茚三酮 號(hào)：485-47-2  
英文名稱：Ninhydrin；1,2,3-Indantrione hydrate；2,2-Dihydroxyinden-1,3-dione；2,2-Dihydroxy-1H-indene-1,3(2H)-dione；Triketohydrindene hydrate；Trioxohydrindene monohydrate   
其他名稱：苯并戊三酮；水合茚三酮；苯駢戊三酮；苯并環(huán)丙三酮；2,2-二羥基-1H-茚并-1,3(2H)-二酮；水合三酮?dú)滠?；寧海?nbsp;  
號(hào)：485-47-2   
C9H6O4=178.14   
級(jí)別：AR   
含量：≥98.0%   
水溶解試驗(yàn)：合格   
對(duì)氨基酸靈敏度試驗(yàn)：合格   
灼燒殘?jiān)?le;0.1%   
性狀(以下信息僅供參考)：白色或淺黃色結(jié)晶或結(jié)晶性粉末。能吸濕結(jié)塊。見光或露置空氣中逐漸變色。在125℃變紅，139℃體積膨脹，241℃分解。溶于水和乙醇，微溶于乙迷和方。   
用途：本品僅供科研，不得用于其它用途。(以下用途僅供參考)測(cè)定蛋白質(zhì)及肽的游離氨基及羧酸。   
保存：RT，避光茚三酮 號(hào)：485-47-2儲(chǔ)存條件：
避光、干燥陰涼處封閉貯存,嚴(yán)禁與有毒、有害物品混放、混運(yùn)。本品為非危險(xiǎn) 產(chǎn)品可按一般化學(xué)品運(yùn)輸,輕搬動(dòng)輕放,防止日曬、雨淋！受熱、受潮、受光后易喪失活力,保存期短,因此貯存和運(yùn)輸條件比較苛刻。
運(yùn)輸：汽車運(yùn)輸、EMS郵政快遞，申通快遞等， 款到上海3天內(nèi)發(fā)貨；
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存儲(chǔ)：應(yīng)貯存在干燥清潔避光的環(huán)境中，嚴(yán)禁與有毒物質(zhì)混放，以免污染（保質(zhì)期為兩年）。
茚三酮 號(hào)：485-47-2主要優(yōu)級(jí)純、分級(jí)純和化學(xué)純3種：
（1）優(yōu)級(jí)純（GR：Guaranteed reagent），又稱一級(jí)品或保證試劑，99.8%，這種試劑純度Z高，雜質(zhì)含量Z低，適合于重要精密的分析工作和科學(xué)研究工作，使用綠色瓶簽。
（2）分析純（AR），又稱二級(jí)試劑，純度很高，99.7%，略次于優(yōu)級(jí)純，適合于重要分析及一般研究工作，使用紅色瓶簽。
（3）化學(xué)純（CP），又稱三級(jí)試劑，≥ 99.5%，純度與分析純相差較大，適用于工礦、學(xué)校一般分析工作。使用藍(lán)色（深藍(lán)色）標(biāo)簽。
（4）實(shí)驗(yàn)試劑（LR：Laboratory reagent），又稱四級(jí)試劑。
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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. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2009].
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 o茚三酮 號(hào)：485-47-2ccur 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. I