123.130.221.191：建立内容为“{{protein |Name=v-akt鼠胸腺瘤病毒癌基因同源物1 |image=3MV5.pdb.jpg |caption= Akt-1-抑制复合体的晶体结构{{…”的新页面

2021-07-21T18:32:26Z

建立内容为“{{protein |Name=v-akt鼠胸腺瘤病毒癌基因同源物1 |image=3MV5.pdb.jpg |caption= Akt-1-抑制复合体的晶体结构<ref name="pmid20481595">{{…”的新页面

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{{protein
|Name=[[AKT1|v-akt鼠胸腺瘤病毒癌基因同源物1]]
|image=3MV5.pdb.jpg
|caption= Akt-1-抑制复合体的晶体结构<ref name="pmid20481595">{{PDB|3MV5}}; {{cite journal | author = Freeman-Cook KD, Autry C, Borzillo G, Gordon D, Barbacci-Tobin E, Bernardo V, Briere D, Clark T, Corbett M, Jakubczak J, Kakar S, Knauth E, Lippa B, Luzzio MJ, Mansour M, Martinelli G, Marx M, Nelson K, Pandit J, Rajamohan F, Robinson S, Subramanyam C, Wei L, Wythes M, Morris J | title = Design of selective, ATP-competitive inhibitors of Akt | journal = J. Med. Chem. | volume = 53 | issue = 12 | pages = 4615–22 | year = 2010 | month = June | pmid = 20481595 | doi = 10.1021/jm1003842 }}</ref>。
|width=
|HGNCid=391
|Symbol=AKT1
|AltSymbols=
|EntrezGene=207
|OMIM=164730
|RefSeq=NM_005163
|UniProt=P31749
|PDB=
|ECnumber=
|Chromosome=14
|Arm=q
|Band=32.32
|LocusSupplementaryData=-32.33
}}
{{protein
|Name=[[AKT1|v-akt鼠胸腺瘤病毒癌基因同源物1]]
|image=Crystal structure of Akt-1-inhibitor complexes.png
|caption= 以丝带模型表示的Akt-1-抑制复合体的晶体结构<ref name="pmid20481595"/>。
|width=
|HGNCid=391
|Symbol=AKT1
|AltSymbols=
|EntrezGene=207
|OMIM=164730
|RefSeq=NM_005163
|UniProt=P31749
|PDB=
|ECnumber=
|Chromosome=14
|Arm=q
|Band=32.32
|LocusSupplementaryData=-32.33
}}
{{protein
|Name=[[AKT2|v-akt鼠胸腺瘤病毒癌基因同源物2]]
|image=3D0E Ribbon.png
|caption=Akt-2-抑制复合体的晶体结构<ref name="pmid18800763">{{PDB|3D0E}}; {{cite journal | author = Heerding DA, Rhodes N, Leber JD, Clark TJ, Keenan RM, Lafrance LV, Li M, Safonov IG, Takata DT, Venslavsky JW, Yamashita DS, Choudhry AE, Copeland RA, Lai Z, Schaber MD, Tummino PJ, Strum SL, Wood ER, Duckett DR, Eberwein D, Knick VB, Lansing TJ, McConnell RT, Zhang S, Minthorn EA, Concha NO, Warren GL, Kumar R | title = Identification of 4-(2-(4-amino-1,2,5-oxadiazol-3-yl)-1-ethyl-7-{[(3S)-3-piperidinylmethyl]oxy}-1H-imidazo[4,5-c]pyridin-4-yl)-2-methyl-3-butyn-2-ol (GSK690693), a novel inhibitor of AKT kinase | journal = J. Med. Chem. | volume = 51 | issue = 18 | pages = 5663–79 | year = 2008 | month = September | pmid = 18800763 | doi = 10.1021/jm8004527 }}</ref>。
|width=
|HGNCid=392
|Symbol=AKT2
|AltSymbols=
|EntrezGene=208
|OMIM=164731
|RefSeq=NM_001626
|UniProt=P31751
|PDB=
|ECnumber=
|Chromosome=19
|Arm=q
|Band=13.1
|LocusSupplementaryData=-13.2
}}
{{protein
|Name=[[AKT3|v-akt鼠胸腺瘤病毒癌基因同源物3（蛋白激酶B，γ）]]
|caption=
|image=
|width=
|HGNCid=393
|Symbol=AKT3
|AltSymbols=
|EntrezGene=10000
|OMIM=
|RefSeq=NM_181690
|UniProt=Q9Y243
|PDB=
|ECnumber=
|Chromosome=1
|Arm=q
|Band=43
|LocusSupplementaryData=-44
}}
'''Akt'''，亦被称为'''蛋白激酶B'''（'''PKB'''），是在如如[[葡萄]][[糖代谢]]、[[凋亡]]、[[细胞]][[增殖]][[转录]]及[[细胞迁移]]等多种细胞过程中起到重要作用的一种[[丝氨酸]]/[[苏氨酸]]特异性[[蛋白激酶]]。

==家族成员==

Akt1通过抑制凋亡过程从而参与细胞存活途径。Akt1亦能诱导[[蛋白合成]]通路，故其在导致[[骨骼肌]]肥大及的一般组织生长的细胞通路中是一种重要信号[[蛋白]]。因其可以阻断凋亡并继而促进细胞存活，现已表明Akt1在多种[[肿瘤]]中起到主要作用。Akt（先亦被称为Akt1）首先是在转化[[逆转录病毒]]AKT8中被鉴定为[[癌基因]]的<ref name="pmid197531">{{cite journal | author = Staal SP, Hartley JW, Rowe WP | title = Isolation of transforming murine leukemia viruses from mice with a high incidence of spontaneous lymphoma | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 74 | issue = 7 | pages = 3065–7 | year = 1977 | month = July | pmid = 197531 | pmc = 431413 | doi = 10.1073/pnas.74.7.3065| url = | issn = }}</ref>。

Akt2在[[胰岛素信号转导通路与血糖调节|胰岛素信号通路]]中是一重要的[[信号分子]]。需要其来诱导[[葡萄糖]]转运。在敲除Akt1但具正常Akt2的小鼠中，[[血糖]][[稳态]]不受干扰，但动物体型会较小，这与Akt1在生长中起得作用是一致的。相反，Akt2缺失但具有正常Akt1的的小鼠生长略缺陷且表现出[[糖尿病]][[表型]]（[[胰岛素]]抵抗），这从另一方面印证了Akt2对胰岛素[[受体]]信号通路更具特异性的这一设想<ref name="pmid12843127">{{cite journal | author = Garofalo RS, Orena SJ, Rafidi K, Torchia AJ, Stock JL, Hildebrandt AL, Coskran T, Black SC, Brees DJ, Wicks JR, McNeish JD, Coleman KG | title = Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta | journal = J. Clin. Invest. | volume = 112 | issue = 2 | pages = 197–208 | year = 2003 | month = July | pmid = 12843127 | pmc = 164287 | doi = 10.1172/JCI16885 | url = }}</ref>。

Akt3似乎主要在脑中表达，但其作用仍未明晰。有报道显示Akt3缺失的小鼠[[脑部]]较小<ref name="pmid15046607">{{cite journal | author = Yang ZZ, Tschopp O, Baudry A, Dümmler B, Hynx D, Hemmings BA | title = Physiological functions of protein kinase B/Akt | journal = Biochem. Soc. Trans. | volume = 32 | issue = Pt 2 | pages = 350–4 | year = 2004 | month = April | pmid = 15046607 | doi = 10.1042/BST0320350}}</ref>。

==参考文献==

<div class="references-small"> <references></references> </div>

==深入阅读==
*{{cite journal | pmid = 19319914 | pmc = 2954189 | doi=10.1002/bies.200900005 | volume=31 | issue=5 | journal = BioEssays | year=2009 | title = Switching Akt: from survival signaling to deadly response | month=May | pages=492–5 | author=Los M, Maddika S, Erb B, Schulze-Osthoff K}}
*{{cite journal | author=Quaresma AJ, Sievert R, Nickerson JA |title=Regulation of mRNA export by the PI3 kinase/AKT signal transduction pathway. |journal=Mol. Biol. Cell. |volume=April |issue= 8 |pages= 1208-21 |year= 2013 |pmid= 23427269 |doi= 10.1091/mbc.E12-06-0450 | pmc=3623641 }}

== 外部链接 ==
* {{MeshName|Proto-Oncogene+Proteins+c-akt}}

{{-}}
{{丝氨酸/苏氨酸特异性蛋白激酶类}}
{{癌基因}}

{{DEFAULTSORT:Akt}}

[[Category:EC 2.7.11]] [[Category:蛋白激酶]]
==参考来源==
*[http://zh.wikipedia.org/wiki/%E8%9B%8B%E7%99%BD%E6%BF%80%E9%85%B6B 维基百科-蛋白激酶B]

蛋白激酶B - 版本历史

123.130.221.191：建立内容为“{{protein |Name=v-akt鼠胸腺瘤病毒癌基因同源物1 |image=3MV5.pdb.jpg |caption= Akt-1-抑制复合体的晶体结构{{…”的新页面