Human TSC1 Alexa Fluor® 750-conjugated Antibody

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IC4379S-100UG
R&D Systems Antibodies
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Human TSC1 Alexa Fluor® 750-conjugated Antibody Summary

Species Reactivity
Human
Specificity
Detects human TSC1 in direct ELISAs and Western blots. In direct ELISAs, no cross-reactivity with recombinant human (rh) TSC2 (aa 550-850), rhTSC2 (aa 1506-1748), or recombinant mouse TSC22 (aa 1-143) is observed.
Source
Monoclonal Mouse IgG2b Clone # 488915
Immunogen
E. coli-derived recombinant human TSC1
Asp156-Thr300
Accession # Q92574
Formulation
Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.
Label
Alexa Fluor 750 (Excitation= 749 nm, Emission= 775 nm)

Applications

Recommended Concentration
Sample
Intracellular Staining by Flow Cytometry
0.25-1 µg/106 cells
Jurkat human acute T cell leukemia cell line fixed with paraformaldehyde and permeabilized with saponin

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

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Preparation and Storage

Shipping
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Store the unopened product at 2 - 8 °C. Do not use past expiration date.

Background: TSC1

TSC1 (Tuberous sclerosis 1), or hamartin, is a tumor suppressor which interacts with tumor suppressor TSC2 (tuberin) to form a cytoplasmic heterodimer. Mutations in either hamartin or tuberin are responsible for tuberous sclerosis (TSC), an autosomal dominant disease characterized by renal dysfunction, seizures, developmental delays, benign hamartomas and low grade neoplasms predominantly affecting the CNS, kidney, lung, skin, and heart. The TSC1/TSC2 complex suppresses cell growth by inhibiting mTOR, with TSC1 acting to inhibit the ubiquitination of TSC2, leading to increased cellular levels of TSC2 and thus enhancing its catalytic activity as a GTPase-activating protein for Rheb. TSC1 and TSC2 are also involved in the G2/M transition of the cell cycle through their interactions with CDK1 and cyclin B1. TSC1 has also been shown to interact with F-actin and ERM (Ezrin-Radixin-Moesin) proteins, implying a role in the modulation of cell adhesion and morphology.

Long Name
Tuberous Sclerosis 1
Entrez Gene IDs
7248 (Human); 64930 (Mouse); 60445 (Rat)
Alternate Names
Hamartin; KIAA0243MGC86987; LAMhamartin; TSC; TSC1; Tuberous sclerosis 1 protein; tuberous sclerosis 1; tumor suppressor

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Product Specific Notices


This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.

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