05-1471
Anti-Rictor Antibody, clone 9F1.2
clone 9F1.2, from mouse
Synonym(s):
Rictor, AVO3, rapamycin-insensitive companion of mTOR, mAVO3
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
9F1.2, monoclonal
species reactivity
human, mouse, rat
technique(s)
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG2aκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... RICTOR(253260)
General description
Rictor, the rapamycin-insensitive complex, is part of the mTORC2 kinase complex which is responsible for phosphorylating the hydrophobic motif kinase of Akt/PKB. This complex also includes mTOR, mSin1 and mLST8/GL. mTORC2 is activated by growth factors and other mitogenic signals.
Specificity
This antibody recognizes Rictor.
Immunogen
Recombinant protein corresponding to human Rictor.
Application
Anti-Rictor Antibody, clone 9F1.2 detects level of Rictor & has been published & validated for use in WB & IP.
Immunoprecipitation:
Representative lot data.
1 ug/mL dilution of this antibody immunoprecipitated Rictor from 100 mg of HEK293 lysate.
Representative lot data.
1 ug/mL dilution of this antibody immunoprecipitated Rictor from 100 mg of HEK293 lysate.
Quality
Evaluated by Western Blotting on 10 mg of HEK293 cell lysate.
Target description
190 kDa Observed
Physical form
Format: Purified
Purified immunoglobulin in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.
Analysis Note
Control
HEK293 cell lysate.
Western Blotting Analysis: 1 µg/mL of this antibody detected Rictor on 10 µg of HEK293 cell lysate.
HEK293 cell lysate.
Western Blotting Analysis: 1 µg/mL of this antibody detected Rictor on 10 µg of HEK293 cell lysate.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Zheng Wang et al.
Neoplasia (New York, N.Y.), 23(11), 1147-1165 (2021-10-28)
Epithelial-mesenchymal transition (EMT) contributes to tumor invasion, metastasis and drug resistance. AKT activation is key in a number of cellular processes. While many positive regulators for either EMT or AKT activation have been reported, few negative regulators are established. Through
Mandy K Losiewicz et al.
Experimental eye research, 197, 108131-108131 (2020-07-06)
The retina is one of the most metabolically active tissues, yet the processes that control retinal metabolism remains poorly understood. The mTOR complex (mTORC) that drives protein and lipid biogenesis and autophagy has been studied extensively in regards to retinal
Sharon K Kuss-Duerkop et al.
PLoS pathogens, 13(9), e1006635-e1006635 (2017-09-28)
Influenza A virus usurps host signaling factors to regulate its replication. One example is mTOR, a cellular regulator of protein synthesis, growth and motility. While the role of mTORC1 in viral infection has been studied, the mechanisms that induce mTORC1
Sanjit K Dhar et al.
Oncogene, 37(48), 6225-6242 (2018-07-25)
Autophagy is a highly regulated evolutionarily conserved metabolic process induced by stress and energy deprivation. Here, we show that DNA polymerase gamma (Polγ) deficiency activates a selective prosurvival autophagic response via mitochondria-mediated reactive oxygen species (ROS) signaling and the mammalian
Mahefatiana Andrianifahanana et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 30(11), 3733-3744 (2016-11-03)
TGF-β plays a central role in the pathogenesis of fibroproliferative disorders. Defining the exact underlying molecular basis is therefore critical for the development of viable therapeutic strategies. Here, we show that expression of the facilitative glucose transporter 1 (GLUT1) is
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