PLA0309
Mouse anti-Rictor Monoclonal Antibody, Affinity Purified
Powered by Bethyl Laboratories, Inc., clone IG3P2C9
别名:
AVO3, AVO3 homolog, KIAA1999, MGC39830, PIA, RPTOR independent companion of MTOR, TORC2-specific protein AVO3, complex 2, hAVO3, pianissimo, rapamycin-insensitive companion of mTOR
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所有图片(1)
About This Item
UNSPSC代码:
12352203
NACRES:
NA.41
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生物来源
mouse
质量水平
抗体形式
affinity purified immunoglobulin
抗体产品类型
primary antibodies
等级
Powered by Bethyl Laboratories, Inc.
克隆
IG3P2C9, monoclonal
种属反应性
human
浓度
1 mg/mL
技术
immunofluorescence: 1:500-1:2,000
immunohistochemistry: 1:100- 1:500
immunoprecipitation (IP): 3 μg/mg
western blot: 1:1,000
同位素/亚型
IgG1κ
登记号
Q6R327
UniProt登记号
运输
wet ice
储存温度
2-8°C
靶向翻译后修饰
unmodified
基因信息
human ... RICTOR(253260)
免疫原
The epitope recognized by PLA0309 maps to a region between residue 1650 and the C-terminus (residue 1708) of human Rapamycin-Insensitive Companion of mTOR using the numbering given in TrEMBL entry Q6R327 (GeneID 253260).
外形
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide
其他说明
Rictor (rapamycin insensitive companion of TOR) is part of the rapamycin insensitive mTORC2 complex which includes mTOR, mLST8/GbetaL, Sin1, and protor 1. The mTORC2 complex appears to function in the regulation of cytoskeletal organization and has been shown to phosphorylate Akt/PKB.
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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储存分类代码
12 - Non Combustible Liquids
WGK
nwg
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
Mario Palma et al.
Cell & bioscience, 13(1), 232-232 (2023-12-23)
mTORC2 is a critical regulator of cytoskeleton organization, cell proliferation, and cancer cell survival. Activated mTORC2 induces maximal activation of Akt by phosphorylation of Ser-473, but regulation of Akt activity and signaling crosstalk upon growth factor stimulation are still unclear.
Kaixuan Shi et al.
Cell death and differentiation, 30(1), 195-207 (2022-09-29)
Despite remarkable efficacy, targeted treatments often yield a subpopulation of residual tumor cells in part due to non-genetic adaptions. Previous mechanistic understanding on the emergence of these drug-tolerant persisters (DTPs) has been limited to epigenetic and transcriptional reprogramming. Here, by
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