Cell Signaling Technology

Product Pathways - Apoptosis

TMS1 Antibody #4628

Applications Reactivity Sensitivity MW (kDa) Source
W H (M) (R) (Mk) Endogenous 22 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

TMS1 Antibody detects endogenous levels of total TMS1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of mouse TMS1. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, mock transfected or transfected with a mouse TMS1 construct, using TMS1 Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1, U-937 and HL-60 cell lines using TMS1 Antibody.

Background

TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

  1. Masumoto, J. et al. (1999) J Biol Chem 274, 33835-8.
  2. Conway, K.E. et al. (2000) Cancer Res 60, 6236-42.
  3. Terasawa, K. et al. (2004) Clin Cancer Res 10, 2000-6.
  4. Stone, A.R. et al. (2004) Am J Pathol 165, 1151-61.
  5. Guan, X. et al. (2003) Int J Cancer 107, 202-8.
  6. Moriai, R. et al. Anticancer Res 22, 4163-8.
  7. Virmani, A. et al. (2003) Int J Cancer 106, 198-204.
  8. Das, P.M. et al. (2006) Mol Cancer 5, 28.
  9. Strong, R. et al. (1991) Brain Res 542, 23-8.
  10. Ohtsuka, T. et al. (2004) Nat Cell Biol 6, 121-8.
  11. Srinivasula, S.M. et al. (2002) J Biol Chem 277, 21119-22.

Application References

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Companion Products

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

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