- 询价
- 上海博湖
- BH-K21030
- 进口、国产
- 2026年01月01日
- WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500
- 详见说明书
- 详见说明书
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- 技术资料
- 抗体名：
乙酰化P53(Lys382)抗体使用说明书
- 抗体英文名：
Anti-Acetyl-p53(K382)
- 靶点：
详见说明书
- 浓度：
1mg/1ml
- 应用范围：
WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500
- 宿主：
详见说明书
- 供应商：
上海博湖
- 库存：
大量
- 级别：
详见说明书
- 目录编号：
详见说明书
- 抗原来源：
Rabbit
- 保质期：
详见说明书
- 适应物种：
详见说明书
- 标记物：
详见说明书
- 克隆性：
多克隆
- 保存条件：
Store at -20 °C
- 形态：
大量
- 亚型：
IgG
- 免疫原：
KLH conjugated Synthesised acetylpeptide derived from human p53 around the acetylation site of K382
- 规格：
0.2ml/200μg
乙酰化P53(Lys382)抗体使用说明书是用于化学反应、分析化验、研究实验、教学实验、化学配方使用的纯净化学品，产品品质卓越，价格实惠，多种规格供应，售后完善。
英文名称 Anti-Acetyl-p53(K382)
中文名称 乙酰化P53(Lys382)抗体使用说明书
别 名 p53 (Acetyl K382); p53 (Acetyl Lys382); Acetyl-p53 (Lys382); Widespread p53; Wtp53; Antigen NY-CO-13; Cellular tumor antigen p53; Cys 51 Stop; HGNC11998; LFS1; p53; p53 Cellular Tumor Antigen; p53 Tumor Suppressor; Phosphoprotein p53; TP53; Transformation
浓 度 1mg/1ml
规 格 0.1ml/100μg 0.2ml/200μg
抗体来源 Rabbit
克隆类型 polyclonal
交叉反应 Human
产品类型 一抗 乙酰化抗体
研究领域 肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡
蛋白分子量 predicted molecular weight: 43kDa
性 状 Lyophilized or Liquid
免 疫 原 KLH conjugated Synthesised acetylpeptide derived from human p53 around the acetylation site of K382
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
乙酰化P53(Lys382)抗体使用说明书产品应用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500
（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.
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.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍 This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons (PMIDs: 12032546, 20937277). [provided by RefSeq, Feb 2013].
Function : Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.
Subunit : Interacts with AXIN1. Probably part of a complex consisting of TP53, HIPK2 and AXIN1 (By similarity). Binds DNA as a homotetramer. Interacts with histone acetyltransferases EP300 and methyltransferases HRMT1L2 and CARM1, and recruits them to promoters. In vitro, the interaction of TP53 with cancer-associated/HPV (E6) viral proteins leads to ubiquitination and degradation of TP53 giving a possible model for cell growth regulation. This complex formation requires an additional factor, E6-AP, which stably associates with TP53 in the presence of E6. Interacts (via C-terminus) with TAF1; when TAF1 is part of the TFIID complex. Interacts with ING4; this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and TP53INP1. Interacts with WWOX. May interact with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1. Interacts with CHD8; leading to recruit histone H1 and prevent transactivation activity (By similarity). Interacts with ARMC10, BANP, CDKN2AIP, NUAK1, STK11/LKB1, UHRF2 and E4F1. Interacts with YWHAZ; the interaction enhances TP53 transcriptional activity. Phosphorylation of YWHAZ on 'Ser-58' inhibits this interaction. Interacts (via DNA-binding domain) with MAML1 (via N-terminus). Interacts with MKRN1. Interacts with PML (via C-terminus). Interacts with MDM2; leading to ubiquitination and proteasomal degradation of TP53. Directly interacts with FBXO42; leading to ubiquitination and degradation of TP53. Interacts (phosphorylated at Ser-15 by ATM) with the phosphatase PP2A-PPP2R5C holoenzyme; regulates stress-induced TP53-dependent inhibition of cell proliferation. Interacts with PPP2R2A. Interacts with AURKA, DAXX, BRD7 and TRIM24. Interacts (when monomethylated at Lys-382) with L3MBTL1. Isoform 1 interacts with isoform 2 and with isoform 4. Interacts with GRK5. Binds to the CAK complex (CDK7, cyclin H and MAT1) in response to DNA damage. Interacts with CDK5 in neurons. Interacts with AURKB, UHRF2 and NOC2L. Interacts (via N-terminus) with PTK2/FAK1; this promotes ubiquitination by MDM2. Interacts with PTK2B/PYK2; this promotes ubiquitination by MDM2. Interacts with PRKCG. Interacts with human cytomegalovirus/HHV-5 protein UL123.
Subcellular Location : Cytoplasm. Nucleus. Nucleus, PML body. Endoplasmic reticulum. Note=Interaction with BANP promotes nuclear localization. Recruited into PML bodies together with CHEK2.
Isoform 2: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.
Isoform 3: Nucleus. Cytoplasm. Note=Localized in the nucleus in most cells but found in the cytoplasm in some cells.
Isoform 4: Nucleus. Cytoplasm. Note=Predominantly nuclear but translocates to the cytoplasm following cell stress.
Isoform 7: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.
Isoform 8: Nucleus. Cytoplasm. Note=Localized in both nucleus and cytoplasm in most cells. In some cells, forms foci in the nucleus that are different from nucleoli.
Isoform 9: Cytoplasm.
Tissue Specificity : Ubiquitous. Isoforms are expressed in a wide range of normal tissues but in a tissue-dependent manner. Isoform 2 is expressed in most normal tissues but is not detected in brain, lung, prostate, muscle, fetal brain, spinal cord and fetal liver. Isoform 3 is expressed in most normal tissues but is not detected in lung, spleen, testis, fetal brain, spinal cord and fetal liver. Isoform 7 is expressed in most normal tissues but is not detected in prostate, uterus, skeletal muscle and breast. Isoform 8 is detected only in colon, bone marrow, testis, fetal brain and intestine. Isoform 9 is expressed in most normal tissues but is not detected in brain, heart, lung, fetal liver, salivary gland, breast or intestine.
Post-translational modifications : Acetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence.
Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1. Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. Phosphorylated on Thr-18 by VRK1. Phosphorylated on Ser-20 by CHEK2 in response to DNA damage, which prevents ubiquitination by MDM2. Phosphorylated on Ser-20 by PLK3 in response to reactive oxygen species (ROS), promoting p53/TP53-mediated apoptosis. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-33 by CDK7 in a CAK complex in response to DNA damage. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. Phosphorylated by NUAK1 at Ser-15 and Ser-392; was initially thought to be mediated by STK11/LKB1 but it was later shown that it is indirect and that STK11/LKB1-dependent phosphorylation is probably mediated by downstream NUAK1 (PubMed:21317932). It is unclear whether AMP directly mediates phosphorylation at Ser-15. Phosphorylated on Thr-18 by isoform 1 and isoform 2 of VRK2. Phosphorylation on Thr-18 by isoform 2 of VRK2 results in a reduction in ubiquitination by MDM2 and an increase in acetylation by EP300. Stabilized by CDK5-mediated phosphorylation in response to genotoxic and oxidative stresses at Ser-15, Ser-33 and Ser-46, leading to accumulation of p53/TP53, particularly in the nucleus, thus inducing the transactivation of p53/TP53 target genes. Phosphorylated at Ser-315 and Ser-392 by CDK2 in response to DNA-damage.
Dephosphorylated by PP2A-PPP2R5C holoenzyme at Thr-55. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A.
May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line.
Ubiquitinated by MDM2 and SYVN1, which leads to proteasomal degradation. Ubiquitinated by RFWD3, which works in cooperation with MDM2 and may catalyze the formation of short polyubiquitin chains on p53/TP53 that are not targeted to the proteasome. Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation. Deubiquitinated by USP10, leading to its stabilization. Ubiquitinated by TRIM24, which leads to proteasomal degradation. Ubiquitination by TOPORS induces degradation. Deubiquitination by USP7, leading to stabilization. Isoform 4 is monoubiquitinated in an MDM2-independent manner.
Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370. Dimethylated at Lys-373 by EHMT1 and EHMT2. Monomethylated at Lys-382 by SETD8, promoting interaction with L3MBTL1 and leading to repress transcriptional activity. Demethylation of dimethylated Lys-370 by KDM1A prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.
Sumoylated by SUMO1.
DISEASE : Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma.
Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:133239].
Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:151623]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.
Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC)
Defects in TP53 are a cause of lung cancer (LNCR) [MIM:211980]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis.
Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:260500]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.
Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:202300]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni yndrome.
Similarity : Belongs to the p53 family.
Database links : NCBI Reference Sequence: NP_001119584.1
UniProtKB/Swiss-Prot: P04637.4
wtp53广泛的研究发现P53肿瘤抑制基因对50%以上的人类癌症具有抑制突变的功能。P53蛋白水平在正常细胞中表达低，在DNA突变时或各种各样细胞遇难信号时反应增加。该基因突变或缺失是导致许多肿瘤发生的原因。
野生型P53(wt-p53)可诱导细胞凋亡，并通过细胞凋亡抑制肿瘤生长，而P53的突变或缺失则可抑制野生型P53的功能，使得缺陷细胞得以存活下来，从而导致肿瘤发生。 P53同时也是细胞凋亡的调控因子。此抗体可用于P53肿瘤抑制基因功能的研究。
乙酰化P53(Lys382)抗体使用说明书具有全、新、优、品、好四大特点：
全：公司提供上万种产品，涵盖了生物试剂，elisa试剂盒，标准品，培养基，原装耗材，抗体、培养基、ATCC细胞等，基本上各种科研所需产品在我司都能找到。
新：产品更新速度较快，基本上每周都有新产品出现。
优：产品质量好，投诉比较少。
好：我公司具有优质的技术团队，产品一旦售出，实验过程中遇到困难可提供在线技术咨询。使您使用产品时没有任何的后顾之忧。
我们提供的标记服务，可根据您科研的需求，满足您的需要，质量保证，价格合理。
一、标记流程
委托标记服务，请下载并详细填写《委托标记申请单》，待我公司标记室技术人员研究、确认后答复，并办理委托标记事宜。
二、各种标记物制备的收费标准（RMB）
我们不但提供抗体和大分子蛋白的标记服务，还提供小分子多肽及小分子蛋白的各种标记服务，提供标记化合物的服务（此化合物必须适用于标记），价格另议。
一抗和二坑的区别：
第一抗体就是平常所说的抗体，即能和抗原特异性结合。
第二抗体是能和抗体结合的，即抗体的抗体。主要用于检测抗体的存在。
一抗是针对抗原的抗体，二抗是针对一抗的抗体。即抗体也可以充当抗原刺激机体产生抗体。也就是说，抗原进入机体刺激机体免疫系统产生免疫应答，由B细胞可以产生与相应抗原发生特异性结合的特殊蛋白质。
一抗二抗都是一种可以特异结合别的物质的基团，而且一抗可以至少结合两种其他基团（底物和二抗）。
一抗：可以特异结合底物，就是识别出我们想要检测的东西。一抗和底物结合与否用肉眼是看不出来的。
二抗：可以和一抗结合，并带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），作用是检测一抗。 如果一抗自己带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），则不需要二抗。但这样成本很高，因为一种一抗只识别一种底物。所以如今的设计一般是二抗带上可检测标记，再来检测一抗。而一抗识别底物。这样，当一抗结合到底物上，就可以通过二抗检测出来。
睾丸精原细胞瘤与淋巴瘤组织芯片 进口/国产
胃癌与胃炎组织芯片 进口/国产
脾脏疾病组织芯片 进口/国产
头颈癌组织芯片 进口/国产
皮肤癌组织芯片 进口/国产
抑癌基因结合蛋白ARID1B抗体 Anti-ARID1B WB IHC-P IHC-F IF 100ul
E3连接酶蛋白ARIH2抗体 Anti-ARIH2 WB IHC-P IHC-F IF 100ul
ADP核糖基化样因子1抗体 Anti-ARFL1 WB IHC-P IHC-F IF 100ul
ADP核糖基化因子样蛋白4抗体 Anti-ARL4 WB IHC-P IHC-F IF 100ul
肌动蛋白相关蛋白2/3抗体 Anti-ARP2 WB IHC-P IHC-F IF 100ul
5甲基胞嘧啶抗体 Anti-5 MethylCytosine WB IHC-P IHC-F IF 100ul
T淋巴细胞分化蛋白MAL2抗体 Anti-MAL2 WB IHC-P IHC-F IF 100ul
环指蛋白61抗体 Anti-RNF61 WB IHC-P IHC-F IF 100ul
毒蕈碱型乙酰胆碱受体M3抗体 Anti-Muscarinic Acetylcholine receptor M3 WB IHC-P IHC-F IF 100ul
错配修复蛋白1抗体 Anti-MLH1 WB IHC-P IHC-F IF 100ul
猕猴皮肤细胞;MMS7
CL-0449SW 780(人膀胱移行细胞癌)5×106cells/瓶×2
PTGFRN Others Cynomolgus 食蟹猴 EWI-F / PTGFRN 人细胞裂解液 (阳性对照)
2BS细胞，胚肺细胞 人前列腺癌细胞,VLcop细胞 人肾小管上皮细胞;HKC
人小细胞肺癌细胞;NCI-H209
TNFRSF21 Others Human 人 DR6 / TNFRSF21 人细胞裂解液 (阳性对照)
人骨骼肌成肌细胞裂解物HSkMML
VTCN1 Others Human 人 B7-H4 / B7S1 / B7x 人细胞裂解液 (阳性对照)
人神经少突起前质胶质细胞完全培养基 100mL
JB6-C30细胞，小鼠皮肤细胞 J82(膀胱癌细胞) 犬肾细胞;MDCK/IgR
EFNA1 Protein Mouse 重组小鼠 Ephrin-A1 / EFNA1 蛋白 (His 标签)
CAL-27(人舌鳞癌细胞) 5×106cells/瓶×2 原代骨细胞特制无血清添加剂Many types of cells包装：1ml
乙酰化P53(Lys382)抗体使用说明书猕猴皮肤细胞;MMS7
CL-0449SW 780(人膀胱移行细胞癌)5×106cells/瓶×2
PTGFRN Others Cynomolgus 食蟹猴 EWI-F / PTGFRN 人细胞裂解液 (阳性对照)
2BS细胞，胚肺细胞 人前列腺癌细胞,VLcop细胞 人肾小管上皮细胞;HKC
人小细胞肺癌细胞;NCI-H209
TNFRSF21 Others Human 人 DR6 / TNFRSF21 人细胞裂解液 (阳性对照)
英文名称 Anti-Acetyl-p53(K382)
中文名称 乙酰化P53(Lys382)抗体使用说明书
别 名 p53 (Acetyl K382); p53 (Acetyl Lys382); Acetyl-p53 (Lys382); Widespread p53; Wtp53; Antigen NY-CO-13; Cellular tumor antigen p53; Cys 51 Stop; HGNC11998; LFS1; p53; p53 Cellular Tumor Antigen; p53 Tumor Suppressor; Phosphoprotein p53; TP53; Transformation
浓 度 1mg/1ml
规 格 0.1ml/100μg 0.2ml/200μg
抗体来源 Rabbit
克隆类型 polyclonal
交叉反应 Human
产品类型 一抗 乙酰化抗体
研究领域 肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡
蛋白分子量 predicted molecular weight: 43kDa
性 状 Lyophilized or Liquid
免 疫 原 KLH conjugated Synthesised acetylpeptide derived from human p53 around the acetylation site of K382
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
乙酰化P53(Lys382)抗体使用说明书产品应用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500
（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.
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.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍 This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons (PMIDs: 12032546, 20937277). [provided by RefSeq, Feb 2013].
Function : Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.
Subunit : Interacts with AXIN1. Probably part of a complex consisting of TP53, HIPK2 and AXIN1 (By similarity). Binds DNA as a homotetramer. Interacts with histone acetyltransferases EP300 and methyltransferases HRMT1L2 and CARM1, and recruits them to promoters. In vitro, the interaction of TP53 with cancer-associated/HPV (E6) viral proteins leads to ubiquitination and degradation of TP53 giving a possible model for cell growth regulation. This complex formation requires an additional factor, E6-AP, which stably associates with TP53 in the presence of E6. Interacts (via C-terminus) with TAF1; when TAF1 is part of the TFIID complex. Interacts with ING4; this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and TP53INP1. Interacts with WWOX. May interact with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1. Interacts with CHD8; leading to recruit histone H1 and prevent transactivation activity (By similarity). Interacts with ARMC10, BANP, CDKN2AIP, NUAK1, STK11/LKB1, UHRF2 and E4F1. Interacts with YWHAZ; the interaction enhances TP53 transcriptional activity. Phosphorylation of YWHAZ on 'Ser-58' inhibits this interaction. Interacts (via DNA-binding domain) with MAML1 (via N-terminus). Interacts with MKRN1. Interacts with PML (via C-terminus). Interacts with MDM2; leading to ubiquitination and proteasomal degradation of TP53. Directly interacts with FBXO42; leading to ubiquitination and degradation of TP53. Interacts (phosphorylated at Ser-15 by ATM) with the phosphatase PP2A-PPP2R5C holoenzyme; regulates stress-induced TP53-dependent inhibition of cell proliferation. Interacts with PPP2R2A. Interacts with AURKA, DAXX, BRD7 and TRIM24. Interacts (when monomethylated at Lys-382) with L3MBTL1. Isoform 1 interacts with isoform 2 and with isoform 4. Interacts with GRK5. Binds to the CAK complex (CDK7, cyclin H and MAT1) in response to DNA damage. Interacts with CDK5 in neurons. Interacts with AURKB, UHRF2 and NOC2L. Interacts (via N-terminus) with PTK2/FAK1; this promotes ubiquitination by MDM2. Interacts with PTK2B/PYK2; this promotes ubiquitination by MDM2. Interacts with PRKCG. Interacts with human cytomegalovirus/HHV-5 protein UL123.
Subcellular Location : Cytoplasm. Nucleus. Nucleus, PML body. Endoplasmic reticulum. Note=Interaction with BANP promotes nuclear localization. Recruited into PML bodies together with CHEK2.
Isoform 2: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.
Isoform 3: Nucleus. Cytoplasm. Note=Localized in the nucleus in most cells but found in the cytoplasm in some cells.
Isoform 4: Nucleus. Cytoplasm. Note=Predominantly nuclear but translocates to the cytoplasm following cell stress.
Isoform 7: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.
Isoform 8: Nucleus. Cytoplasm. Note=Localized in both nucleus and cytoplasm in most cells. In some cells, forms foci in the nucleus that are different from nucleoli.
Isoform 9: Cytoplasm.
Tissue Specificity : Ubiquitous. Isoforms are expressed in a wide range of normal tissues but in a tissue-dependent manner. Isoform 2 is expressed in most normal tissues but is not detected in brain, lung, prostate, muscle, fetal brain, spinal cord and fetal liver. Isoform 3 is expressed in most normal tissues but is not detected in lung, spleen, testis, fetal brain, spinal cord and fetal liver. Isoform 7 is expressed in most normal tissues but is not detected in prostate, uterus, skeletal muscle and breast. Isoform 8 is detected only in colon, bone marrow, testis, fetal brain and intestine. Isoform 9 is expressed in most normal tissues but is not detected in brain, heart, lung, fetal liver, salivary gland, breast or intestine.
Post-translational modifications : Acetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence.
Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1. Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. Phosphorylated on Thr-18 by VRK1. Phosphorylated on Ser-20 by CHEK2 in response to DNA damage, which prevents ubiquitination by MDM2. Phosphorylated on Ser-20 by PLK3 in response to reactive oxygen species (ROS), promoting p53/TP53-mediated apoptosis. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-33 by CDK7 in a CAK complex in response to DNA damage. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. Phosphorylated by NUAK1 at Ser-15 and Ser-392; was initially thought to be mediated by STK11/LKB1 but it was later shown that it is indirect and that STK11/LKB1-dependent phosphorylation is probably mediated by downstream NUAK1 (PubMed:21317932). It is unclear whether AMP directly mediates phosphorylation at Ser-15. Phosphorylated on Thr-18 by isoform 1 and isoform 2 of VRK2. Phosphorylation on Thr-18 by isoform 2 of VRK2 results in a reduction in ubiquitination by MDM2 and an increase in acetylation by EP300. Stabilized by CDK5-mediated phosphorylation in response to genotoxic and oxidative stresses at Ser-15, Ser-33 and Ser-46, leading to accumulation of p53/TP53, particularly in the nucleus, thus inducing the transactivation of p53/TP53 target genes. Phosphorylated at Ser-315 and Ser-392 by CDK2 in response to DNA-damage.
Dephosphorylated by PP2A-PPP2R5C holoenzyme at Thr-55. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A.
May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line.
Ubiquitinated by MDM2 and SYVN1, which leads to proteasomal degradation. Ubiquitinated by RFWD3, which works in cooperation with MDM2 and may catalyze the formation of short polyubiquitin chains on p53/TP53 that are not targeted to the proteasome. Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation. Deubiquitinated by USP10, leading to its stabilization. Ubiquitinated by TRIM24, which leads to proteasomal degradation. Ubiquitination by TOPORS induces degradation. Deubiquitination by USP7, leading to stabilization. Isoform 4 is monoubiquitinated in an MDM2-independent manner.
Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370. Dimethylated at Lys-373 by EHMT1 and EHMT2. Monomethylated at Lys-382 by SETD8, promoting interaction with L3MBTL1 and leading to repress transcriptional activity. Demethylation of dimethylated Lys-370 by KDM1A prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.
Sumoylated by SUMO1.
DISEASE : Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma.
Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:133239].
Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:151623]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.
Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC)
Defects in TP53 are a cause of lung cancer (LNCR) [MIM:211980]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis.
Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:260500]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.
Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:202300]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni yndrome.
Similarity : Belongs to the p53 family.
Database links : NCBI Reference Sequence: NP_001119584.1
UniProtKB/Swiss-Prot: P04637.4
wtp53广泛的研究发现P53肿瘤抑制基因对50%以上的人类癌症具有抑制突变的功能。P53蛋白水平在正常细胞中表达低，在DNA突变时或各种各样细胞遇难信号时反应增加。该基因突变或缺失是导致许多肿瘤发生的原因。
野生型P53(wt-p53)可诱导细胞凋亡，并通过细胞凋亡抑制肿瘤生长，而P53的突变或缺失则可抑制野生型P53的功能，使得缺陷细胞得以存活下来，从而导致肿瘤发生。 P53同时也是细胞凋亡的调控因子。此抗体可用于P53肿瘤抑制基因功能的研究。
乙酰化P53(Lys382)抗体使用说明书具有全、新、优、品、好四大特点：
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我们提供的标记服务，可根据您科研的需求，满足您的需要，质量保证，价格合理。
一、标记流程
委托标记服务，请下载并详细填写《委托标记申请单》，待我公司标记室技术人员研究、确认后答复，并办理委托标记事宜。
二、各种标记物制备的收费标准（RMB）
我们不但提供抗体和大分子蛋白的标记服务，还提供小分子多肽及小分子蛋白的各种标记服务，提供标记化合物的服务（此化合物必须适用于标记），价格另议。
一抗和二坑的区别：
第一抗体就是平常所说的抗体，即能和抗原特异性结合。
第二抗体是能和抗体结合的，即抗体的抗体。主要用于检测抗体的存在。
一抗是针对抗原的抗体，二抗是针对一抗的抗体。即抗体也可以充当抗原刺激机体产生抗体。也就是说，抗原进入机体刺激机体免疫系统产生免疫应答，由B细胞可以产生与相应抗原发生特异性结合的特殊蛋白质。
一抗二抗都是一种可以特异结合别的物质的基团，而且一抗可以至少结合两种其他基团（底物和二抗）。
一抗：可以特异结合底物，就是识别出我们想要检测的东西。一抗和底物结合与否用肉眼是看不出来的。
二抗：可以和一抗结合，并带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），作用是检测一抗。 如果一抗自己带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），则不需要二抗。但这样成本很高，因为一种一抗只识别一种底物。所以如今的设计一般是二抗带上可检测标记，再来检测一抗。而一抗识别底物。这样，当一抗结合到底物上，就可以通过二抗检测出来。
睾丸精原细胞瘤与淋巴瘤组织芯片 进口/国产
胃癌与胃炎组织芯片 进口/国产
脾脏疾病组织芯片 进口/国产
头颈癌组织芯片 进口/国产
皮肤癌组织芯片 进口/国产
抑癌基因结合蛋白ARID1B抗体 Anti-ARID1B WB IHC-P IHC-F IF 100ul
E3连接酶蛋白ARIH2抗体 Anti-ARIH2 WB IHC-P IHC-F IF 100ul
ADP核糖基化样因子1抗体 Anti-ARFL1 WB IHC-P IHC-F IF 100ul
ADP核糖基化因子样蛋白4抗体 Anti-ARL4 WB IHC-P IHC-F IF 100ul
肌动蛋白相关蛋白2/3抗体 Anti-ARP2 WB IHC-P IHC-F IF 100ul
5甲基胞嘧啶抗体 Anti-5 MethylCytosine WB IHC-P IHC-F IF 100ul
T淋巴细胞分化蛋白MAL2抗体 Anti-MAL2 WB IHC-P IHC-F IF 100ul
环指蛋白61抗体 Anti-RNF61 WB IHC-P IHC-F IF 100ul
毒蕈碱型乙酰胆碱受体M3抗体 Anti-Muscarinic Acetylcholine receptor M3 WB IHC-P IHC-F IF 100ul
错配修复蛋白1抗体 Anti-MLH1 WB IHC-P IHC-F IF 100ul
猕猴皮肤细胞;MMS7
CL-0449SW 780(人膀胱移行细胞癌)5×106cells/瓶×2
PTGFRN Others Cynomolgus 食蟹猴 EWI-F / PTGFRN 人细胞裂解液 (阳性对照)
2BS细胞，胚肺细胞 人前列腺癌细胞,VLcop细胞 人肾小管上皮细胞;HKC
人小细胞肺癌细胞;NCI-H209
TNFRSF21 Others Human 人 DR6 / TNFRSF21 人细胞裂解液 (阳性对照)
人骨骼肌成肌细胞裂解物HSkMML
VTCN1 Others Human 人 B7-H4 / B7S1 / B7x 人细胞裂解液 (阳性对照)
人神经少突起前质胶质细胞完全培养基 100mL
JB6-C30细胞，小鼠皮肤细胞 J82(膀胱癌细胞) 犬肾细胞;MDCK/IgR
EFNA1 Protein Mouse 重组小鼠 Ephrin-A1 / EFNA1 蛋白 (His 标签)
CAL-27(人舌鳞癌细胞) 5×106cells/瓶×2 原代骨细胞特制无血清添加剂Many types of cells包装：1ml
乙酰化P53(Lys382)抗体使用说明书猕猴皮肤细胞;MMS7
CL-0449SW 780(人膀胱移行细胞癌)5×106cells/瓶×2
PTGFRN Others Cynomolgus 食蟹猴 EWI-F / PTGFRN 人细胞裂解液 (阳性对照)
2BS细胞，胚肺细胞 人前列腺癌细胞,VLcop细胞 人肾小管上皮细胞;HKC
人小细胞肺癌细胞;NCI-H209
TNFRSF21 Others Human 人 DR6 / TNFRSF21 人细胞裂解液 (阳性对照)
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乙酰化P53(Lys382)抗体使用说明书
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