重组抗小鼠PD-1(CD279)抗体 RMP1-14.1 | Syd Labs PA007162.r2a

重组抗小鼠PD-1(CD279)单克隆抗体

重组抗小鼠PD-1(CD279)抗体 RMP1-14.1 | Syd Labs PA007162.r2a

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体内实验级重组抗小鼠PD-1单克隆抗体,大鼠IgG2a Kappa(克隆号:RMP1-14.1,货号:PA007162.r2a)是用哺乳动物细胞生产的重组抗体,与大鼠抗小鼠PD-1抗体(克隆号:RMP1-14)有相同的可变区序列,可用于免疫组织化学(IHC),流式细胞术(FC),以及各种体外和体内功能分析,比如动物体内实验。Syd Labs PA007162.r2a不变区为大鼠IgG2a kappa (rIgG2a或r2a),可与重组大鼠IgG2a同型对照抗体配套使用。2025年6月促销活动:买抗小鼠PD-1重组抗体(克隆号RMP1-14)送配套同型对照抗体

货号 PA007162.r2a
产品名称重组抗小鼠PD-1(CD279)抗体 RMP1-14.1 | Syd Labs PA007162.r2a
英文名 In Vivo Grade Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Rat IgG2a Kappa
供货商名称 Syd Labs, Inc.
品牌名 悉得(Syd Labs)
别称 PA007162 抗小鼠PD 1抗体,抗小鼠pd-1单抗,小鼠PD-1单抗,小鼠CD279抗体,RMP1-14抗体
概述 重组抗小鼠PD-1(CD279)单克隆抗体的可变区序列是从大鼠抗小鼠PD-1单抗(克隆号:RMP1-14)中提取的。重组大鼠和嵌合小鼠版本的RMP1-14抗体也可用。
克隆号 RMP1-14.1,与大鼠抗小鼠PD1单克隆抗体(克隆号:RMP1-14)的可变区和不变区序列相同。
同种型 大鼠 IgG2a, kappa
应用 抗小鼠pd-1抗体用于免疫组织化学(IHC),流式细胞术(FC),以及各种体外和体内功能分析。
免疫源 原大鼠杂交瘤(克隆号:RMP1-14)是用小鼠pd -1转染的BHK细胞免疫大鼠产生的。
抗体形式 0.2 μM过滤溶液,1x PBS
内毒素 根据 LAL 方法,≤1 EU每1mg 蛋白质。提供特级体内实验级重组抗小鼠PD 1单克隆抗体,大鼠IgG2a Kappa(RMP1-14.1)(内毒素≤0.05 EU/mg)。
纯度 >95%(在还原条件下通过SDS-PAGE测定)
运输 体内实验级重组抗小鼠PD-1(CD279)单克隆抗体(克隆号RMP1-14.1),大鼠IgG2a Kappa用冰袋运输。收到后,请立即将其存放在下面建议的温度下。
稳定性与存储 抗小鼠PD-1单抗使用手动除霜冰箱并避免重复冻融循环。 如果保存在2 至 8°C,自收到之日起可保存1个月。 如果保存在-20 至 -70°C,自收到之日起可保存 12个月。
注意事项 PA007162.r2a Syd Labs 体内实验级重组抗小鼠PD-1单克隆抗体(克隆号RMP1-14.1),大鼠IgG2a Kappa的可变区序列是从大鼠抗小鼠PD-1单克隆抗体(克隆号:RMP1-14)中提取的。Syd Labs还提供重组大鼠和嵌合小鼠版本的重组RMP1-14抗体。
产品咨询 悉得(Syd Labs)在国内只通过代理商销售其产品,不做直销。终端用户咨询价格请联系悉得(Syd Labs)中国代理商
关于悉得(Syd Labs)产品如果有任何技术或其它问题,欢迎随时联系悉得(Syd Labs)国内市场推广合作伙伴:武汉多找找科技有限公司企业微信:duozhaozhao2024 联系电话:18162581039(龙经理)

描述

了解更多抗小鼠PD-1单克隆抗体(clone:RMP1-14)引用文献,请查看:抗小鼠PD-1单抗(克隆号RMP1-14)引用文献

抗小鼠PD-1抗体(RMP1-14)参考文献:

1. PD-L1/PD-1 checkpoint pathway regulates hippocampal neuronal excitability and learning and memory behavior
Junli Zhao,et al.Neuron. 2023.PMCID: PMC10529885
“Programmed death protein 1 (PD-1) and its ligand PD-L1 constitute an immune checkpoint pathway. We report that neuronal PD-1 signaling regulates learning/memory in health and disease. Mice lacking PD-1 (encoded by Pdcd1) exhibit enhanced long-term potentiation (LTP) and memory. Intraventricular administration of anti-mouse PD-1 monoclonal antibody (RMP1-14) potentiated learning and memory. Selective deletion of PD-1 in excitatory neurons (but not microglia) also enhanced LTP and memory. Traumatic brain injury (TBI) impairs learning and memory, which is rescued by Pdcd1 deletion or intraventricular PD-1 blockade. Conversely, re-expression of Pdcd1 in PD-1 deficient hippocampal neurons suppresses memory and LTP. Exogenous PD-L1 suppressed learning/memory in mice and the excitability of mouse and NHP hippocampal neurons through PD-1. Notably, neuronal activation suppressed PD-L1 secretion, and PD-L1/PD-1 signaling is distinctly regulated by learning and TBI. Thus, conditions that reduce PD-L1 levels or PD-1 signaling could promote memory in both physiological and pathological conditions.”
2. PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration
Wenji Piao,et al.Nat Commun. 2022.PMCID: PMC9023578
“Programmed death-1 (PD-1) and its ligand PD-L1 are checkpoint molecules which regulate immune responses. Little is known about their functions in T cell
migration and there are contradictory data about their roles in regulatory T cell (Treg) function. Here we show activated Tregs and CD4 effector T cells (Teffs) use PD-1/PD-L1 and CD80/PD-L1, respectively, to regulate transendothelial migration across lymphatic endothelial cells (LECs). Antibody blockade of Treg PD-1, Teff CD80 (the alternative ligand for PD-L1), or LEC PD-L1 impairs Treg or Teff migration in vitro and in vivo. PD-1/PD-L1 signals through PI3K/Akt and ERK to regulate zipper junctional VE-cadherin, and through NFκB-p65 to up-regulate VCAM-1 expression on LECs. CD80/PD-L1 signaling up-regulates VCAM-1 through ERK and NFκB-p65. PD-1 and CD80 blockade reduces tumor egress of PD-1high fragile Tregs and Teffs into draining lymph nodes, respectively, and promotes tumor regression. These data provide roles for PD-L1 in cell migration and immune regulation.”
3. Macrophages Impair TLR9 Agonist Antitumor Activity through Interacting with the Anti-PD-1 Antibody Fc Domain
Simone Camelliti,et al.Cancers (Basel) 2021.PMCID: PMC8391891
“Simple Summary: We evaluated the contribution of macrophages to the effect of combinatorial immunotherapeutic treatments based on TLR9 stimulation (with CpG-ODNs) and PD-1 blockade in an ovarian cancer preclinical model. We observed a strong reduction in the antitumor efficacy of a TLR9 agonist upon anti-PD-1 antibody administration. Specifically, we found that TLR9-stimulated macrophages, through interacting with the fragment crystallizable (Fc) domain of the anti-PD-1 antibody, acquire an immunoregulatory phenotype leading to dampening of CpG-ODN antitumor effect. Since the stimulation of macrophage TLRs can be achieved not only by synthetic agonists but also by molecules present in the tumor microenvironment, the data we are presenting may represent another possible mechanism of anti-PD-1 antibody therapy resistance. Indeed, it is possible that when delivered as a monotherapy, anti-PD-1 antibody Fc domain may interact with macrophages in which TLR signaling has already been triggered by endogenous ligands, mirroring the biological effects described in the present study. Abstract: Background. A combination of TLR9 agonists and an anti-PD-1 antibody has been reported to be effective in immunocompetent mice but the role of innate immunity has not yet been completely elucidated. Therefore, we investigated the contribution of the innate immune system to this combinatorial immunotherapeutic regimens using an immunodeficient mouse model in which the effector functions of innate immunity can clearly emerge without any interference from T lymphocytes. Methods. Athymic mice xenografted with IGROV-1 human ovarian cells, reported to be sensitive to TLR9 agonist therapy, were treated with cytosine–guanine (CpG)-oligodeoxynucleotides (ODNs), an anti-PD-1 antibody or their combination. Results. We found that PD-1 blockade dampened CpG-ODN antitumor activity. In vitro studies indicated that the interaction between the anti-PD-1 antibody fragment crystallizable (Fc) domain and macrophage Fc receptors caused these immune cells to acquire an immunoregulatory phenotype, contributing to a decrease in the efficacy of CpG-ODNs. Accordingly, in vivo macrophage depletion abrogated the detrimental effect exerted by the anti-PD-1 antibody. Conclusion. Our data suggest that if TLR signaling is active in macrophages, coadministration of an anti-PD-1 antibody can reprogram these immune cells towards a polarization state able to negatively affect the immune response and eventually promote tumor growth.”

Syd Labs抗小鼠PD-1重组抗体(克隆号RMP1-14.1)(货号:PA007162.r2a)推荐同型对照抗体:

重组大鼠IgG2a同型对照抗体,体内实验级(In vivo Grade Recombinant Rat IgG2a Isotype Control Antibody)

Syd Labs相关重组IgG同型对照抗体(Recombinant IgG Reference Antibodies):

重组小鼠IgG1同型对照抗体和突变体,体内实验级(In vivo Grade Recombinant Mouse IgG1 Isotype Control Antibody and Mutants)
重组小鼠IgG2a同型对照抗体和突变体,体内实验级(In vivo Grade Recombinant Mouse IgG2a Isotype Control Antibody and Mutants)
重组小鼠IgG2c同型对照抗体和突变体,体内实验级(In vivo Grade Recombinant Mouse IgG2c Isotype Control Antibody and Mutants)

Syd Labs提供以下抗小鼠PD 1抗体(anti-mouse PD 1 antibodies):

重组抗小鼠PD1单克隆抗体(克隆号29F.1A12.1),体内实验级(In vivo grade recombinant anti-mouse PD1 monoclonal antibodies (Clone 29F.1A12.1))
重组抗小鼠PD-1(CD279)单克隆抗体(克隆号RMP1-14.1),体内实验级(In vivo grade recombinant anti-mouse PD-1 monoclonal antibodies (Clone RMP1-14.1))
重组鼠化抗小鼠PD 1单克隆抗体,体内实验级(In Vivo Grade Recombinant Murinized Anti-mouse PD-1 Mouse Monoclonal Antibody (Clone RMP1-14.1) 

Syd Labs提供以下体内实验级重组抗小鼠PD-1单克隆抗体(克隆号RMP1-14.1)突变体:

体内实验级重组抗小鼠PD-1小鼠IgG2c-L234A L235A P329G (LALAPG) Kappa单克隆抗体(克隆号RMP1-14.1)
体内实验级重组抗小鼠PD-1小鼠IgG2a-L234A L235A P329G (LALAPG) Kappa单克隆抗体(克隆号RMP1-14.1)

请记住我们的产品信息: Syd Labs(货号:PA007162.r2a)重组抗小鼠PD-1单克隆抗体,大鼠IgG2a Kappa,体内实验级(克隆号RMP1-14.1): Syd Labs PA007162.r2a In Vivo Grade Recombinant Anti-mouse PD-1 Monoclonal Antibody (Clone RMP1-14.1), Rat IgG2a Kappa

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