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產(chǎn)品訂購(gòu)信息：
英文名稱  Anti-PTEN/MMAC1(NT) 

中文名稱   一種抑制基因抗體（N端）規(guī)格 

別    名  ITGA 2; MGC11227; MHAM; MMAC 1; MMAC1; Bannayan Zonana; BZS a; Multiple hamartoma (Cowden syndrome); Mutated in Mutiple Advanced Cancers 1; Phosphatase and Tensin Homolog; Phosphatidylinositol 345 trisphosphate 3 phosphatase and dual specificity protein phosphatase PTEN; Phosphatidylinositol 345 trisphosphate 3 phosphatase; Platelet antigen BR; PTEN 1; PTEN1; Tensin homolog; TEP 1; TEP1; VLA 2 Receptor Alpha Subunit.

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, Mouse, Rat 

產(chǎn)品類型   一抗  

研究領(lǐng)域     細(xì)胞生物 細(xì)胞周期蛋白 激酶和磷酸酶 表觀遺傳學(xué)

蛋白分子量  predicted molecular weight: 44kDa

性    狀   Lyophilized or Liquid

免 疫 原 KLH conjugated synthetic peptide derived from human PTEN 

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

一種抑制基因抗體（N端）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 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 Potential tumor suppressor. Acts as a phosphoinositide3-phosphatase by regulating PtdIns (3,4,5)P3 levels. Involved in regulation of the AKT1 signaling pathway. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation.The PTEN/MMAC1 discovers the first to have the suppress of the phosphoric acid enzyme activity cancer gene currently.The gene of PTEN locates the chromosome10q23 area, sending forth sex tumor and a few households cancers with the variety to suffer from the comprehensive disease easilyrelevant.The activity that passes to repress the Akt regulates the cell period, the cell ground rule decease and glues to connect.This text discussed PTEN structure, function and its correlationses, the PTEN is in tumor repress function mechanism.

Function : Tumor suppressor. Acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine-phosphorylated proteins. Also acts as a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring from phosphatidylinositol 3,4,5-trisphosphate, phosphatidylinositol 3,4-diphosphate, phosphatidylinositol 3-phosphate and inositol 1,3,4,5-tetrakisphosphate with order of substrate preference in vitro PtdIns(3,4,5)P3 > PtdIns(3,4)P2 > PtdIns3P > Ins(1,3,4,5)P4. The lipid phosphatase activity is critical for its tumor suppressor function. Antagonizes the PI3K-AKT/PKB signaling pathway by dephosphorylating phosphoinositides and thereby modulating cell cycle progression and cell survival. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation. Dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. Plays a role as a key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. The nuclear monoubiquitinated form possesses greater apoptotic potential, whereas the cytoplasmic nonubiquitinated form induces less tumor suppressive ability.

Subunit : Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro. Interacts with MAGI2, MAGI3, MAST1 and MAST3, but neither with MAST4 nor with DLG5. Interaction with MAGI2 increases protein stability. Interacts with NEDD4. Interacts with NDFIP1 and NDFIP2; in the presence of NEDD4 or ITCH, this interaction promotes PTEN ubiquitination. Interacts (via C2 domain) with FRK. Interacts with USP7; the interaction is direct. Interacts with ROCK1. Interacts with XIAP/BIRC4.

Subcellular Location : Cytoplasm. Nucleus. Nucleus, PML body. Note=Monoubiquitinated form is nuclear. Nonubiquitinated form is cytoplasmic. Colocalized with PML and USP7 in PML nuclear bodies. XIAP/BIRC4 promotes its nuclear localization.

Post-translational modifications : Constitutively phosphorylated by CK2 under normal conditions. Phosphorylated in vitro by MAST1, MAST2 and MAST3. Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit or promote PDZ-binding. Phosphorylation at Tyr-336 by FRK/PTK5 protects this protein from ubiquitin-mediated degradation probably by inhibiting its binding to NEDD4. Phosphorylation by ROCK1 is essential for its stability and activity. Phosphorylation by PLK3 promotes its stability and prevents its degradation by the proteasome.

Monoubiquitinated; monoubiquitination is increased in presence of retinoic acid. Deubiquitinated by USP7; leading to its nuclear exclusion. Monoubiquitination of one of either Lys-13 and Lys-289 amino acid is sufficient to modulate PTEN compartmentalization. Ubiquitinated by XIAP/BIRC4.

DISEASE : Defects in PTEN are a cause of Cowden disease (CD) [MIM:158350]; also known as Cowden syndrome (CS). CD is an autosomal dominant cancer predisposition syndrome associated with elevated risk for tumors of the breast, thyroid and skin. The predominant phenotype for CD is multiple hamartoma syndrome, in many organ systems including the breast (70% of CD patients), thyroid (40-60%), skin, CNS (40%), gastrointestinal tract. Affected individuals are at an increased risk of both breast and thyroid cancers. Trichilemmomas (benign tumors of the hair follicle infundibulum), and mucocutaneous papillomatosis (99%) are hallmarks of CD.

Defects in PTEN are the cause of Lhermitte-Duclos disease (LDD) [MIM:158350]; also known as cerebelloparenchymal disorder VI. LDD is characterized by dysplastic gangliocytoma of the cerebellum which often results in cerebellar signs and seizures. LDD and CD seem to be the same entity, and are considered as hamartoma-neoplasia syndromes.

Defects in PTEN are a cause of Bannayan-Zonana syndrome (BZS) [MIM:153480]; also known as Ruvalcaba-Myhre-Smith syndrome (RMSS) or Bannayan-Riley-Ruvalcaba syndrome (BRRS). In BZS there seems not to be an increased risk of malignancy. It has a partial clinical overlap with CD. BZS is characterized by the classic triad of macrocephaly, lipomatosis and pigmented macules of the gland penis.

Defects in PTEN are a cause of head and neck squamous cell carcinomas (HNSCC) [MIM:275355]; also known as squamous cell carcinoma of the head and neck.

Defects in PTEN are a cause of susceptibility to endometrial cancer (ENDMC) [MIM:608089].

Note=PTEN mutations are found in a subset of patients with Proteus syndrome, a genetically heterogeneous condition. The molecular diagnosis of PTEN mutation positive cases classifies Proteus syndrome patients as part of the PTEN hamartoma syndrome spectrum. As such, patients surviving the early years of Proteus syndrome are likely at a greater risk of developing malignancies.

Defects in PTEN are a cause of susceptibility to glioma type 2 (GLM2) [MIM:613028]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas.

[DISEASE] Defects in PTEN are a cause of VACTERL association with hydrocephalus (VACTERL-H) [MIM:276950]. VACTERL is an acronym for vertebral anomalies, anal atresia, congenital cardiac disease, tracheoesophageal fistula, renal anomalies, radial dysplasia, and other limb defects.

Defects in PTEN may be a cause of susceptibility to prostate cancer (PC) [MIM:176807]. It is a malignancy originating in tissues of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma.

Defects in PTEN are a cause of macrocephaly/autism syndrome (MCEPHAS) [MIM:605309]. Patients have autism spectrum disorders and macrocephaly, with head circumferences ranging from +2.5 to +8 SD for age and sex (average head circumference +4.0 SD).

Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.

Similarity : Contains 1 C2 tensin-type domain.

Contains 1 phosphatase tensin-type domain.

Database links : UniProtKB/Swiss-Prot: P60484.1

PTEN是一種抑制基因（N端抗體），在維持細(xì)胞的增殖、分化和凋亡平衡起重要作用，該基因在許多常表現(xiàn)為突變或雜合性丟失，NMAC1主要用于、乳腺、、非何杰金氏各種的研究.

Anti-CD158b2/KIR2DL3/NKAT2a/FITC 熒光素標(biāo)記NK細(xì)胞抑制性受體2DL3抗體IgGMulti-class antibodies規(guī)格： 0.2ml

Anti-IL-3R Alpha/CD123/FITC 熒光素標(biāo)記白介素3受體a鏈抗體IgGMulti-class antibodies規(guī)格： 0.2ml

Rhesus antibody Rh CD33/Siglec-3 CD33抗體 規(guī)格 0.1ml

N-cadherin N-鈣粘附分子抗原 0.5mg

Id1 英文名稱： DNA結(jié)合抑制因子1抗體 0.2ml

Rhesus antibody Rh SULT1A1 芳基磺基轉(zhuǎn)移酶1抗體 規(guī)格 0.2ml

Anti-IL-3R Alpha/CD123/FITC 熒光素標(biāo)記白介素3受體a鏈抗體IgGMulti-class antibodies規(guī)格： 0.2ml

human Mus musculus similar to 60S ribosomal protein L12,LOC382344 ELISA kit 人類似60S核糖體蛋白L21Multi-class antibodies規(guī)格： 48T

Anti-Phospho-SHIP2 (Tyr986/987) 磷酸化蛋白酪氨酸磷酸酶2抗體Multi-class antibodies規(guī)格： 0.1ml

Rhesus antibody Rh Goat Anti-rat IgG/PE-Cy3 PE-Cy3標(biāo)記的羊抗大鼠IgG 規(guī)格 0.1ml

Alpha-Fodrin IgG/IgA ELISA Kit 大鼠抗α-胞襯蛋白抗體IgG/IgA 96T

NFIC 英文名稱： 核因子1C型抗體 0.2ml

BCNP 英文名稱： B淋巴細(xì)胞新型蛋白1抗體 0.2ml

Anti-Phospho-SHIP2 (Tyr986/987) 磷酸化蛋白酪氨酸磷酸酶2抗體Multi-class antibodies規(guī)格： 0.1ml

PAPP-A(Human pregnancy associated plasma protein A) ELISA Kit 人相關(guān)血漿蛋白AMulti-class antibodies規(guī)格： 48T

Anti-Phospho-PKR (Thr446) 磷酸化蛋白激酶R抗體Multi-class antibodies規(guī)格： 0.1ml

Rhesus antibody Rh HEATR3 HEATR3蛋白抗體 規(guī)格 0.2ml

SHBG ELISA Kit 大鼠性激素結(jié)合球蛋白 96T

phospho-P53(Ser315) 英文名稱： 磷酸化抑制基因P53抗體 0.1ml

Cytohesin 2 英文名稱： 胞粘蛋白2抗體 0.2ml

Anti-Phospho-PKR (Thr446) 磷酸化蛋白激酶R抗體Multi-class antibodies規(guī)格： 0.1ml

CL-0168Neuro-2a/N2a(小鼠腦神經(jīng)瘤細(xì)胞)5×106cells/瓶×2

GSK3B Others Human 人 GSK3B 桿狀病毒-昆蟲細(xì)胞裂解液 (陽(yáng)性對(duì)照)

人視網(wǎng)膜色素上皮細(xì)胞裂解物HRPEpiCL

NCI-H1755[H1755]細(xì)胞，人細(xì)胞 人胚,HELF細(xì)胞 卵巢上皮細(xì)胞Many types of cells包裝：5 × 105次方(1ml)

兔主動(dòng)脈平滑肌細(xì)胞;SMC

TIMP2 Others Human 人 TIMP2 / TIMP-2 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)

CL-0167NCI-H292(人細(xì)胞)5×106cells/瓶×2

CD8B Others Human 人 CD8B / P37 / LEU2 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)

小鼠腸內(nèi)皮細(xì)胞完全培養(yǎng)基 100mL

marc-145猴胚胎腎上皮細(xì)胞 Marc-145 monkey embryonic kidney epithelial cells DMEM+10% FBS

LIF Protein Human 重組人 LIF 蛋白 (Fc 標(biāo)簽)

RK1(大鼠腎細(xì)胞) 5×106cells/瓶×2 786-0(腎透明細(xì)胞腺癌)

一種抑制基因抗體（N端）規(guī)格 KLK6 Others Human 人 KLK6 / Kallikrein 6 / Neurosin 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)

人腦微內(nèi)皮細(xì)胞

大鼠視網(wǎng)膜色素上皮細(xì)胞完全培養(yǎng)基 100mL

Tca-8113人舌鱗癌細(xì)胞 Tca-8113 human tongue squamous cell carcinoma 1640+10% FBS

IL11RA Protein Canine 重組狗 IL11RA / IL-11RA / IL11Rα 蛋白 (His 標(biāo)簽)

NCI-H2452(人間皮瘤細(xì)胞) 5×106cells/瓶×2 L1210(細(xì)胞)

抗體的生物素化標(biāo)記實(shí)驗(yàn)要點(diǎn)：

1. 一種抑制基因抗體（N端）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、異咪唑基及苯酚基,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）一種抑制基因抗體（N端）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?？贵w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。