NFKBIB Monoclonal Antibody
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中文名称:NFKBIB鼠单克隆抗体
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货号:CSB-MA869384
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规格:¥1090
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图片:
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其他:
产品详情
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产品描述:CUSABIO货号:CSB-MA869384 NFKBIB单克隆抗体是针对核因子κB抑制蛋白β(IκBβ)研发的高特异性科研试剂,该靶点作为IκB家族关键成员,通过调控NF-κB信号通路在炎症反应、免疫应答及细胞增殖中发挥重要作用,是肿瘤发生与免疫性疾病机制研究的重要分子标记物。本产品采用杂交瘤技术制备,经严格验证可特异性识别人类、小鼠及大鼠种属的NFKBIB蛋白,适用于ELISA酶联免疫吸附实验与IHC免疫组织化学技术,为研究者提供稳定的抗原-抗体结合性能。在基础科研领域,该抗体可广泛应用于体外培养细胞中NF-κB信号通路的动态监测、炎症相关疾病模型的分子机制解析,以及肿瘤微环境中蛋白互作网络的实验研究。其卓越的种属兼容性使其成为跨物种比较研究的理想工具,特别适用于神经退行性疾病、自身免疫疾病及癌症生物学等领域的蛋白表达水平分析,为探索NFKBIB在病理生理过程中的调控机制提供可靠检测方案。
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Uniprot No.:
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基因名:
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别名:I kappa B beta antibody; I-kappa-B-beta antibody; IkappaBbeta antibody; IKB beta antibody; IkB-B antibody; IkB-beta antibody; IKBB antibody; IKBB_HUMAN antibody; IkBbeta antibody; NF kappa BIB antibody; NF-kappa-B inhibitor beta antibody; NF-kappa-BIB antibody; Nfkbib antibody; Thyroid receptor interacting protein 9 antibody; Thyroid receptor-interacting protein 9 antibody; TR interacting protein 9 antibody; TR-interacting protein 9 antibody; TRIP-9 antibody; TRIP9 antibody
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宿主:Mouse
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反应种属:Human,Mouse,Rat
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免疫原:Recombinant Protein
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免疫原种属:Homo sapiens (Human)
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标记方式:Non-conjugated
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纯化方式:The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
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克隆号:24G3
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浓度:It differs from different batches. Please contact us to confirm it.
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保存缓冲液:Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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产品提供形式:Liquid
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应用范围:ELISA,IHC
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推荐稀释比:
Application Recommended Dilution IHC 1:100-1:200 -
Protocols:
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储存条件:Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
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货期:Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
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用途:For Research Use Only. Not for use in diagnostic or therapeutic procedures.
相关产品
靶点详情
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功能:Inhibits NF-kappa-B by complexing with and trapping it in the cytoplasm. However, the unphosphorylated form resynthesized after cell stimulation is able to bind NF-kappa-B allowing its transport to the nucleus and protecting it to further NFKBIA-dependent inactivation. Association with inhibitor kappa B-interacting NKIRAS1 and NKIRAS2 prevent its phosphorylation rendering it more resistant to degradation, explaining its slower degradation.
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基因功能参考文献:
- The subcellular distributions of IkappaB and NFkappaB are indicative of carcinogenesis. Inhibition of XPO1 results in intranuclear retention of IkappaB, which inhibits NFkappaB and thereby provides a novel mechanism for drug therapy in sarcoma. This effect can be further enhanced in relatively selinexor-resistant sarcoma cell lines by pretreatment with the proteasome inhibitor carfilzomib. PMID: 28314790
- data suggest that miRNA-4776 modulates Influenza A virus production in infected cells through NFKBIB expression, possibly through the modulation of NF-kappaB. PMID: 28448456
- our data establish the importance of a novel tumor suppressive IKBB gene in abrogating angiogenesis in NPC via the NF-kappaB signalling pathway. PMID: 26227166
- NFKBIBrs3136641TT single nucleotide polymorphism was associated with a significantly decreased risk of developing wheezing. PMID: 25326706
- IkappaBbeta may be a novel target for transcription factors of the HMG-box SRY/Sox family and imply a potential role for NF-kappaB/IkappaBbeta in spermatogenesis PMID: 12475944
- VEGF increased Mn-superoxide dismutase promoter activity, an effect that was dependent on a second intronic NF-kappaB consensus motif. PMID: 15308628
- data indicate that inhibition of NFkappa-B activity by the hepatitis C virus core protein might be related to its physical interaction with and interrupted nuclear localization of IKKbeta PMID: 15919917
- None of the NFKBIB SNPs are associated with pneumococcal susceptibility. PMID: 17463416
- increased I-kappaBbeta expression reversed NF-kappaB activation in cancer cells, compensating for the loss of I-kappaBalpha via TGase 2 polymerization. PMID: 18950638
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亚细胞定位:Cytoplasm. Nucleus.
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蛋白家族:NF-kappa-B inhibitor family
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组织特异性:Expressed in all tissues examined.
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数据库链接: