Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

Phospho-Tuberin/TSC2 (Ser664) (D3B9Z) Rabbit mAb #40729

No. Size Price
40729S 100 µl ( 10 western blots ) ¥4,050.00 现货查询 购买询价 防伪查询
40729 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 200 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

Phospho-Tuberin/TSC2 (Ser664) (D3B9Z) Rabbit mAb recognizes endogenous levels of Tuberin/TSC2 protein only when phosphorylated at Ser664. This antibody cross-reacts with a 140kD protein of unknown origin.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser664 of human Tuberin/TSC2 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, untreated (-) or treated with TPA #4174 (200 nM, 20 minutes, +), using Phospho-Tuberin/TSC2 (Ser664) (D3B9Z) Rabbit mAb (upper) and Tuberin/TSC2 (D93F12) XP® Rabbit mAb #4308 (lower).

Background

Tuberin is a product of the TSC2 tumor suppressor gene and an important regulator of cell proliferation and tumor development (1). 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 (2). Tuberin is directly phosphorylated at Thr1462 by Akt/PKB (3). Phosphorylation at Thr1462 and Tyr1571 regulates tuberin-hamartin complexes and tuberin activity (3-5). In addition, tuberin inhibits the mammalian target of rapamycin (mTOR), which promotes inhibition of p70 S6 kinase, activation of eukaryotic initiation factor 4E binding protein 1 (4E-BP1, an inhibitor of translation initiation), and eventual inhibition of translation (3,6,7).

p44/42 MAPK (Erk1/2) phosphorylates of TSC2 at Ser664 which leads to TSC1-TSC2 dissociation and considerably decreases the ability of TSC2 to inhibit mTOR signaling, cell proliferation and oncogenic transformation (8,9). Furthermore, studies have indicated that cancer patients with TSC2 phosphorylation at Ser664 may benefit from MAPK and mTOR inhibitors (10).

  1. Soucek, T. et al. (1998) Proc Natl Acad Sci U S A 95, 15653-8.
  2. Sparagana, S.P. and Roach, E.S. (2000) Curr Opin Neurol 13, 115-9.
  3. Manning, B.D. et al. (2002) Mol Cell 10, 151-62.
  4. Aicher, L.D. et al. (2001) J Biol Chem 276, 21017-21.
  5. Dan, H.C. et al. (2002) J Biol Chem 277, 35364-70.
  6. Goncharova, E.A. et al. (2002) J Biol Chem 277, 30958-67.
  7. Inoki, K. et al. (2002) Nat Cell Biol 4, 648-57.
  8. Ma, L. et al. (2005) Cell 121, 179-93.
  9. Ballif, B.A. et al. (2005) Proc Natl Acad Sci U S A 102, 667-72.
  10. Ma, L. et al. (2007) Cancer Res 67, 7106-12.

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For Research Use Only. Not For Use In Diagnostic Procedures.

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