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Phospho-NFKB p65(Ser468) antib

ody
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  • ¥1580
  • 康朗生物
  • kl-3485R
  • 中国/美国/德国
  • 2025年07月08日
  • WB=1:100-200 IHC-P=1:400-800 IHC-F=1:100-200 Flow-Cyt=0.2μg /test IF=1:100-200
  • Rabbit
  • Human, Mouse, Rat, Dog, Pig, Cow, Horse,
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 供应商

      上海康朗生物科技有限公司

    • 库存

      大量

    • 目录编号

      kl-3485R

    • 克隆性

      多克隆

    • 抗原来源

      Rabbit

    • 保质期

      12个月

    • 抗体英文名

      Phospho-NFKB p65(Ser468) antibody

    • 抗体名

      磷酸化细胞核因子NF-κB p65抗体

    • 宿主

      Rabbit

    • 适应物种

      Human, Mouse, Rat, Dog, Pig, Cow, Horse,

    • 免疫原

      KLH conjugated Synthesised phosphopeptide derived from human NFKBp65 around the phosphorylation site of Ser468:LA(p-S)VD

    • 亚型

      IgG

    • 形态

      冻干粉或液体

    • 应用范围

      WB=1:100-200 IHC-P=1:400-800 IHC-F=1:100-200 Flow-Cyt=0.2μg /test IF=1:100-200

    • 浓度

      1mg/ml

    • 保存条件

      -20 °C

    • 规格

      100ul

    Phospho-NFKB p65(Ser468) antibody
    中文名称 磷酸化细胞核因子NF-κB p65抗体
    别    名 NF-kB p65 (phospho S468); p-NF-kB p65 (phospho S468); RELA(phospho S468); NF kB P65; NF-kB p65; NFKBp65; NF-κBp65; p65 NF kappaB; p65 NFkB; NFKBp65; RELA; Transcription Factor p65; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)); V Rel Avian Reticuloendotheliosis Viral Oncogene Homolog A; v rel reticuloendotheliosis viral oncogene homolog A (avian); v-rel reticuloendotheliosis viral oncogene homolog A; p65NFKB; Avian reticuloendotheliosis viral (v rel) oncogene homolog A; MGC131774; NFKB 3; NFKB3; Nuclear Factor NF Kappa B p65 Subunit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3; Nuclear Factor Of Kappa Light Polypeptide Gene Enhancer In B Cells.  NFκB-p65; NFκB p65; NF κB-p65; NFκBp65;
    规格价格 100ul/1580元 购买        大包装/询价
    说 明 书 100ul  
    产品类型 磷酸化抗体 
    研究领域 肿瘤  细胞生物  免疫学  信号转导  细胞凋亡  转录调节因子  激酶和磷酸酶  通道蛋白  
    抗体来源 Rabbit
    克隆类型 Polyclonal
    交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Horse, 
    产品应用 WB=1:100-200 IHC-P=1:400-800 IHC-F=1:100-200 Flow-Cyt=0.2μg /test IF=1:100-200 (石蜡切片需做抗原修复) 
    not yet tested in other applications.
    optimal dilutions/concentrations should be determined by the end user.
    分 子 量 61kDa
    细胞定位 细胞核 细胞浆 
    性    状 Lyophilized or Liquid
    浓    度 1mg/ml
    免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human NFKBp65 around the phosphorylation site of Ser468:LA(p-S)VD 
    亚    型 IgG
    纯化方法 affinity purified by Protein A
    储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
    保存条件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
    PubMed PubMed
    产品介绍 background:
    NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor, NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene, RELA. Four transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2011].

    Function:
    NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1.

    Subunit:
    Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-c-Rel complex. Homodimer; component of the NF-kappa-B p65-p65 complex. Component of the NF-kappa-B p65-p52 complex. May interact with ETHE1. Binds AES and TLE1. Interacts with TP53BP2. Binds to and is phosphorylated by the activated form of either RPS6KA4 or RPS6KA5. Interacts with ING4 and this interaction may be indirect. Interacts with CARM1, USP48 and UNC5CL. Interacts with IRAK1BP1 (By similarity). Interacts with NFKBID (By similarity). Interacts with NFKBIA. Interacts with GSK3B. Interacts with NFKBIB (By similarity). Interacts with NFKBIE. Interacts with NFKBIZ. Interacts with EHMT1 (via ANK repeats) (By similarity). Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HDAC3; HDAC3 mediates the deacetylation of RELA. Interacts with HDAC1; the interaction requires non-phosphorylated RELA. Interacts with CBP; the interaction requires phosphorylated RELA. Interacts (phosphorylated at 'Thr-254') with PIN1; the interaction inhibits p65 binding to NFKBIA. Interacts with SOCS1. Interacts with UXT. Interacts with MTDH and PHF11. Interacts with ARRB2. Interacts with human respiratory syncytial virus (HRSV) protein M2-1. Interacts with NFKBIA (when phosphorylated), the interaction is direct; phosphorylated NFKBIA is part of a SCF(BTRC)-like complex lacking CUL1. Interacts with RNF25. Interacts (via C-terminus) with DDX1. Interacts with UFL1 and COMMD1. Interacts with BRMS1; this promotes deacetylation of 'Lys-310'. Interacts with NOTCH2 (By similarity). Directly interacts with MEN1; this interaction represses NFKB-mediated transactivation. Interacts with AKIP1, which promotes the phosphorylation and nuclear retention of RELA. Interacts (via the RHD) with GFI1; the interaction, after bacterial lipopolysaccharide (LPS) stimulation, inhibits the transcriptional activity by interfering with the DNA-binding activity to target gene promoter DNA.

    Subcellular Location:
    Nucleus. Cytoplasm. Note=Colocalized with DDX1 in the nucleus upon TNF-alpha induction. Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B). Colocalizes with GFI1 in the nucleus after LPS stimulation.

    Post-translational modifications:
    Ubiquitinated, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response. 
    Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes. 
    Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity. Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity. Phosphorylation at Ser-276 by RPS6KA4 and RPS6KA5 promotes its transactivation and transcriptional activities. 
    Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3 and SIRT2. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of Lys-310. Lys-310 is deacetylated by SIRT2. 
    S-nitrosylation of Cys-38 inactivates the enzyme activity. 
    Sulfhydration at Cys-38 mediates the anti-apoptotic activity by promoting the interaction with RPS3 and activating the transcription factor activity. 
    Sumoylation by PIAS3 negatively regulates DNA-bound activated NF-kappa-B.

    Similarity:
    Contains 1 RHD (Rel-like) domain.

    SWISS:
    Q04206

    Gene ID:
    5970

    Database links:

    Entrez Gene: 5970 Human

    Omim: 164014 Human

    SwissProt: Q04206 Human

    Unigene: 502875 Human



    Important Note:
    This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

    转录调节因子(Transcriptin Regulators) NF-κBp65是一种重要的转录因子,NF-kBp65可激活参与炎症、细胞增殖、细胞凋亡等基因的调节,影响着细胞的凋亡,同时影响着肿瘤细胞对细胞毒性药物及离子辐射的敏感性。ras基因诱导的致癌突变作用需NFkB的活化,提示NFkB在致癌发生方面可能起一定作用;另有文献报道,在乳腺癌、非小细胞性肺癌、甲状腺癌、T或B淋巴细胞白血病及病毒诱变导致的肿瘤等人类肿瘤中,NFkB活化或表达。 经研究认为:NFKBp65蛋白在静息状态下以结合态的方式存在于胞浆中,当NFKBp65蛋白被激活后解离进入细胞核。 NF-кB可以保护细胞免受肿瘤坏死因子以及电离辐射等引起的凋亡作用,而抑制NFkB的表达可以增加TNF等引起的细胞凋亡,以及增加化疗及放疗对肿瘤细胞的敏感性。
    产品图片 产品细节图片1
    Sample: 
    A431(Human) Cell Lysate at 40 ug
    Hela(Human) Cell Lysate at 40 ug
    Primary: Anti-Phospho-NFKB p65(Ser468) (bs-3485R) at 1/300 dilution
    Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
    Predicted band size: 61 kD
    Observed band size: 61 kD

    产品细节图片2
    Sample:
    Lane1:HL-60 (Human) Whole Cell Lysate at 30 ug
    Lane2:Lung (Mouse) Tissue Lysate at 30 ug
    Primary: Anti-phospho-NFKB p65(Ser468) (bs-3485R)at 1/300 dilution
    Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
    Predicted band size: 61 kD
    Observed band size: 61 kD

    产品细节图片3
    Sample: 
    Spleen (Mouse) Lysate at 40 ug
    Primary: Anti-Phospho-NFKB p65(Ser468) (bs-3485R) at 1/300 dilution
    Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
    Predicted band size: 61 kD
    Observed band size: 61 kD

    产品细节图片4
    Sample: 
    Lymph node (Mouse) Lysate at 40 ug
    Primary: Anti-Phospho-NFKB p65(Ser468) (bs-3485R) at 1/300 dilution
    Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
    Predicted band size: 61 kD
    Observed band size: 61 kD

    产品细节图片5
    Paraformaldehyde-fixed, paraffin embedded (Rat bladder); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (Phospho-NFKB p65(Ser468)) Polyclonal Antibody, Unconjugated (bs-3485R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.
    产品细节图片6
    Blank control (blue line): Hela (fixed with 70% ethanol (Overnight at 4℃) and then permeabilized with 90% ice-cold methanol for 30 min on ice). 
    Primary Antibody (green line): Rabbit Anti-Phospho-NFKB p65(Ser468) antibody (bs-3485R),Dilution: 0.2μg /10^6 cells; 
    Isotype Control Antibody (orange line): Rabbit IgG .
    Secondary Antibody (white blue line): Goat anti-rabbit IgG-FITC, Dilution: 1μg /test. 

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    相关实验
    • 【求助】nfkb促凋亡通过jnk通路?

      sakura042 本新手欲研究nfkb引起内皮细胞凋亡的机制:是否通过jnk通路。 这是否是一个信号通路串话的问题? 我们用特异性抑制剂阻断nfkb后发现jnk活性下降,是否就能说明nfkb促进内皮细胞凋亡是通过jnk通路呢?还需要再阻断或者过表达jnk通路来反证吗? 这个问题困扰了我好久,请教各位高手。 sakura042 自己顶一下 三叶虫 请问一下

    • 【求助】于NF-KB 激活,P65磷酸化位点是ser536还是ser276?

      激活。所以蛋白的磷酸化或去磷酸化不是简单的孤立现象,它始终与细胞信号转导有关系。最终将达到细胞增殖、分化、激活等功能的实现。 magichunter 楼上回答的是什么啊?人家问的是:于NF-KB 激活,P65磷酸化位点是ser536还是ser276? 你也没回答到底是哪个啊? 伽利略 chenlydd wrote: 我认为蛋白的磷酸化与其功能有关系。蛋白可被磷酸化,也可被去磷

    • 【求助】矛盾的实验结果:IKb alpha和NFKB同时升高

      吴佰霖 我的基因过表达,结合文献,推理应该是IKb alpha下降,而NFKB升高 (IKb可磷酸化NFKB,使后者降低) 但现在我的结果是两者同时升高,请问可能的原因有哪些呢? 谢谢 woxingwosu 可否检测一下NFKB的磷酸化情况? erik NFKB是检测核内的吗?检测p65还是p50/ 吴佰霖 检测总蛋白

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