|Sample-dependent, check data in validation data gallery|
20004-1-AP targets Tuberin-Specific in WB, IF,ELISA applications and shows reactivity with human, mouse samples.
|Tested Reactivity||human, mouse|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Full Name||tuberous sclerosis 2|
|Calculated molecular weight||201 kDa|
|GenBank accession number||NM_000548|
|Gene ID (NCBI)||7249|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
TSC2, also named as TSC4, FLJ43106 and LAM, acts as a GTPase-activating protein (GAP) for the small GTPase RHEB, a direct activator of the protein kinase activity of mTORC1. In complex with TSC1, TSC2 inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of S6K1 and EIF4EBP1 by negatively regulating mTORC1 signaling. TSC2 implicated as a tumor suppressor. It is involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling. TSC2 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. Mutations in either TSC2 or the related TSC1 (hamartin) gene cause tuberous sclerosis complex (TSC), an autosomal dominant disorder characterized by development of multiple, widespread non-malignant tumors. The antibody is specific to TSC2.
Tuberous sclerosis complex exhibits a new renal cystogenic mechanism.
Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response.