|Application ||WB, IHC|
|Calculated MW||200608 Da|
|Other Names||Tuberin, Tuberous sclerosis 2 protein, TSC2, TSC4|
|Target/Specificity||A synthetic peptide corresponding to residues of human Tuberin was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Tuberin Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||In complex with TSC1, inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of S6K1 and EIF4EBP1 by negatively regulating mTORC1 signaling. Acts as a GTPase- activating protein (GAP) for the small GTPase RHEB, a direct activator of the protein kinase activity of mTORC1. Implicated as a tumor suppressor. Involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling. Stimulates weakly the intrinsic GTPase activity of the Ras-related proteins RAP1A and RAB5 in vitro. Mutations in TSC2 lead to constitutive activation of RAP1A in tumors.|
|Cellular Location||Cytoplasm. Membrane; Peripheral membrane protein. Note=At steady state found in association with membranes|
|Tissue Location||Liver, brain, heart, lymphocytes, fibroblasts, biliary epithelium, pancreas, skeletal muscle, kidney, lung and placenta|
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Provided below are standard protocols that you may find useful for product applications.
Tuberous sclerosis complex-2 (TSC2 also known as Tuberin) is a tumor suppressor that forms a complex with TSC1 (Hamartin ) and this complex is known to control various cellular functions including cell cycle, endocytosis, adhesion, and transcription (1). The C-terminal region of TSC2 contains a GTPase-activating protein (GAP) domain which interacts with Rap1, Rab5 and Rheb (2). The TSC1/TSC2 complex inhibits phosphorylation of S6kinase and 4E-BP1 through inactivation of mTOR (3). Additionally, binding of 14-3-3 beta to TSC2 at Ser1210 reduce the ability of the complex to inhibit phosphorylation of S6 kinase (4). Phosphorylation by ATK at Ser924 and Thr1518 inactivates TSC2 and disrupts its interaction with TSC1 (5). Tuberous sclerosis (TSC), an autosomal dominant disorder that affects 1 in 6000 individuals, is caused by a mutation in either the TSC1 or TSC2 tumor suppressor gene.
1. Lamb,et al. Nature Cell Biol. 2: 281-287
2. Xiao, et al. J. Biol. Chem. 272: 6097-6100
3. Manning, BD, et al. Molec. Cell 10: 151-162, 2002.
4. Shumway, SD, et al. J. Biol. Chem. 278: 2089-2092, 2003.
5. Inoki, K, et al. Nat Cell Biol: 4: 648-657, 2002.
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