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| 產(chǎn)地 | 進(jìn)口、國(guó)產(chǎn) |
| 品牌 | 上海莼試 |
| 保存條件 | Store at -20 °C |
| 貨號(hào) | CS10630 |
| 應(yīng)用范圍 | 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 |
| CAS編號(hào) | |
| 抗體名 | Anti-Acetyl-p53(K382) |
| 克隆性 | |
| 靶點(diǎn) | 詳見說(shuō)明書 |
| 適應(yīng)物種 | 詳見說(shuō)明書 |
| 形態(tài) | 詳見說(shuō)明書 |
| 宿主 | 詳見說(shuō)明書 |
| 亞型 | IgG |
| 標(biāo)識(shí)物 | 詳見說(shuō)明書 |
| 濃度 | 1mg/1ml% |
| 免疫原 | KLH conjugated Synthesised acetylpeptide derived from human p53 around the acetylation site of K382 |
產(chǎn)品訂購(gòu)信息：
英文名稱 Anti-Acetyl-p53(K382)
中文名稱 乙?；疨53(Lys382)抗體規(guī)格
別 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 related protein 53; TRP53; Tumor protein p53; Tumour Protein p53; P53_HUMAN; TP53.
濃 度 1mg/1ml
規(guī) 格 0.1ml/100μg 0.2ml/200μg
抗體來(lái)源 Rabbit
克隆類型 polyclonal
交叉反應(yīng) Human
產(chǎn)品類型 一抗 乙酰化抗體
研究領(lǐng)域 細(xì)胞生物 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡
蛋白分子量 predicted molecular weight: 43kDa
性 狀 Lyophilized or Liquid
免 疫 原 KLH conjugated Synthesised acetylpeptide derived from human p53 around the acetylation site of K382
亞 型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
乙?；疨53(Lys382)抗體規(guī)格 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 ICC=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 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廣泛的研究發(fā)現(xiàn)P53。P53蛋白水平在正常細(xì)胞中表達(dá)低，在DNA突變時(shí)或各種各樣細(xì)胞遇難信號(hào)時(shí)反應(yīng)增加。該基因突變或缺失是導(dǎo)致許多發(fā)生的原因。
野生型P53(wt-p53)可誘導(dǎo)細(xì)胞凋亡，并通過(guò)細(xì)胞凋亡抑制，而P53的突變或缺失則可抑制野生型P53的功能，使得缺陷細(xì)胞得以存活下來(lái)，從而導(dǎo)致發(fā)生。 P53同時(shí)也是細(xì)胞凋亡的調(diào)控因子。此抗體可用于P53的研究。
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Anti-Phospho-Mcl1 (Ser159/Thr163)/FITC 熒光素標(biāo)記磷酸化髓樣細(xì)胞-1抗體IgGMulti-class antibodies規(guī)格： 0.2ml
Rhesus antibody Rh CACH2/CaV1.2 L型鈣通道蛋白抗體 規(guī)格 0.1ml
C-Mer/MERTK (proto-oncogene tyrosine kinase) c-mer原癌基因酪酸激酶抗原 0.5mg
HSPA6 英文名稱： 熱休克蛋白70家族蛋白6抗體 0.2ml
Rhesus antibody Rh Sema6A Sema6A抗體 規(guī)格 0.1ml
Anti-Phospho-Mcl1 (Ser159/Thr163)/FITC 熒光素標(biāo)記磷酸化髓樣細(xì)胞-1抗體IgGMulti-class antibodies規(guī)格： 0.2ml
CAM(Human calmodulin) ELISA Kit 人鈣調(diào)素Multi-class antibodies規(guī)格： 48T
Anti-Phospho-Stathmin (Ser38) 磷酸化原癌基因蛋白18Multi-class antibodies規(guī)格： 0.1ml
Rhesus antibody Rh Lactoferrin 乳鐵蛋白抗體 規(guī)格 0.1ml
GM-CSF ELISA Kit 大鼠粒細(xì)胞巨噬細(xì)胞集落刺激因子 96T
PPP2R1A 英文名稱： 蛋白質(zhì)磷酸酶2調(diào)節(jié)亞基1A抗體 0.2ml
Contactin 4 + 6 英文名稱： 軸突相關(guān)粘附分子抗體 0.2ml
Anti-Phospho-Stathmin (Ser38) 磷酸化原癌基因蛋白18Multi-class antibodies規(guī)格： 0.1ml
MYS(Human Myosin) ELISA Kit 人肌球蛋白Multi-class antibodies規(guī)格： 48T
Anti-PAF 血小板活化因子抗體Multi-class antibodies規(guī)格： 0.1ml
Rhesus antibody Rh HPV18 E6 monoclonal 人類狀瘤病毒18 E6單克隆抗體 規(guī)格 0.2ml
GnRH ELISA Kit 大鼠激素釋放激素 96T
Phospho-PBK (Thr9) 英文名稱： 磷酸化PDZ連接激酶/T-LAK細(xì)胞源蛋白激酶抗體 0.1ml
CDC45L 英文名稱： 細(xì)胞分裂周期調(diào)控蛋白45抗體 0.2ml
Anti-PAF 血小板活化因子抗體Multi-class antibodies規(guī)格： 0.1ml
CL-0264C918(人眼脈絡(luò)細(xì)胞)5×106cells/瓶×2
HA Others H4N8 甲型 H4N8 (A/chicken/Alabama/1/1975) 血凝素 (Hemagglutinin / HA) 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)
小鼠上皮細(xì)胞完全培養(yǎng)基 100mL
NCTC clone 929 [L cell, L-929, derivative of Sain L]小鼠成纖維細(xì)胞 NCTC clone 929 [L cell, L-929, derivative of Sain L] mouse fibroblast cells MEM(NaHCO3 1.5g/L, Sodium Pyruvate 0.11g/L)+10%FBS
IL1B Protein Human 重組人 IL-1 beta / IL1B 蛋白
PC-12(大鼠腎上腺嗜鉻細(xì)胞瘤細(xì)胞) 5×106cells/瓶×2 RSC96(大鼠雪旺細(xì)胞)
CL-0261BC-022(人癌細(xì)胞)5×106cells/瓶×2
IFNB1 Others Mouse 小鼠 IFNB1 / IFN-beta / Ierferon beta 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)
人髓核細(xì)胞cDNAHNPC cDNA
T47D細(xì)胞，人管癌細(xì)胞 豬腎細(xì)胞系,IBRS-2細(xì)胞 Many types of cells包裝：5 × 105次方(1ml)
MC3T3-E1(小鼠胚胎成骨細(xì)胞前體細(xì)胞) 5×106cells/瓶×2
HCMEC Pellet 人微內(nèi)皮細(xì)胞團(tuán)塊 > 1 mio.cells 纖維母細(xì)胞粘附檢測(cè)試劑盒Fibro
乙?；疨53(Lys382)抗體規(guī)格 JAM2 Others Rat 大鼠 JAM-2 / JAM-B 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)
人成纖維細(xì)胞總RNAHPrF NA
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抗體的生物素化標(biāo)記實(shí)驗(yàn)要點(diǎn)：
1. 乙酰化P53(Lys382)抗體規(guī)格 如在反應(yīng)混合液中有疊氮鈉或游離氨基存在,會(huì)抑制標(biāo)記反應(yīng)。因此,蛋白質(zhì)在反應(yīng)前要對(duì) 0.1mol/L碳酸氫鈉緩沖液或0.5mol/L硼酸緩沖液充分透析；
2.所用的NHSB及待生物素化蛋白質(zhì)之間的分子比按蛋白質(zhì)表面的ε-氨基的密度會(huì)有所不同,選擇不當(dāng)則影響標(biāo)記的效率,應(yīng)先用幾個(gè)不同的分子比來(lái)篩選最適條件；
3.用NHSB量過(guò)量也是不利的,抗原的結(jié)合位點(diǎn)可能因此被封閉,導(dǎo)致抗體失活；
4.由于抗體的氨基不易接近可能造成生物素化不足,此時(shí)可加入去污劑如 Triton x-100, Tween20等；
5.當(dāng)游離ε-氨基(賴氨酸殘基的氨基)存在于抗體的抗原結(jié)合位點(diǎn)時(shí),或位于酶的催化位點(diǎn)時(shí),生物素化會(huì)降低或損傷抗體蛋白的結(jié)合力或活性；
6.生物素還可能與不同的功能基團(tuán),如羰基、氨基、巰基、異咪唑基及*基,也可與糖基共價(jià)結(jié)合；
7.交聯(lián)反應(yīng)后,應(yīng)充分透析,否則,殘余的生物素會(huì)對(duì)生物素化抗體與親和素的結(jié)合產(chǎn)生競(jìng)爭(zhēng)作用；
8.在細(xì)胞的熒光標(biāo)記實(shí)驗(yàn)中,中和親和素的本底低,但由于鏈霉親和素含有少量正電荷,故對(duì)某些細(xì)胞可導(dǎo)致高本底。
抗體的鑒定：
1）乙酰化P53(Lys382)抗體規(guī)格 抗體的效價(jià)鑒定：不管是用于診斷還是用于,制備抗體的目的都是要求較高效價(jià)。不同的抗原制備的抗體,要求的效價(jià)不一。鑒定效價(jià)的方法很多,包括有試管凝集反應(yīng),瓊脂擴(kuò)散試驗(yàn),酶聯(lián)免疫吸附試驗(yàn)等。常用的抗原所制備的抗體一般都有約成的鑒定效價(jià)的方法,以資比較。如制備抗抗體的效價(jià),一般就采用瓊脂擴(kuò)散試驗(yàn)來(lái)鑒定。
2）抗體的特異性鑒定：抗體的特異性是指與相應(yīng)抗原或近似抗原物質(zhì)的識(shí)別能力?？贵w的特異性高,它的識(shí)別能力就強(qiáng)。衡量特異性通常以交叉反應(yīng)率來(lái)表示。交叉反應(yīng)率可用競(jìng)爭(zhēng)抑制試驗(yàn)測(cè)定。以不同濃度抗原和近似抗原分別做競(jìng)爭(zhēng)抑制曲線,計(jì)算各自的結(jié)合率,求出各自在IC50時(shí)的濃度,并按公式計(jì)算交叉反應(yīng)率。
如果所用抗原濃度IC50濃度為pg/管,而一些近似抗原物質(zhì)的IC50濃度幾乎是無(wú)窮大時(shí),表示這一抗血清與其他抗原物質(zhì)的交叉反應(yīng)率近似為0,即該血清的特異性較好。
3）抗體親和力：是指抗體和抗原結(jié)合的牢固程度。親和力的高低是由抗原分子的大小,抗體分子的結(jié)合位點(diǎn)與抗原決定簇之間立體構(gòu)型的合適度決定的。有助于維持抗原抗體復(fù)合物穩(wěn)定的分子間力有氫鍵,疏水鍵,側(cè)鏈相反電荷基因的庫(kù)侖力,范德華力和空間斥力。親和力常以親和常數(shù)K表示,K的單位是L/mol。抗體親和力的測(cè)定對(duì)抗體的篩選,確定抗體的用途,驗(yàn)證抗體的均一性等均有重要意義。
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