Technical Data
ASC (Apoptosis-associated Speck-like Protein Containing a CARD, hASC, Caspase Recruitment Domain-containing Protein 5, PYD and CARD Domain-containing Protein, Target of Methylation-induced Silencing 1, PYCARD, CARD5, TMS1)
ASC [apoptosis-associated speck-like protein containing a CARD (caspase-recruitment domain)] is a bimodel protein containing a pyrin:paad domain (PYD/PAAD) and a caspase recruitment domain (CARD) (reviewed in McConnell and Vertino, 2004). ASC is also known as TMS1 (target of methylation-induced silencing). ASC was first identified in 1999 as a protein that forms cytoplasmic specks during retinoic acid induced differentiation or drug-induced apoptosis in HL60 cells. It was later independently identified in 2000 in a screen for targets of methylation-mediated silencing. In general proteins, like ASC/TMS1, containing PYD/PAAD and CARD domains play key roles in regulating apoptosis and inflammation signaling pathways. Mutations in a number of PYD/PAAD- and CARD-containing proteins have been linked to inflammatory diseases and cancer. There is evidence that ASC/TMS1 has roles in both apoptosis and inflammation signaling pathways. For example, ASC/TMS1 has been reported to function as a proapoptotic protein and has been shown to trigger apoptosis upon over expression in tumor cell lines. With respect to inflammation, ASC/TMS1 interacts with the CARD of procaspase-1 and induces aggregation of a protein complex called the inflammasome, thereby regulating caspase-1 activation and secretion of IL-1b. Additionally, ASC/TMS1 has been found to be subjected to methylation-mediated silencing in a significant proportion of human breast tumors and other cancers, including melanomas, glioblastomas, non-small lung cancers, gastric and colorectal cancers (reviewed in Parsons and Vertino, 2006). The loss of ASC/TMS1 expression in breast tumors and other cancers through methylation-mediated (epigenetic) silencing suggests that ASC/TMS1 has a role in tumorigenesis. In general, it is thought that methylation-mediated gene silencing contributes to tumorigenesis by inactivating genes involved in tumor suppression, and by conferring resistance to cell death signals by silencing genes that promote apoptosis. Thus methylation-mediated silencing of ASC/TMS1 may confer a survival advantage to tumor cells by enabling them to escape apoptosis. However, the precise role of ASC/TMS1 in the pathogenesis of cancer remains to be fully elucidated. Human ASC/TMS1 (isoform a) is a 195aa protein (~22kD), GenBank no. NP_037390.2. Three transcript variants encoding different isoforms have been identified for the ASC:TMS1 gene. ASC/TMS1 is normally highly expressed in immune cells, especially in neutrophils and cells of the macrophage:monocyte lineage; it is also expressed in many epithelial cell types (reviewed in Parsons and Vertino, 2006).

Suitable for use in Western Blot, Immunohistochemistry and Immunoprecipitation. Other applications not tested.

Recommended Dilution:
Western Blot: 1:1000-1:2000
Immunohistochemistry (formalin fixed paraffin embedded): 1:1000-1:5000
Immunoprecipitation: 1:50-1:200
Immunohistochemistry: Frozen
Optimal dilutions to be determined by the researcher.

Positive Control:
Spleen, lymphoid, many cancer cell lines

Storage and Stability:
May be stored at 4C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
50ul-20CBlue IceHumanRabbit
Not determined.
Synthetic peptide corresponding to aa83-102 (GQLQAATHQGSGAAPAGIQA) of human ASC/TMS1; GenBank no. NP_037390.2, which is also referred-as ASC/TMS1 isoform a. Isoform a is a 195 aaprotein.
Supplied as a liquid, 0.05% sodium azide.
Recognizes human ASC/TMS1.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.
1. McConnell BB and PM Vertino. 2004. TMS1/ASC: The cancer connection. Apoptosis 9:5-18. 2. Parsons MJ and PM Vertino. 2006. Dual role of TMS1/ASC in death receptor signaling. Oncogene doi:10.1038/sj.onc.1209684.