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ASC/TMS1 (D2W8U) Rabbit Monoclonal Antibody (Alexa Fluor® 647 Conjugate) #23640
Filter:
- IF
Product Specifications
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- M-Mouse
Product Information
Product Description
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 647 fluorescent dye and tested in-house for direct immunofluorescent analysis in mouse cells. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated ASC/TMS1 (D2W8U) Rabbit mAb #67824.
Product Usage Information
| Application | Dilution |
|---|---|
| Immunofluorescence (Frozen) | 1:50 |
| Immunofluorescence (Immunocytochemistry) | 1:50 |
Storage
Supplied in PBS (pH 7.2), less than 0.1% sodium azide and 2 mg/ml BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze.
Protocol
Specificity / Sensitivity
ASC/TMS1 (D2W8U) Rabbit Monoclonal Antibody (Alexa Fluor® 647 Conjugate) recognizes endogenous levels of total ASC protein.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant mouse ASC 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 redistributed 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.
Alternate Names
9130417A21Rik; Apoptosis-associated speck-like protein containing a CARD; Asc; CARD5; mASC; OTTMUSP00000030782; Pycard; PYD and CARD domain containing; PYD and CARD domain-containing protein; TMS-; TMS-1; TNS1
限制使用
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For Research Use Only. Not for Use in Diagnostic Procedures.
Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
This product is provided under an intellectual property license from Life Technologies Corporation. The transfer of this product is conditioned on the buyer using the purchased product solely in research conducted by the buyer, excluding contract research or any fee for service research, and the buyer must not (1) use this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; or (c) manufacturing or quality assurance or quality control, and/or (2) sell or transfer this product or its components for resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or [email protected].
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