Alexa Fluor® 647 Anti-Argonaute-2 antibody [EPR10411],Abcam,AB310088

How are conjugated primary antibodies validated? This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling. For suitable applications and species reactivity, please refer to the unconjugated version of this clone. What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies . Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents .

Host

Rabbit

Reactivity

Human, Mouse, Rat

Application

IHC-P, Antibody Labelling, Target Binding Affinity, ICC/IF, Flow Cyt (Intra)

Conjugate

Alexa Fluor® 647

Platform ID

BAB118676095

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAlexa Fluor® 647 Anti-Argonaute-2 antibody [EPR10411]
Cat. No.AB310088
HostRabbit
IsotypeIgG
ReactivityHuman, Mouse, Rat
ConjugationAlexa Fluor® 647
ApplicationIHC-P, Antibody Labelling, Target Binding Affinity, ICC/IF, Flow Cyt (Intra)
ClonalityMonoclonal
Clone NumberEPR10411
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data Required for RNA-mediated gene silencing (RNAi) by the RNA-induced silencing complex (RISC). The 'minimal RISC' appears to include AGO2 bound to a short guide RNA such as a microRNA (miRNA) or short interfering RNA (siRNA). These guide RNAs direct RISC to complementary mRNAs that are targets for RISC-mediated gene silencing. The precise mechanism of gene silencing depends on the degree of complementarity between the miRNA or siRNA and its target. Binding of RISC to a perfectly complementary mRNA generally results in silencing due to endonucleolytic cleavage of the mRNA specifically by AGO2. Binding of RISC to a partially complementary mRNA results in silencing through inhibition of translation, and this is independent of endonuclease activity. May inhibit translation initiation by binding to the 7-methylguanosine cap, thereby preventing the recruitment of the translation initiation factor eIF4-E. May also inhibit translation initiation via interaction with EIF6, which itself binds to the 60S ribosomal subunit and prevents its association with the 40S ribosomal subunit. The inhibition of translational initiation leads to the accumulation of the affected mRNA in cytoplasmic processing bodies (P-bodies), where mRNA degradation may subsequently occur. In some cases RISC-mediated translational repression is also observed for miRNAs that perfectly match the 3' untranslated region (3'-UTR). Can also up-regulate the translation of specific mRNAs under certain growth conditions. Binds to the AU element of the 3'-UTR of the TNF mRNA and up-regulates translation under conditions of serum starvation. Also required for transcriptional gene silencing (TGS), in which short RNAs known as antigene RNAs or agRNAs direct the transcriptional repression of complementary promoter regions.. (Microbial infection) Upon Sars-CoV-2 infection, associates with viral miRNA-like small RNA, CoV2-miR-O7a, and may repress mRNAs, such as BATF2, to evade the IFN response. See full target information AGO2

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