最近搜索:細胞培養 微生物學 分子生物 生物化學
    首頁>>免疫學>>一抗>>細胞核因子/k基因結合核因子單克隆抗體
    細胞核因子/k基因結合核因子單克隆抗體
    • 產品貨號:
      BN41988M
    • 中文名稱:
      細胞核因子/k基因結合核因子單克隆抗體
    • 英文名稱:
      Mouse anti-NFKB p65 Monoclonal antibody
    • 品牌:
      Biorigin
    • 貨號

      產品規格

      售價

      備注

    • BN41988M-50ul

      50ul

      ¥1486.00

      交叉反應:Human,Mouse(predicted:Rat) 推薦應用:WB,ELISA

    • BN41988M-100ul

      100ul

      ¥2360.00

      交叉反應:Human,Mouse(predicted:Rat) 推薦應用:WB,ELISA

    產品描述

    英文名稱NFKB p65
    中文名稱細胞核因子/k基因結合核因子單克隆抗體
    別    名NF kB P65; NF-kB p65; NFKBp65; NF-κBp65; NF-kBp65; 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; p65; p65 NF kappaB; p65 NFkB; 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; TF65_HUMAN.  




    研究領域細胞生物  免疫學  神經生物學  信號轉導  細胞凋亡  轉錄調節因子  
    抗體來源Mouse
    克隆類型Monoclonal
    克 隆 號12G3
    交叉反應Human, Mouse,  (predicted: Rat, )
    產品應用WB=1:500-2000 ELISA=1:5000-10000 ICC=1:100 
    not yet tested in other applications.
    optimal dilutions/concentrations should be determined by the end user.
    分 子 量61kDa
    細胞定位細胞核 細胞漿 
    性    狀Liquid
    濃    度1mg/ml
    免 疫 原KLH conjugated synthetic peptide derived from human NFKB p65: 
    亞    型IgG1
    純化方法affinity purified by Protein G
    儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
    保存條件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
    PubMedPubMed
    產品介紹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. Interacts with NFKBID. Interacts with NFKBIA. Interacts with GSK3B. Interacts with NFKBIB. Interacts with NFKBIE. Interacts with NFKBIZ. Interacts with EHMT1 (via ANK repeats). 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. 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

    Entrez Gene: 19697 Mouse

    Entrez Gene: 309165 Rat

    Omim: 164014 Human

    SwissProt: Q04206 Human

    SwissProt: Q04207 Mouse

    Unigene: 502875 Human

    Unigene: 249966 Mouse

    Unigene: 19480 Rat



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


    亚洲av无码无线在线观看| 亚洲妇熟XXXX妇色黄| 中文字幕无码精品亚洲资源网| 亚洲国产成人精品激情| 亚洲AV日韩AV天堂一区二区三区 | 亚洲色偷精品一区二区三区| 亚洲国产美女视频| 亚洲视频免费在线播放| 1区1区3区4区产品亚洲| 亚洲一区精品中文字幕| 亚洲人成网址在线观看 | 亚洲三级中文字幕| 亚洲日韩乱码中文无码蜜桃臀| 久久精品国产精品亚洲毛片| 久久精品国产亚洲av日韩| 亚洲激情在线观看| 亚洲黄色三级网站| 亚洲美女色在线欧洲美女| 亚洲熟妇无码久久精品| 亚洲欧洲日本精品| 亚洲午夜一区二区电影院| 亚洲一区二区三区免费观看| 亚洲w码欧洲s码免费| 国产99在线|亚洲| 亚洲国产综合AV在线观看| 亚洲AV无码之国产精品| 狠狠综合亚洲综合亚洲色| 成人伊人亚洲人综合网站222| 亚洲国产综合精品一区在线播放| 亚洲一区二区精品视频| 亚洲无线码一区二区三区| 亚洲av午夜福利精品一区人妖| 久久亚洲精精品中文字幕| 亚洲熟妇av一区| 亚洲色大成网站www久久九| 毛片亚洲AV无码精品国产午夜| 亚洲婷婷国产精品电影人久久| 亚洲爽爽一区二区三区| 亚洲国产精品无码专区在线观看| 亚洲va久久久噜噜噜久久天堂 | 国产A在亚洲线播放|