ASC/TMS1 is a CARD domain containing protein that is expressed in a variety of human and mouse tissues. Ectopic expression of ASC/TMS1 is known to inhibit cell survival and cause cell death in human breast cancer tissues by activating caspase-9. Furthermore, overexpression of ASC/TMS1 can induce DNA fragmentation,,,. Rabbit anti-ASC/TMS1 recognizes human ASC/TMS1 (approximately 25 kDa) by immunoblotting.
Immunogen
synthetic peptide corresponding to amino acids 182-195 of human ASC.
Application
Rabbit anti-ASC/TMS1 antibody can be used for western blot assays at a concentration of 1 μg/ml.
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Physical form
Solution in phophate buffered saline containing 0.02% sodium azide
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
The Journal of biological chemistry, 274(48), 33835-33838 (1999-11-24)
The cytoskeletal and/or nuclear matrix molecules responsible for morphological changes associated with apoptosis were identified using monoclonal antibodies (mAbs). We developed mAbs against Triton X-100-insoluble components of HL-60 cells pretreated with all-trans retinoic acid. In particular, one mAb recognized a
ASC (apoptosis-associated speck-like protein containing a CARD) was first identified as a cytosolic soluble protein that forms insoluble aggregates and enhances etoposide-induced apoptosis. We have cloned a murine ortholog of ASC (mASC) comprising 193 amino acids with a well-conserved pyrin
Genetic and epigenetic alterations affecting proteins involved in apoptosis can contribute to the establishment and progression of cancer. Recently, our laboratory has isolated a novel gene, TMS1, that is aberrantly methylated and silenced in a significant proportion of human breast
Gene silencing associated with aberrant methylation of promoter region CpG islands is an acquired epigenetic alteration that serves as an alternative to genetic defects in the inactivation of tumor suppressor and other genes in human cancers. The hypothesis that aberrant
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