鄰甲* 號：596-27-0  
英文名稱：o-Cresolphthalein；3,3′-Dimethylphenolphthalein；3,3-Bis(4-hydroxy-3methylphenyl)-1-(3H)-isobenzofuranone    
其他名稱：鄰甲酚呋酞；2-甲*, 3,3′-二甲基*；3,3-雙(4-羥基-3-甲基苯基)-1(3H)-異苯并呋喃酮；鄰甲苯*；3,3'-二甲*；鄰甲酚酜酞   
號：596-27-0    
C22H18O4=346.38    
級別：IND   
pH變色域：8.2(無色)～9.8(紅色)   
紅外光譜鑒定：和對照品匹配   
性狀(以下信息僅供參考)：白色或黃色結晶性粉末。易溶于乙醇、乙迷和冰乙酸，溶于稀堿溶液呈紫色，微溶于水，不溶于苯。熔點223℃。Z大吸收波長 566(381)nm   
用途：本品僅供科研，不得用于其它用途。(以下用途僅供參考)酸堿指示劑   
保存：RT鄰甲* 號：596-27-0儲存條件：
避光、干燥陰涼處封閉貯存,嚴禁與有毒、有害物品混放、混運。本品為非危險 產品可按一般化學品運輸,輕搬動輕放,防止日曬、雨淋！受熱、受潮、受光后易喪失活力,保存期短,因此貯存和運輸條件比較苛刻。
運輸：汽車運輸、EMS郵政快遞，申通快遞等， 款到上海3天內發貨；
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存儲：應貯存在干燥清潔避光的環境中，嚴禁與有毒物質混放，以免污染（保質期為兩年）。
鄰甲* 號：596-27-0主要優級純、分級純和化學純3種：
（1）優級純（GR：Guaranteed reagent），又稱一級品或保證試劑，99.8%，這種試劑純度Z高，雜質含量Z低，適合于重要精密的分析工作和科學研究工作，使用綠色瓶簽。
（2）分析純（AR），又稱二級試劑，純度很高，99.7%，略次于優級純，適合于重要分析及一般研究工作，使用紅色瓶簽。
（3）化學純（CP），又稱三級試劑，≥ 99.5%，純度與分析純相差較大，適用于工礦、學校一般分析工作。使用藍色（深藍色）標簽。
（4）實驗試劑（LR：Laboratory reagent），又稱四級試劑。
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1inactive 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.