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About This Item
NACRES:
NA.41
UNSPSC Code:
12352203
Conjugate:
unconjugated
Clone:
IG3P2C9, monoclonal
Application:
IF, IHC, IP, WB
Citations:
2
biological source
mouse
conjugate
unconjugated
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
IG3P2C9, monoclonal
species reactivity
human
concentration
1 mg/mL
technique(s)
immunofluorescence: 1:500-1:2,000, immunohistochemistry: 1:100- 1:500, immunoprecipitation (IP): 3 μg/mg, western blot: 1:1,000
isotype
IgG1κ
accession no.
Q6R327
UniProt accession no.
shipped in
wet ice
storage temp.
2-8°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... RICTOR(253260)
Immunogen
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).
Physical form
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide
Other Notes
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.
Disclaimer
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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Storage Class
12 - Non Combustible Liquids
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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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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