Anti-TMS1/ASC Rabbit mAb

Primary Antibodies

TMS1/ASC

Store at -20°C. Avoid freeze/thaw cycles.

Target of methylation-induced silencing (TMS1)/Apoptosis-associated speck-like protein containing a CARD (ASC), 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). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells, and has since been found to be silenced in a number of other cancers, including ovarian cancer, glioblastoma, melanoma, gastric cancer, lung cancer, and prostate cancer. Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli. 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. 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.

PBS, Glycerol, BSA

Recombinant Monoclonal

Target of methylation-induced silencing (TMS1)/Apoptosis-associated speck-like protein containing a CARD (ASC), 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). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells, and has since been found to be silenced in a number of other cancers, including ovarian cancer, glioblastoma, melanoma, gastric cancer, lung cancer, and prostate cancer. Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli. 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. 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.