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磷酸化細胞核因子p50/k基因結(jié)合核因子抗體說明書 英文名稱  Anti-Phospho-NFKB1(Ser932)

中文名稱  磷酸化細胞核因子p50/k基因結(jié)合核因子抗體說明書 

別    名 DKFZp686C01211; DNA binding factor KBF1; DNA binding factor KBF1 EBP1; DNA binding factor KBF1 EBP1; DNA-binding factor KBF1; EBP 1; EBP-1; EBP1; KBF1; MGC54151; NF kappa B; NF kappabeta; NF kB1; NFKB 1; NFKB p105; NFKB p50; NFKB1; NFKB1_HUMAN; Nuclear factor kappa B DNA binding subunit; Nuclear factor NF kappa B p105 subunit; Nuclear factor NF kappa B p50 subunit; Nuclear factor NF-kappa-B p50 subunit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 1; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1; p84/NF-kappa-B1 p98.

產(chǎn)品屬性：

濃    度  1mg/1ml

規(guī) 格  0.1ml/100μg

抗體來源  Rabbit

克隆類型   polyclonal

交叉反應(yīng)   Human, Mouse, Rat, Chicken, Dog, Pig, Cow

產(chǎn)品類型   一抗 磷酸化抗體  

研究領(lǐng)域     細胞生物 免疫學(xué) 染色質(zhì)和核信號 信號轉(zhuǎn)導(dǎo) 細胞凋亡 轉(zhuǎn)錄調(diào)節(jié)因子 表觀遺傳學(xué)

蛋白分子量  predicted molecular weight: 48/105kDa 

性    狀   Lyophilized or Liquid

免 疫 原  KLH conjugated Synthesised phosphopeptide derived from human NF KappaB p105 around the phosphorylation site of Ser932 [ET(p-S)FR]

亞    型  IgG

純化方法   affinity purified by Protein A

儲 存 液   0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide

磷酸化細胞核因子p50/k基因結(jié)合核因子抗體說明書 產(chǎn)品應(yīng)用   WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500

（石蠟切片需做抗原修復(fù)） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存條件  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. 

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

產(chǎn)品介紹 This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. SUBUNIT: Active NF-kappa-B is a heterodimer of an about 50 kDa DNA-binding subunit and the weak DNA-binding subunit p65. Two heterodimers might form a labile tetramer. Also interacts with MAP3K8. NF-kappa-B p50 subunit interacts with NCOA3 coactivator, which may coactivate NF-kappa-B dependent expression via its histone acetyltransferase activity. Interacts with DSIPI; this interaction prevents nuclear translocation and DNA-binding. Interacts with SPAG9 and UNC5CL.

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 RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.Subunit : Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-p50 complex. Homodimer; component of the NF-kappa-B p50-p50 complex. Component of the NF-kappa-B p105-p50 complex. Component of the NF-kappa-B p50-c-Rel complex. Component of a complex consisting of the NF-kappa-B p50-p50 homodimer and BCL3. Also interacts with MAP3K8. NF-kappa-B p50 subunit interacts with NCOA3 coactivator, which may coactivate NF-kappa-B dependent expression via its histone acetyltransferase activity. Interacts with DSIPI; this interaction prevents nuclear translocation and DNA-binding. Interacts with SPAG9 and UNC5CL. NFKB1/p105 interacts with CFLAR; the interaction inhibits p105 processing into p50. NFKB1/p105 forms a ternary complex with MAP3K8 and TNIP2. Interacts with GSK3B; the interaction prevents processing of p105 to p50. NFKB1/p50 interacts with NFKBIE. NFKB1/p50 interacts with NFKBIZ. Nuclear factor NF-kappa-B p50 subunit interacts with NFKBID. Directly interacts with MEN1. Interacts with HIF1AN.Subcellular Location : Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).Post-translational modifications : While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p50 making it an acceptable substrate for the proteasome. This process is known as cotranslational processing. The processed form is active and the unprocessed form acts as an inhibitor (I kappa B-like), being able to form cytosolic complexes with NF-kappa B, trapping it in the cytoplasm. Complete folding of the region downstream of the GRR repeat precludes processing.Phosphorylation at 'Ser-903' and 'Ser-907' primes p105 for proteolytic processing in response to TNF-alpha stimulation. Phosphorylation at 'Ser-927' and 'Ser-932' are required for BTRC/BTRCP-mediated proteolysis.Polyubiquitination seems to allow p105 processing.S-nitrosylation of Cys-61 affects DNA binding.The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.Similarity : Contains 7 ANK repeats.Contains 1 death domain.Contains 1 RHD (Rel-like) domain.Database links : UniProtKB/Swiss-Prot: P19838.2

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