Rabbit Recombinant Monoclonal RHEB antibody - conjugated to Alexa Fluor® 647.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application Target Binding Affinity | Reactivity Expected | Dilution info - | Notes - |
Application Antibody Labelling | Reactivity Expected | Dilution info - | Notes - |
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Small GTPase that acts as an allosteric activator of the canonical mTORC1 complex, an evolutionarily conserved central nutrient sensor that stimulates anabolic reactions and macromolecule biosynthesis to promote cellular biomass generation and growth (PubMed:12172553, PubMed:12271141, PubMed:12842888, PubMed:12869586, PubMed:12906785, PubMed:15340059, PubMed:15854902, PubMed:16098514, PubMed:20381137, PubMed:22819219, PubMed:24529379, PubMed:29416044, PubMed:32470140, PubMed:33157014). In response to nutrients, growth factors or amino acids, specifically activates the protein kinase activity of MTOR, the catalytic component of the mTORC1 complex: acts by causing a conformational change that allows the alignment of residues in the active site of MTOR, thereby enhancing the phosphorylation of ribosomal protein S6 kinase (RPS6KB1 and RPS6KB2) and EIF4EBP1 (4E-BP1) (PubMed:29236692, PubMed:33157014). RHEB is also required for localization of the TSC-TBC complex to lysosomal membranes (PubMed:24529379). In response to starvation, RHEB is inactivated by the TSC-TBC complex, preventing activation of mTORC1 (PubMed:24529379, PubMed:33157014). Has low intrinsic GTPase activity (PubMed:15340059).
RHEB2, RHEB, GTP-binding protein Rheb, Ras homolog enriched in brain
Rabbit Recombinant Monoclonal RHEB antibody - conjugated to Alexa Fluor® 647.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 68% PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
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. This conjugated antibody is eligible for the Abcam trial program.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
RHEB also known as Ras homolog enriched in brain is a small GTPase with a molecular mass of approximately 21 kDa. It is a member of the Ras superfamily and plays a role in the regulation of cell growth and proliferation. RHEB is widely expressed with concentrations found in the brain skeletal muscle and various other tissues. It functions as a molecular switch cycling between active GTP-bound and inactive GDP-bound states influencing signaling pathways linked to growth and metabolism.
RHEB interacts with several components within the mTORC1 complex a major regulator of cell growth and autophagy. This protein positively regulates the mTORC1 pathway by activating mTOR leading to protein synthesis and cell growth when nutrients such as amino acids and energy are available. RHEB's regulation of mTORC1 is influenced by upstream modulation through the TSC1/2 complex acting as a sensor for cellular energy levels and growth signals. The role of RHEB in these regulatory mechanisms highlights its fundamental importance in cellular metabolic processes.
RHEB plays a significant role in the mechanistic target of rapamycin (mTOR) signaling pathway which is important for regulating protein synthesis and cellular growth. RHEB acts downstream of the TSC1/2 complex with TSC2 acting as a GTPase-activating protein for RHEB. This interaction points RHEB as an essential regulator of mTORC1 activation. In connection with other proteins RHEB functions alongside mTOR and TSC1/2 to mediate responses to cellular nutrient status thereby adjusting growth and proliferation accordingly.
Mutations or dysregulation of RHEB have been linked to tuberous sclerosis complex (TSC) and cancer. In TSC where aberrant signaling occurs through the mTOR pathway RHEB's activity influences the mTORC1 pathway in cells lacking functional TSC1 or TSC2 leading to benign tumors. Additionally RHEB overexpression has been implicated in certain cancers due to its capacity to enhance cell proliferation via mTORC1. The interaction of RHEB with mTOR highlights its role in disease states where cell growth control is altered suggesting the potential for targeted therapies in treating these conditions.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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