国产毛片高清-国产毛片电影-国产码欧美日韩高清综合一区-国产麻豆永久视频-日批视频网站-日批视频免费在线观看

最近搜索:細胞培養 微生物學 分子生物 生物化學
首頁>>免疫學>>一抗>>磷酸化蛋白激酶B抗體
磷酸化蛋白激酶B抗體
  • 產品貨號:
    BN40277R
  • 中文名稱:
    磷酸化蛋白激酶B抗體
  • 英文名稱:
    Rabbit anti-phospho-AKT1(Ser129) Polyclonal antibody
  • 品牌:
    Biorigin
  • 貨號

    產品規格

    售價

    備注

  • BN40277R-100ul

    100ul

    ¥2470.00

    交叉反應:Human,Mouse(predicted:Rat,Chicken,Dog,Horse) 推薦應用:WB,IHC-P,IHC-F,ICC,IF,Flow-Cyt,ELISA

產品描述

英文名稱phospho-AKT1(Ser129)
中文名稱磷酸化蛋白激酶B抗體
別    名AKT1 (phospho S129); p-AKT1 (phospho S129); AKT 1; AKT; AKT1; AKT-1; AKT1_HUMAN; C AKT; cAKT; MGC9965; MGC99656; Oncogene AKT1; PKB; PKB alpha; PKB-ALPHA; PRKBA; Protein Kinase B Alpha; Protein kinase B; Proto-oncogene c-Akt; RAC Alpha; RAC alpha serine/threonine protein kinase; RAC; RAC PK Alpha; Rac protein kinase alpha; RAC Serine/Threonine Protein Kinase; RAC-alpha serine/threonine-protein kinase; RAC-PK-alpha; v akt murine thymoma viral oncogene homolog 1; vAKT Murine Thymoma Viral Oncogene Homolog 1.  
產品類型磷酸化抗體 
抗體來源Rabbit
克隆類型Polyclonal
交叉反應Human, Mouse,  (predicted: Rat, Chicken, Dog, Horse, )
產品應用WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=2ug/Test ICC=1:100 IF=1:100-500 (石蠟切片需做抗原修復)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量56kDa
細胞定位細胞核 細胞漿 細胞膜 
性    狀Liquid
濃    度1mg/ml
免 疫 原KLH conjugated Synthesised phosphopeptide derived from human Akt1 around the phosphorylation site of Ser129:DN(p-S)GA 
亞    型IgG
純化方法affinity purified by Protein A
儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMedPubMed
產品介紹The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Mutations in this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2011]

Function:
AKT1 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface. Phosphorylation of PTPN1 at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling. Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport. AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity. Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven. AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase). Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization. In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'. FOXO3 and FOXO4 are phosphorylated on equivalent sites. AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein). The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1. AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis. Activates the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis. Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI(3)P-5 activity. The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth. AKT plays a role as 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. Signals downstream of phosphatidylinositol 3-kinase (PI(3)K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). AKT mediates the antiapoptotic effects of IGF-I. Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly. May be involved in the regulation of the placental development. Phosphorylates STK4/MST1 at 'Thr-120' and 'Thr-387' leading to inhibition of its: kinase activity, nuclear translocation, autophosphorylation and ability to phosphorylate FOXO3. Phosphorylates STK3/MST2 at 'Thr-117' and 'Thr-384' leading to inhibition of its: cleavage, kinase activity, autophosphorylation at Thr-180, binding to RASSF1 and nuclear translocation. Phosphorylates SRPK2 and enhances its kinase activity towards SRSF2 and ACIN1 and promotes its nuclear translocation. Phosphorylates RAF1 at 'Ser-259' and negatively regulates its activity. Phosphorylation of BAD stimulates its pro-apoptotic activity.
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.

Subunit:
Interacts (via the C-terminus) with CCDC88A (via its C-terminus). Interacts with GRB10; the interaction leads to GRB10 phosphorylation thus promoting YWHAE-binding. Interacts with AGAP2 (isoform 2/PIKE-A); the interaction occurs in the presence of guanine nucleotides. Interacts with AKTIP. Interacts (via PH domain) with MTCP1, TCL1A AND TCL1B. Interacts with CDKN1B; the interaction phosphorylates CDKN1B promoting 14-3-3 binding and cell-cycle progression. Interacts with MAP3K5 and TRAF6. Interacts with BAD, PPP2R5B, STK3 and STK4. Interacts (via PH domain) with SIRT1. Interacts with SRPK2 in a phosphorylation-dependent manner. Interacts with RAF1. Interacts with TRIM13; the interaction ubiquitinates AKT1 leading to its proteasomal degradation. Interacts with TNK2 and CLK2. Interacts (via the C-terminus) with THEM4 (via its C-terminus). Interacts with and phosphorylated by PDPK1.

Subcellular Location:
Cytoplasm. Nucleus. Cell membrane. Note=Nucleus after activation by integrin-linked protein kinase 1 (ILK1). Nuclear translocation is enhanced by interaction with TCL1A. Phosphorylation on Tyr-176 by TNK2 results in its localization to the cell membrane where it is targeted for further phosphorylations on Thr-308 and Ser-473 leading to its activation and the activated form translocates to the nucleus.

Tissue Specificity:
Expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.

Post-translational modifications:
O-GlcNAcylation at Thr-305 and Thr-312 inhibits activating phosphorylation at Thr-308 via disrupting the interaction between AKT1 and PDPK1. O-GlcNAcylation at Ser-473 also probably interferes with phosphorylation at this site.
Phosphorylation on Thr-308, Ser-473 and Tyr-474 is required for full activity. Activated TNK2 phosphorylates it on Tyr-176 resulting in its binding to the anionic plasma membrane phospholipid PA. This phosphorylated form localizes to the cell membrane, where it is targeted by PDPK1 and PDPK2 for further phosphorylations on Thr-308 and Ser-473 leading to its activation. Ser-473 phosphorylation by mTORC2 favors Thr-308 phosphorylation by PDPK1. Ser-473 phosphorylation is enhanced by interaction with AGAP2 isoform 2 (PIKE-A). Ser-473 phosphorylation is enhanced in focal cortical dysplasias with Taylor-type balloon cells. Ser-473 phosphorylation is enhanced by signaling through activated FLT3. Dephosphorylated at Thr-308 and Ser-473 by PP2A phosphatase. The phosphorylated form of PPP2R5B is required for bridging AKT1 with PP2A phosphatase.
Ubiquitinated via 'Lys-48'-linked polyubiquitination by ZNRF1, leading to its degradation by the proteasome. Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. TRAF6-induced 'Lys-63'-linked AKT1 ubiquitination is critical for phosphorylation and activation. When ubiquitinated, it translocates to the plasma membrane, where it becomes phosphorylated. When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome. Also ubiquitinated by TRIM13 leading to its proteasomal degradation.
Acetylated on Lys-14 and Lys-20 by the histone acetyltransferases EP300 and KAT2B. Acetylation results in reduced phosphorylation and inhibition of activity. Deacetylated at Lys-14 and Lys-20 by SIRT1. SIRT1-mediated deacetylation relieves the inhibition.

DISEASE:
Defects in AKT1 are a cause of susceptibility to breast cancer (BC) [MIM:114480]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.
Defects in AKT1 are associated with colorectal cancer (CRC) [MIM:114500].
Note=Genetic variations in AKT1 may play a role in susceptibility to ovarian cancer.
Defects in AKT1 are a cause of Proteus syndrome (PROTEUSS) [MIM:176920]. A highly variable, severe disorder of asymmetric and disproportionate overgrowth of body parts, connective tissue nevi, epidermal nevi, dysregulated adipose tissue, and vascular malformations. Many features of Proteus syndrome overlap with other overgrowth syndromes.

Similarity:
Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. RAC subfamily.
Contains 1 AGC-kinase C-terminal domain.
Contains 1 PH domain.
Contains 1 protein kinase domain.

SWISS:
P31749

Gene ID:
207

Database links:

Entrez Gene: 207 Human

Entrez Gene: 11651 Mouse

Entrez Gene: 24185 Rat

Omim: 164730 Human

SwissProt: O57513 Chicken

SwissProt: P31749 Human

SwissProt: P31750 Mouse

SwissProt: P47196 Rat

Unigene: 525622 Human

Unigene: 6645 Mouse

Unigene: 11422 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.


无码秘 蜜桃一区二区三区| 日韩欧美人妻一区二区三区| 成人免费午夜无码视频| 同学要做吗PO爱喝花茶的小酥肉| 国内A级毛片免费观看| 一区二区三区AV高清免费波多| 欧美人与性囗牲恔配| 国产XXXX做受视频国语对白L| 亚洲成人在线观看av| 蜜桃色欲AV久久无码精品软件| 成人嘿咻漫画免费入口| 亚洲AⅤ无码一区二区波多野 | 日日婷婷夜日日天干| 国模小黎大尺度精品(02)[ | 国内女人喷潮完整视频| 再灬再灬再灬深一点舒服| 日本肉体裸交XXXXBBBB| 国语自产少妇精品视频| 坐着轮流提双腿能起到什么效果| 色综合久久无码五十路人妻| 狠狠躁日日躁夜夜躁2020| 8Ⅹ8X擦拨擦拨成人免费视频| 少妇特殊按摩高潮爽翻天| 精品卡一卡三卡四卡AⅤ新区| AV无码不卡一区二区三区| 亭亭玉立国色天香四月天| 久久成人国产精品免费| 被蹂躏的她 电影| 亚洲不卡无码永久在线| 女人自熨全过程直播| 国产精品YY9299在线观看| 夜夜躁天天躁很很躁| 日韩精品卡2卡3卡4卡5| 精品国产麻豆免费人成网站 | 中文字幕一区二区三区乱码视频 | 国产超薄肉色丝袜视频| 亚洲日韩精品无码专区网站| 人妻无码一区二区19P| 国色精品卡一卡2卡3卡4卡在线| 50岁老熟女一级毛片| 我和公GONG在厨房日本电影 | 黑人顶到深处高潮颤抖| FREEⅩXX性欧美HD丝袜| 亚洲AV成人精品日韩一区18p| 男人猛躁进女人免费播放| 国产精品一区二区久久国产| 中文字幕成熟丰满人妻| 无码精品A∨在线观看十八禁| 蜜桃AV秘 无码一区二区三欧| 国产精品 高清 尿 小便 嘘嘘 | 亚洲AV无码一区二区三区在线| 欧美JIZZ18性欧美| 国产永久AV福利在线观看| AV成人羞羞漫画永久入口| 亚洲AV成人无码精品综合网站| 欧美日韩精品一区二区三区不卡| 国模少妇一区二区三区| 八戒八戒WWW资源网在线观看| 亚洲精品乱码久久久久久不卡| 日本JAPANESE猛男GAY| 久久精品AⅤ无码中文字字幕重口| 成人午夜福利无码不卡视频| 亚洲最大综合久久网成人| 少妇粉嫩小泬喷水视频在线观看| 久久人妻蜜桃一区二区三区| 国产成人一区二区青青草原| 18禁无遮挡无码网站免费| 亚洲AV无码成人精品区狼人影院| 人妻少妇被猛烈进入中文字幕| 精品国产V无码大片在线观看| 粗大的内捧猛烈进出无码| 又色又爽又黄18禁美女裸身无遮| 无码AV免费一区二区三区试看| 欧美AⅤ精品一区二区三区| 狠狠色丁香婷婷亚洲综合| 成人片黄网站色大片免费| 永久免费观看国产裸体美女| 香蕉国产成版人视频APP| 人妻大战黑人白浆狂泄| 久久久久久久精品无码AV少妇| 国产成人久久综合一区| 99国精产品灬源码1688钻| 亚洲国产美女精品久久久| 少妇高潮喷水惨叫久久久久电影| 免费 黄 色 人成 视频 在| 国内精品伊人久久久久777| 成人午夜福利视频| 综合一区无套内射中文字幕| 亚洲AV综合色区无码一区偷拍| 日日碰狠狠添天天爽| 娜娜的YIN荡生涯H全文阅读| 黑人双人RAPPER的特点| 公与憩止痒小说400章| 99国精品午夜福利视频不卡99| 亚洲国产成人久久精品软件 | WWW一区二区WWW免费| 亚洲综合一区二区三区四区五区| 无码午夜福利片在线观看 | 免费观看的AV毛片的网站| 好嗨哟片在线观看| 国产AV无码专区亚洲AV桃花庵| CAOPOREN超碰| 幼儿交1300部多少钱| 亚洲成AV人片天堂网久久| 天堂M和天堂2M区别| 漂亮人妻洗澡被公强 日日躁| 久久无码AV中文出轨人妻| 国内精品伊人久久久久影院对白| 疯狂做受XXXX高潮不断| JAPANESE军人强迫| 中国女人大白屁股ASS| 亚洲精品无码专区在线播放| 无码一区二区三区老色鬼| 日韩AV午夜在线观看| 欧美大波少妇在厨房被| 巨粗进入警花哭喊求饶| 精产国品一二三产区区别在哪儿呢| 国产高清自产拍AV在线| 趁夫不在给给公侵犯了| 97日日碰人人模人人澡| 永久免费AⅤ无码网站国产| 亚洲精品V天堂中文字幕| 香港三日本三级少妇三级视频 | 成人伊人亚洲人综合网站| 99久久免费国产精品2021| 永久免费看啪啪的网站| 亚洲人成人无码一区二区三区| 亚洲AV成人片乱码色午夜| 偷拍东北熟女BBWW| 色狠狠AV老熟女| 人妻体内射精一区二区三四| 女局长白白嫩嫩大屁股| 麻花豆传媒剧国产MV免费天美| 久久国产精品成人无码网站| 黑人大战欲求不满人妻| 国产日产欧产美韩系列| 国产成人艳妇AA视频在线| 多毛BGMBGMBGM胖在| 成 人 黄 色 网站 小说 免| Chinese老熟女老女人HD| 24种男女插秧法| 中国熟妇毛多多裸交视频| 艳妇乳肉豪妇荡乳ⅩXXOO| 亚洲欧洲日产国码中文字幕| 亚洲AV最新在线网址| 性色AV免费观看| 香蕉久久夜色精品国产| 无码专区—VA亚洲V专区VR| 无码AV最新无码AV专区| 特殊重囗味SM在线观看无码| 色噜噜狠狠色综合网| 日韩午夜理论免费TV影院| 日本真人无遮挡啪啪免费| 人人做天天爱夜夜爽2020| 人人妻人人澡人人爽人人DVD| 亲孑伦视频一区二区三区一| 欧美日韩XXOO无码专区| 欧美人和黑人牲交网站上线| 女人被弄高潮视频免费| 女人被弄到高潮的免费视频APP | 久久精品国产久精国产思思| 精品人妻中文AV一区二区三区| 精产国品一二三产区区别在线观看| 狠狠躁天天躁男人| 精品久久人妻AV中文字幕| 精品国产AV 无码一区二区三区| 教官在我腿间疯狂驰聘视频| 精品久久久久久无码人妻| 精品久久亚洲中文字幕| 久久精品AⅤ无码中文字字幕重口| 久久国产免费直播| 久久久综合九色综合88| 乱码一卡二卡新区永久入口| 蜜芽国产尤物AV尤物在线看| 妺妺窝人体色WWW在线观看婚闹 | 欧美极品小妇另类xXXX性| 欧美丰满熟妇性XXXX| 强行暴力肉体进入HDⅩXXX| 人妻少妇中文字幕在线一区| 日韩AV片无码一区二区不卡电影| 日韩亚洲欧美精品综合| 视频一区二区三区在线观看密桃| 爽到高潮无码视频在线观看| 无码人妻精一区二区三区| 亚洲A∨国产AV综合AV网站| 亚洲SSS整片AV在线播放| 亚洲欧洲日产国码无码久久99| 亚洲最新无码中文字幕久久| 中文成人久久久久影院免费观看| 91精品人妻一区二区三区蜜桃| JIZZJIZZ国产精品久久| 成人无码区免费AⅤ片WWW| 国产A V无码专区亚洲AV| 国产精品一国产精品| 护士奶头又白又大又好摸| 久久精品国产精品亚洲| 美女下部裸体张开腿视频| 欧美婷婷丁香五月社区| 日产无人区一线二线三线最新版| 私人医生H1忘记密码了怎么办|