ASC/TMS1 (D2W8U) Rabbit mAb #67824
- WB
- IP
- IHC
- IF
- F
Supporting Data
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 22 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| Immunohistochemistry (Paraffin) | 1:100 - 1:400 |
| Immunofluorescence (Frozen) | 1:400 - 1:1600 |
| Immunofluorescence (Immunocytochemistry) | 1:400 - 1:1600 |
| Flow Cytometry (Fixed/Permeabilized) | 1:400 - 1:1600 |
Storage
For a carrier free (BSA and azide free) version of this product see product #37953.
Protocol
Specificity / Sensitivity
ASC/TMS1 (D2W8U) Rabbit mAb recognizes endogenous levels of total ASC/TMS1 protein.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant mouse ASC/TMS1 protein.
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 ASC/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 ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/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).
- Masumoto, J. et al. (1999) J Biol Chem 274, 33835-8.
- Conway, K.E. et al. (2000) Cancer Res 60, 6236-42.
- Terasawa, K. et al. (2004) Clin Cancer Res 10, 2000-6.
- Stone, A.R. et al. (2004) Am J Pathol 165, 1151-61.
- Guan, X. et al. (2003) Int J Cancer 107, 202-8.
- Moriai, R. et al. (2002) Anticancer Res 22, 4163-8.
- Virmani, A. et al. (2003) Int J Cancer 106, 198-204.
- Das, P.M. et al. (2006) Mol Cancer 5, 28.
- Strong, R. et al. (1991) Brain Res 542, 23-8.
- Ohtsuka, T. et al. (2004) Nat Cell Biol 6, 121-8.
- Srinivasula, S.M. et al. (2002) J Biol Chem 277, 21119-22.
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