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Rat IgG2a Isotype Control Antibody(Clone: 12B9) | PA007143

Rat IgG2a Isotype Control Antibody PA007143 Ushelf

Rat IgG2a Isotype Control Antibody(Clone: 12B9) | PA007143

$150.00$800.00

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$150.00$800.00

Recombinant rat IgG2a kappa isotype control good for in vitro and in vivo studies. Low or no specific binding to mouse samples tested. Mouse variable regions and rat IgG2a kappa constant regions.

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Order Offline:
Phone: 1-617-401-8149
Fax: 1-617-606-5019
Email: message@sydlabs.com
Catalog No. PA007143
Product NameRat IgG2a Isotype Control Antibody(Clone: 12B9) | PA007143
Supplier Name Syd Labs, Inc.
Brand Name Syd Labs
Synonyms

Recombinant Rat IgG2a Isotype Control, Rat IgG2a Negative Control Antibody, rtIgG2a Isotype Control

Summary The in vivo grade recombinant rat IgG2a isotype control antibody (rtIgG2a isotype control) was produced in HEK 293 cells.
Clone 12B9.
Isotype rat IgG2a, kappa.
Applications an isotype-matched negative control for rat IgG2a kappa antibodies used in ELISA, Western Blot (WB), Flow Cytometry (Flow), Immunoprecipitation (IP), Immunohistochemistry (Paraffin) (IHC (P)), Immunohistochemistry (Frozen) (IHC (F)), and in vivo animal model research.
Immunogen N/A.
Form Of Antibody 0.2 μM filtered solution of 1x PBS.
Endotoxin Less than 1 EU/mg of protein as determined by LAL method.
Purity >95% by SDS-PAGE under reducing conditions.
Shipping The recombinant rtIgG2a isotype control is shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage Use a manual defrost freezer and avoid repeated freeze-thaw cycles. 1 month from date of receipt, 2 to 8°C as supplied. 3 months from date of receipt, -20°C to -70°C as supplied.
Order Offline Phone: 1-617-401-8149 Fax: 1-617-606-5022 Email: message@sydlabs.com Or leave a message with a formal purchase order (PO) Or credit card.

Description

PA007143: Recombinant Rat IgG2a Isotype Control Antibody(Clone: 12B9), In Vivo Grade

The in vivo grade recombinant rat IgG2a isotype control antibody (rtIgG2a isotype control) was produced in HEK 293 cells.

Rat IgG2a isotype control and mutants (natural and engineered rtIgG2a isotype controls) are useful for functional study using animal model among a number of in vitro and in vivo research applications including ELISA, Western Blot (WB), Flow Cytometry (Flow), Immunoprecipitation (IP), Immunohistochemistry (Paraffin) (IHC (P)), and Immunohistochemistry (Frozen) (IHC (F)). Rat IgG2a and IgG1 antibodies are more like mouse IgG1 than rat IgG2b antibodies. Most of rat antibodies are used to study mouse and human target proteins.

Please contact us to ask for a quote for the engineered rat IgG2a isotype control mutants, rtIgG2a isotype control and mutants with Avi-, His-, and Flag-tags, and biotinylated rtIgG2a isotype control and mutants. A variety of conjugates (such as dyes and fluorophores) with the rat IgG2a isotype control and Fc mutants are available.

References of Rat IgG2a Isotype Control Antibody:

1、LAG3+ Regulatory T Cells Restrain Interleukin-23-Producing CX3CR1+ Gut-Resident Macrophages during Group 3 Innate Lymphoid Cell-Driven Colitis.
Bauché, D., et al. Immunity. 2018 Aug 21;49(2):342-352.e5. doi: 10.1016/j.immuni.2018.07.007. PMID: 30097293.
“Rag2-/- mice were injected in i.p with 1mg of depleting anti-CSF1R mAb (BioXCell, clone AFS98) or isotype control (BioXCell, Rat IgG2a) 3 and 2 days prior anti-CD40 treatment and then 500ug of depleting antibody or control every 2 two days. …Instead we demonstrated that Treg cells directly limit CX3CR1+ macrophage function in a contact-dependent manner. …We found that LAG-3-Fc can suppress multiple inflammatory genes including Il1b, Il23a, Cd80, and Nrpl3 in an MHCII-dependent manner. …Although Ctla4 and Tim3 expression was also higher, these molecules were not required for Treg cell-mediated suppression of anti-CD40-driven colitis (data not shown). …In the colon lamina propria, ILC3 are clustered close to the base of the crypt, where stem cells reside.”

2、TIGIT predominantly regulates the immune response via regulatory T cells.
Kurtulus, S., et al. J Clin Invest. 2015 Nov 2;125(11):4053-62. doi: 10.1172/JCI81187. PMID: 26413872.
“In some experiments, mice were treated with 250 μg isotype (rat IgG2a) or anti–TIM-3 (clone RMT3-23; Bio X Cell) Abs on the days indicated in the legend for Figure 7. …Adoptive transfers. For adoptive transfer experiments, CD4+ (FOXP3+ and FOXP3–) and CD8+ T cells from either WT or Tigit–/– Foxp3-GFP–KI reporter mice were isolated by cell sorting using a BD FACSAria. …For the examination of TIGIT signaling, CD4+ FOXP3+ cells from naive Foxp3-GFP–KI mice were isolated by cell sorting and stimulated with plate-bound anti-CD3 (1 μg/ml) and anti-CD28 (2 μg/ml), together with either agonist anti-TIGIT (4D4, generated in-house, ref. 9) (50 μg/ml) or isotype control. …Importantly, our data do not exclude a direct role for TIGIT in promoting a dysfunctional phenotype in CD8+ T cells. …Our data add a dimension to our current understanding of how TIGIT modulates antitumor immunity by showing that the function of TIGIT in Tregs is dominant over its function in CD8+ T cells.”

3、TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.
Ellis, G. T., et al. EMBO Rep. 2015 Sep;16(9):1203-18. doi: 10.15252/embr.201540473. PMID: 26265006.
“Influenza A virus (IAV) is a major human respiratory pathogen 1, and deaths after influenza infections are frequently due to complications associated with secondary bacterial infections. …The majority of previous studies typically investigated two broad factors: direct viral‐mediated lung damage allowing increased bacterial colonization, or impairment of the antibacterial immune response. …Although a strong immune response is frequently observed, many studies have reported prior influenza impairs the antibacterial response. …However, for many functions in the immune response, it is still unclear whether they are impaired and whether they are protective or pathogenic during IAV–S. pneumoniae coinfection. …Inflammatory monocytes are among the most abundant cells to be recruited into coinfected lungs, but their role in coinfection has not been addressed.”

4、Curing mice with large tumors by locally delivering combinations of immunomodulatory antibodies.
Dai, M., et al. Clin Cancer Res. 2015 Mar 1;21(5):1127-38. doi: 10.1158/1078-0432.CCR-14-1339. PMID: 25142145.
“Immunomodulatory mAbs can treat cancer, but cures are rare except for small tumors. …Immunomodulatory mAbs have shown efficacy in both preclinical models and patients with cancer. …Regression was always associated with a strong Th1-type response in tumor, tumor-draining lymph nodes, and spleen and was accompanied by severe reduction of the number of CD19 cells in tumors and draining lymph nodes. …However, the role of immunologic responses to most human cancers was questioned for many years and therapeutic tumor vaccination has not been sufficiently effective to become part of the clinical mainstay. …Responses were consistently associated with a shift in the tumor microenvironment from the Th2 type to Th1 immunity with long-term memory T cells and expression of genes encoding IFNγ and TNFα, and therapy-resistant cells were not detected.”

5、A Threshold Level of Intratumor CD8+ T-cell PD1 Expression Dictates Therapeutic Response to Anti-PD1.
Ngiow, S. F., et al. Cancer Res. 2015 Sep 15;75(18):3800-11. doi: 10.1158/0008-5472.CAN-15-1082. PMID: 26208901.
“The authors thank Liam Town, Kate Elder, and Joanne Sutton for breeding, genotyping, and maintenance and care of the mice used in this study. …It is important to note that our findings may apply to tumors where significant T-cell infiltrates are present. …In concordance with the expression of CTLA-4 by Treg, we showed that Treg were induced in anti-PD1–treated MC38-bearing hosts. …We demonstrated that induction of intratumor Treg was, in part, a mechanism responsible for the development of anti-PD1–resistant tumors and PD1hi CD8+ T cells. …However, the role of Treg in regulating T-cell PD1 expression has not been examined.”

6、The E3 ubiquitin ligase Itch is required for the differentiation of follicular helper T cells.
Xiao, N., et al. Nat Immunol. 2014 Jul;15(7):657-66. doi: 10.1038/ni.2912. PMID: 24859451.
“Follicular helper T cells (TFH cells) are responsible for effective B cell–mediated immunity, and Bcl-6 is a central factor for the differentiation of TFH cells. …However, the molecular mechanisms that regulate the induction of TFH cells remain unclear. …Itch acted intrinsically in CD4+ T cells at early stages of TFH cell development. …Itch seemed to act upstream of Bcl-6 expression, as Bcl-6 expression was substantially impaired in Itch−/− cells, and the differentiation of Itch−/− T cells into TFH cells was restored by enforced expression of Bcl-6. …The defective TFH differentiation of Itch−/− T cells was rectified by deletion of Foxo1.”

7、Animal model of respiratory syncytial virus: CD8+ T cells cause a cytokine storm that is chemically tractable by sphingosine-1-phosphate 1 receptor agonist therapy.
Teijaro, J. R., et al. J Virol. 2014 Jun;88(11):6281-93. doi: 10.1128/JVI.00464-14. PMID: 24672024.
“Rat IgG2a (2A3; Bioxcell) was administered at equivalent concentrations for isotype control-treated mice within the cell depletion experiments. …Disruption of CD8+ T cells, which induced and maintained the cytokine storm, was chemically tractable, with oral S1P1R agonist therapy resulting in significant blunting of disease. …The tracheas of euthanized mice were exposed, transected, and intubated with a blunt 18-gauge needle. …Tissues were harvested and placed in PBS-buffered formalin. …Slides were analyzed by three separate pathologists, who were blinded to the various experimental treatments.”

8、Antimetastatic effects of blocking PD-1 and the adenosine A2A receptor.
Mittal, D., et al. Cancer Res. 2014 Jul 15;74(14):3652-8. doi: 10.1158/0008-5472.CAN-14-0957. PMID: 24986517.
“Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiologic immune responses in peripheral tissues to minimize collateral damage. …One promising molecule that is a new target in preclinical studies is immunosuppressive adenosine. …The protumor effects of CD73 are believed to be largely because of adenosine-mediated immunosuppression. …In this study, we investigated whether dual immune checkpoint blockade and A2AR inhibitor could increase the magnitude of immune responses to metastasis. …All experiments were approved by the QIMR Berghofer Medical Research Institute Animal Ethics Committee.”

9、Autoreactive Th1 cells activate monocytes to support regional Th17 responses in inflammatory arthritis.
Oh, S., et al. J Immunol. 2013 Apr 1;190(7):3134-41. doi: 10.4049/jimmunol.1203212. PMID: 23420889.
“We have examined mechanisms underlying the formation of pathologic Th17 cells using a transgenic mouse model in which autoreactive CD4+ T cells recognize influenza virus hemagglutinin (HA) as a ubiquitously expressed self-Ag and induce inflammatory arthritis. …The lymph nodes of arthritic mice contain elevated numbers of inflammatory monocytes (iMO) with an enhanced capacity to promote CD4+ Th17 cell differentiation, and a regional inflammatory response develops in the paw-draining lymph nodes by an IL-17–dependent mechanism. …The activation of these Th17-trophic iMO precedes arthritis development and occurs in the context of an autoreactive CD4+ Th1 cell response. Adoptive transfer of HA-specific CD4+ T cells into nonarthritic mice expressing HA as a self-Ag similarly led to the formation of Th1 cells and of iMO that could support Th17 cell formation, and, notably, the accumulation of these iMO in the lymph nodes was blocked by IFN-γ neutralization. …These studies show that autoreactive CD4+ Th1 cells directed to a systemically distributed self-Ag can promote the development of a regional Th17 cell inflammatory response by driving the recruitment of Th17-trophic iMO to the lymph nodes.”

10、Toll-like receptor 9 inhibition confers protection from liver ischemia-reperfusion injury.
Bamboat, Z. M., et al. Hepatology. 2010 Feb;51(2):621-32. doi: 10.1002/hep.23365. PMID: 19902481.
“Endogenous ligands such as high-mobility group box 1 (HMGB1) and nucleic acids are released by dying cells and bind Toll-like receptors (TLRs). …Mice were subjected to 1 hour of ischemia and 12 hours of reperfusion before assessment of liver injury, cytokines, and reactive oxygen species (ROS). …Liver damage was mediated by bone marrow–derived cells because WT mice transplanted with TLR9−/− bone marrow were protected from hepatic I/R injury. …Injury in WT mice partly depended on TLR9 signaling in neutrophils, which enhanced production of ROS, interleukin-6 (IL-6), and tumor necrosis factor (TNF).In vitro, DNA released from necrotic hepatocytes increased liver nonparenchymal cell (NPC) and neutrophil cytokine secretion through a TLR9-dependent mechanism. …Inhibition of both TLR9 and HMGB1 caused maximal inflammatory cytokine suppression in neutrophil cultures and conferred even greater protection from I/R injuryin vivo.”

For more references about Rat IgG2a Isotype Control Antibody please contact our scientific support team with message@sydlabs.com.

Other in vivo grade Recombinant IgG Isotype Control Antibodies and Mutants:
Recombinant Human IgG1 Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Human IgG2 Isotype Control Antibody, In vivo Grade
Recombinant Human IgG3 Isotype Control Antibody, In vivo Grade
Recombinant Human IgG4-S228P Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG1 Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2a Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2b Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2c Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG3 Isotype Control Antibody, In vivo Grade
Recombinant Rat IgG1 Isotype Control Antibody, In vivo Grade
Recombinant Rat IgG2a Isotype Control Antibody, In vivo Grade
Recombinant Rat IgG2b Isotype Control Antibody, In vivo Grade
Recombinant Rat IgG2c Isotype Control Antibody, In vivo Grade
Recombinant Hamster IgG1 Isotype Control Antibody, In vivo Grade
Recombinant Hamster IgG2 Isotype Control Antibody, In vivo Grade

In vivo Grade Recombinant IgG Fc Proteins:
Recombinant Human IgG1 Fc Protein (hIgG1), In vivo Grade
Recombinant Human IgG2 Fc Protein (hIgG2), In vivo Grade
Recombinant Human IgG4 Fc Protein (hIgG4), In vivo Grade
Recombinant Mouse IgG1 Fc Protein (mIgG1), In vivo Grade
Recombinant Mouse IgG2a Fc Protein (mIgG2a), In vivo Grade
Recombinant Mouse IgG2b Fc Protein (mIgG2b), In vivo Grade
Recombinant Rat IgG2a Fc Protein (rtIgG2a), In vivo Grade
Recombinant Rat IgG2b Fc Protein (rtIgG2b), In vivo Grade
Recombinant Llama IgG2b Fc Protein (lIgG2b), In vivo Grade
Recombinant Rabbit IgG Fc Protein (rIgG), In vivo Grade

Rat IgG2a Isotype Control(12B9) from: In Vivo Grade Recombinant Rat IgG2a Isotype Control Antibody: PA007143 Syd Labs

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