|Positive WB detected in||HeLa cells|
|Positive IF detected in||HeLa cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunofluorescence (IF)||IF : 1:10-1:100|
|Sample-dependent, check data in validation data gallery|
20988-1-AP targets Hamartin in WB, IP, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Full Name||tuberous sclerosis 1|
|Calculated molecular weight||130 kDa|
|Observed molecular weight|
|GenBank accession number||NM_000368|
|Gene ID (NCBI)||7248|
|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.|
TSC1, also named as KIAA0243 and TSC, is implicated as a tumor suppressor. It is involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling. In complex with TSC2, TSC1 inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of S6K1 and EIF4EBP1 by negatively regulating mTORC1 signaling. It seems not to be required for TSC2 GAP activity towards RHEB. It is involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling. Defects in TSC1 are the cause of tuberous sclerosis complex (TSC). Defects in TSC1 may be a cause of focal cortical dysplasia of Taylor balloon cell type (FCDBC). The antibody is specific to TSC1. This antibody can recognize two isoforms: 70 kDa (667aa) and 130 kDa.
Tuberous sclerosis complex exhibits a new renal cystogenic mechanism.
Wound Repair Regen
Activation of mTORC1 in fibroblasts accelerates wound healing and induces fibrosis in mice.
Biochem Biophys Res Commun
UBE2S exerts oncogenic activities in urinary bladder cancer by ubiquitinating TSC1.
mTORC1 promotes mineralization via p53 pathway.
Tsc1 deficiency impairs mammary development in mice by suppression of AKT, nuclear ERα, and cell-cycle-driving proteins.
Mol Ther Nucleic Acids
miR-301a Suppression within Fibroblasts Limits the Progression of Fibrosis through the TSC1/mTOR Pathway.