别名：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.
研究领域：肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡 激酶和磷酸酶
抗体来源：Mouse
克隆类型：Monoclonal
克 隆 号：10D8
交叉反应：Human
产品应用：WB=1:500-1000, ICC=1:100, ELISA=1:5000-10000
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理论分子量：56kDa
细胞定位：细胞核 细胞浆 细胞膜
性 状：Liquid
浓 度：1mg/ml
免 疫 原：KLH conjugated synthetic peptide derived from human AKT: 420-479/479
亚 型：IgG
纯化方法：affinity purified by Protein G
缓 冲 液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件：Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
注意事项：This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed：PubMed
产品介绍：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
激酶和磷酸酶（Kinases and Phosphatases）
Akt/PKB(Protein kinase B;Protein kinase beta, gamma;PKB gamma;STK-2 )是丝氨酸/苏氨酸蛋白激酶家族成员，可使蛋白磷酸化，也可自身磷酸化,在调节细胞存活中起重要作用。
Akt1/PKBa是一种丝氨酸/苏氨酸蛋白激酶，其激酶活力在包括细胞凋亡、糖原合成和细胞生长等的各种细胞功能中起着关键作用。Akt1/PKBa 被各种生长因子和存活因子所活化。其308位苏氨酸残基、473位丝氨酸残基和474位酪氨酸残基的磷酸化对于该酶的充分活化是不可或缺的。Akt1/PKBa通过对包括胱冬酶-9在内的几种靶标的磷酸化和失活而抑制细胞凋亡。 Akt1/PKBa 通过对糖原合酶激酶-3a和3b的磷酸化和失活来调节糖原合成。已鉴定了3种亚型的哺乳动物Akt1/PKBa。在很多种癌症中AKT都有非正常表达或过表达。
Murine thymoma viral(v-akt) oncogene homolog-2(AKT-2;PRKBB)—蛋白激酶AKT-2，被认为也是原癌基因之一。受PDGF，EGF，FGF激活，经过phosphatidylinositol 3-kinase作用而活化。通过对凋亡调控蛋白的磷酸化而灭活其活性，抑制细胞的凋亡.
研究领域：肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡 激酶和磷酸酶
抗体来源：Mouse
克隆类型：Monoclonal
克 隆 号：10D8
交叉反应：Human
产品应用：WB=1:500-1000, ICC=1:100, ELISA=1:5000-10000
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理论分子量：56kDa
细胞定位：细胞核 细胞浆 细胞膜
性 状：Liquid
浓 度：1mg/ml
免 疫 原：KLH conjugated synthetic peptide derived from human AKT: 420-479/479
亚 型：IgG
纯化方法：affinity purified by Protein G
缓 冲 液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件：Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
注意事项：This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed：PubMed
产品介绍：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
激酶和磷酸酶（Kinases and Phosphatases）
Akt/PKB(Protein kinase B;Protein kinase beta, gamma;PKB gamma;STK-2 )是丝氨酸/苏氨酸蛋白激酶家族成员，可使蛋白磷酸化，也可自身磷酸化,在调节细胞存活中起重要作用。
Akt1/PKBa是一种丝氨酸/苏氨酸蛋白激酶，其激酶活力在包括细胞凋亡、糖原合成和细胞生长等的各种细胞功能中起着关键作用。Akt1/PKBa 被各种生长因子和存活因子所活化。其308位苏氨酸残基、473位丝氨酸残基和474位酪氨酸残基的磷酸化对于该酶的充分活化是不可或缺的。Akt1/PKBa通过对包括胱冬酶-9在内的几种靶标的磷酸化和失活而抑制细胞凋亡。 Akt1/PKBa 通过对糖原合酶激酶-3a和3b的磷酸化和失活来调节糖原合成。已鉴定了3种亚型的哺乳动物Akt1/PKBa。在很多种癌症中AKT都有非正常表达或过表达。
Murine thymoma viral(v-akt) oncogene homolog-2(AKT-2;PRKBB)—蛋白激酶AKT-2，被认为也是原癌基因之一。受PDGF，EGF，FGF激活，经过phosphatidylinositol 3-kinase作用而活化。通过对凋亡调控蛋白的磷酸化而灭活其活性，抑制细胞的凋亡.
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一． 买方对产品的使用：产品应当用于实验室研究目的，不可用作其他用途（包括但不限于：体外诊断、食品、药物、医疗器械、人用或兽用治疗、化妆品或其他商业用途）。购买方应明确清楚知道此声明，并严格遵守。如有任何因购买方隐瞒真实购买意图，由此引起的法律责任以及一切法律后果，由购买方承担。
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三． 质量责任：我司保证所供产品质量与随货COA所列标准相符。买方应以产品制造商的标准作为验收标准。鉴于化学品的特殊性，卖方对未使用之前的产品质量负责，对化学品的应用不负有任何直接与间接的责任。卖方提醒买方：在做实验之前，预先按照技术规范检验产品质量。在产品开始使用之后，买方对应用及其结果负有全部责任。若有质量异议，买方需在收到货物后10个工作日内书面通知卖方，过期无效。
四． 有限保证：在适用法律允许的最大限度内，卖方提供的产品均“按现状条件”提供给买方，卖方不作对产品和/或其使用的各种明示或默示的保证（包括但不限于对适销性、适合用于特殊用途及不侵权的所有明示或默示保证）或卖方产品会达到任何特定结果或不会被中断或不会有错误的保证。
五． 责任限制：在适用法律允许的最大限度内，卖方不对以任何方式由本合同、卖方产品或使用卖方产品引起的或与此有关的任何利润或收入损失或其他后果性损失、随附性损失、特殊损失、惩罚性损失或任何其他间接损失或损害承担责任。在适用法律允许的最大限度内，卖方的最高赔偿限额为买方就所涉及的卖方产品实际支付给卖方的价格。
六． 如卖方因不可抗拒力原因无法供货，卖方将及时通知买方，双方将视情况决定部分不履行、全部不履行或延期履行；如供货期限届满日为国内外重大节日或国家法定假日，则供货期限顺延；若因缺货导致延期交货或无法供货，卖方将及时告知买方，并不视为卖方违约。不可抗力：因火灾、洪水、风暴、爆炸、恐怖事件、战争、政府行为或任何其他卖方无法预见、无法避免和无法克服的事件造成延期交货或无法交货的，卖方不承担任何责任。
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支付：
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电话 021-60543596
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帐号 454663168779
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运输：
（1）生物试剂需要冷冻运输，运输需要泡沫盒和一定量的冰袋（特殊商品需要干冰），运费金额会开进发票里。运费以显示为准
（2）常规试剂采用快递，运费以显示为准。
（3）大物件一般默认发德邦物流，运费需联系客服计算。
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通用销售条款
一． 买方对产品的使用：产品应当用于实验室研究目的，不可用作其他用途（包括但不限于：体外诊断、食品、药物、医疗器械、人用或兽用治疗、化妆品或其他商业用途）。购买方应明确清楚知道此声明，并严格遵守。如有任何因购买方隐瞒真实购买意图，由此引起的法律责任以及一切法律后果，由购买方承担。
二． 准确订货：下订单时，买方应预先仔细审阅产品的技术指标，确认无误。不详之处应立即查询。订单及产品一经发出，即视为买方认可有关产品的技术指标。
三． 质量责任：我司保证所供产品质量与随货COA所列标准相符。买方应以产品制造商的标准作为验收标准。鉴于化学品的特殊性，卖方对未使用之前的产品质量负责，对化学品的应用不负有任何直接与间接的责任。卖方提醒买方：在做实验之前，预先按照技术规范检验产品质量。在产品开始使用之后，买方对应用及其结果负有全部责任。若有质量异议，买方需在收到货物后10个工作日内书面通知卖方，过期无效。
四． 有限保证：在适用法律允许的最大限度内，卖方提供的产品均“按现状条件”提供给买方，卖方不作对产品和/或其使用的各种明示或默示的保证（包括但不限于对适销性、适合用于特殊用途及不侵权的所有明示或默示保证）或卖方产品会达到任何特定结果或不会被中断或不会有错误的保证。
五． 责任限制：在适用法律允许的最大限度内，卖方不对以任何方式由本合同、卖方产品或使用卖方产品引起的或与此有关的任何利润或收入损失或其他后果性损失、随附性损失、特殊损失、惩罚性损失或任何其他间接损失或损害承担责任。在适用法律允许的最大限度内，卖方的最高赔偿限额为买方就所涉及的卖方产品实际支付给卖方的价格。
六． 如卖方因不可抗拒力原因无法供货，卖方将及时通知买方，双方将视情况决定部分不履行、全部不履行或延期履行；如供货期限届满日为国内外重大节日或国家法定假日，则供货期限顺延；若因缺货导致延期交货或无法供货，卖方将及时告知买方，并不视为卖方违约。不可抗力：因火灾、洪水、风暴、爆炸、恐怖事件、战争、政府行为或任何其他卖方无法预见、无法避免和无法克服的事件造成延期交货或无法交货的，卖方不承担任何责任。
订购方式：
（1）直接注册www.ruichubio.com网站会员后直接在线订购支持支付宝、微信和公务卡支付；
（2）拨打021-59145618订购热线订购;
（3）登录www.ruichubio.com下载中心下载订购单发送至：order@ruichubio.com订购
注：在邮件确认合同或订购单情况下，可以货物和发票一起寄送，对公转账。
发票：
本公司出具增值税普通发票和增值税专用发票，适合您报销。发票面额为含税后的货物价格和运费，请您放心购买，我们会将运费开进发票里。请在拍下时在备注一栏里写上发票抬头。
支付：
开票账户：
公司名称 上海瑞楚生物科技有限公司
电话 021-60543596
纳税人识别号 91310116057685530X
开户银行全称 中国银行股份有限公司上海市长宁支行
帐号 454663168779
帐 户 名 上海瑞楚生物科技有限公司
账 号 epay@ruichubio.com
为了方便高校科研单位公务卡结算，本网站开通了公务卡支付。可以在线下单选择支付宝付款，登录支付宝账号添加银行卡（输入公务卡号就可以）（公务卡一般就是信用卡,请按信用卡支付方式支付)。
运输：
（1）生物试剂需要冷冻运输，运输需要泡沫盒和一定量的冰袋（特殊商品需要干冰），运费金额会开进发票里。运费以显示为准
（2）常规试剂采用快递，运费以显示为准。
（3）大物件一般默认发德邦物流，运费需联系客服计算。
