expressing, CD103(-)CD11b(hi) dendritic cells (DCs) at later times in the primary response. As a consequence, they maintained CD25 expression and responded to interleukin-2 (IL-2) and CD27, which together programmed their robust secondary proliferative capacity and interferon-gamma (IFN-gamma)-producing ability. In contrast, polymerase (PA)-specific CD8(+) T cells did not encounter antigen-bearing, CD40-activated DCs at later times in the primary response, did not receive CD27 and CD25 signals, and were not programmed to become memory CD8(+) T cells with strong proliferative and cytokine-producing ability. As a result, CD8(+) T cells responding to abundant antigens, like NP, dominated the secondary response.
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Imai, Y., et al (2015). "Cutting Edge: PD-1 Regulates Imiquimod-Induced Psoriasiform Dermatitis through Inhibition of IL-17A Expression by Innate gammadelta-Low T Cells" J Immunol 195(2): 421-425.
PubMed
Programmed cell death 1 (PD-1) is a key regulatory molecule that has been targeted in human cancers, including melanoma. In clinical testing, Abs against PD-1 have resulted in psoriasiform dermatitis (PsD). To determine whether PD-1 regulates PsD, we compared skin responses of PD-1-deficient (PD-1KO) mice and wild-type (WT) controls in an imiquimod (IMQ)-induced murine model of psoriasis. PD-1KO mice showed severe epidermal hyperplasia, greater neutrophilic infiltration, and higher expression of Th17 cytokines (versus WT mice). IMQ exposure increased PD-1 expression by skin gammadelta-low (GDL) T cells and enhanced expression of PD-L1 by keratinocytes. Three-fold increases in the percentage of IL-17A(+) GDL T cells were observed in skin cell suspensions derived from IMQ-treated PD-1KO mice (versus WT controls), suggesting that the lack of PD-1 has a functional effect not only on alphabeta T cells, but also on GDL T cells, and that PD-1 may play a regulatory role in PsD.
Product Citations
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Ionic regulation of cancer cell stiffness and metastatic colonization via the MRTFA-KCNMB1 axis.
In Dev Cell on 10 June 2026 by Gajda, A. M., Haloul, M., et al.
PubMed
Cellular stiffness impacts multiple steps of cancer metastasis, but mechanisms that regulate the stiffness of cancer cells remain poorly understood. Here, we identified potassium efflux and potassium calcium-activated channel subfamily M regulatory beta subunit 1 (KCNMB1), an auxiliary subunit of the large conductance calcium-activated potassium (BK) channels, as regulators of cellular stiffness downstream of myocardin-related transcription factor A (MRTFA). In primary pericytes, KCNMB1 knockdown increased cellular stiffness, which is consistent with the role of potassium efflux in promoting relaxation during excitation-contraction coupling. In a striking contrast, however, KCNMB1 knockdown decreased cancer cells' stiffness. Softer cancer cells were resistant to natural killer (NK) cell mediated cytotoxicity and the low KCNMB1 expression was associated with reduced survival in breast cancer patients. Importantly, pharmacological activation of BK channels reduced metastatic burden in mice and improved lysis of cancer cells by cytotoxic T lymphocytes. These results highlight the ionic regulation of stiffness in cancer cells and point to BK channel agonism as a therapeutic approach.
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Xiaoyao San alleviates emotional distress - induced TNBC growth through augmenting intratumoral CD8+T cell infiltration mediated by Rela/NF-kB-Cxcl9 axis.
In Front Immunol on 23 February 2026 by Liang, Y., Wu, Y., et al.
PubMed
Emotional distress (ED) is closely associated with the progression of triple-negative breast cancer (TNBC). Xiaoyao San (XYS), a classical Chinese herbal prescription traditionally used for mood regulation, has demonstrated potential therapeutic efficacy in emotion-related breast cancer. However, the molecular mechanisms through which XYS mitigates ED-induced TNBC (ED-TNBC) remain insufficiently characterized. This study aimed to investigate the therapeutic effects of XYS on ED-TNBC and elucidate its underlying molecular mechanisms.
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WNT pathway inhibition sensitizes HAT1-high lung cancers to treatment with PD-1 inhibitors.
In Cancer Cell Int on 24 October 2025 by Yang, T., Xie, Z., et al.
PubMed
BACKGROUND: Immunotherapies change the paradigm of current pulmonary oncological clinics, although majority of patients fail to benefit from these treatment modalities. HAT1 overexpression is frequently diagnosed in lung cancer patients. Effective immunotherapeutic scheme remains to be determined for this portion of patients. METHODS : In vitro experiments were used to verify the transcriptional regulation of PD-L1 by HAT1 in lung cancer cells. Mouse syngeneic lung tumors with sgHAT1 were treated with PD-1 antibodies to determine the impact of deficiency of HAT1 on the sensitivity of lung cancers to PD-1 inhibitors. RNA-seq and Chip-seq analyses revealed the effect of HAT1 on the WNT pathway. The impact of HAT1 on WNT signaling on stemness of lung cancer cells and their ability to escape immune surveillance were evaluated through a series of in vitro and in vivo experiments. Clinical relevance of expression level of HAT1 on prognosis of lung cancer patients were assessed using data from multiple public datasets. Carcinogenicity of HAT1 was evaluated using a transgenic mouse model in vivo. RESULTS: Silencing HAT1 expression downregulated PD-L1 expression in murine and human lung cancer cells. Notably, HAT1-knockout sensitized lung cancers to PD-1 antibody treatment. We found that HAT1 enhanced the stemness of lung cancer cells through enhancing expression of WNT ligands by direct binding of their promoter regions. WNT pathway inhibitor, ICG001, sensitized lung tumors to treatment with PD-1 antibody. HAT1 overexpression was highly frequent among lung cancer patients and was found transforming in vitro and tumorigenic in vivo. CONCLUSION: This study demonstrates that overexpression HAT1 plays a critical role in mediating immune evasion in lung cancer. Mechanistically, on one hand, HAT1 upregulate PD-L1 expression in lung cancer cells. On the other hand, HAT1 enhances stem-like properties of lung cancer cells by upregulating several WNT ligands. Consequently, combined inhibition of the WNT pathway and PD-1 signaling effectively shrinks HAT1-high lung cancers. These findings highlight the critical role of HAT1 overexpression in lung cancer development and shed light on potential precision medicine for this portion of lung cancer patients.
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Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury.
In Exp Neurol on 1 October 2025 by Celorrio, M., Shumilov, K., et al.
PubMed
The gut microbiota has emerged as a pivotal regulator of host inflammatory processes after traumatic brain injury (TBI). However, the mechanisms by which the gut microbiota communicates to the brain in TBI are still under investigation. We previously reported that gut microbiota depletion (GMD) using antibiotics after TBI resulted in increased microglial activation, reduced neurogenesis, and reduced T cell infiltration. In the present study, we have demonstrated that intestinal T cells contribute to the pool of cells infiltrating the brain after TBI. Depletion or genetic deletion of T cells before injury reversed GMD induced reductions in post-TBI neurogenesis. Short-chain fatty acid supplementation increased T regulatory and T helper 1 cell infiltration to the brain along with restoring neurogenesis and microglia activation after TBI with GMD. These data suggest that T cell subsets are essential cellular mediators by which the gut microbiota modulates TBI pathogenesis, a finding with important therapeutic implications.