ANTI-DAXX , DEVELOPED IN RABBIT

Description_x000D_ General description_x000D_ Death domain associated protein (Daxx), also known as ETS associated protein 1 (EAP1), is an adaptor protein that binds to the death domain of Fas. Daxx is a 120 kDa protein with a nuclear localization signal sequence. It is highly acidic due to extended glutamic acid-rich domains. Daxx mRNA is extensively expressed in fetal and adult human and mouse tissues. Daxx has also been found in the nucleus where it localizes with the promyelocytic leukemia protein (PML), a gene of acute promyelocytic leukemia (APL)._x000D_ Specificity_x000D_ Anti-Daxx specifically recognizes human Daxx (120 kDa)._x000D_ Immunogen_x000D_ Synthetic peptide corresponding to the C-terminus of human Daxx. This sequence is identical in mouse and monkey._x000D_ Application_x000D_ Anti-Daxx antibody is suitable for:_x000D_ • western blot (1:4,000 using human acute lymphoma Jurkat whole cell extract)_x000D_ • microarray_x000D_ • the detection and localization of Daxx by immunoblotting_x000D_ Anti-Daxx antibody produced in rabbit has been used to visualize hDaxx._x000D_ Physical form_x000D_ Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide._x000D_ Disclaimer_x000D_ 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._x000D_ Biochem/physiol Actions_x000D_ The death domain-associated protein (Daxx) is a protein that interacts with FAS and subsequently regulates cellular apoptosis. Daxx also interacts with H3.3 histone and α-thalassemia X-linked mental retardation protein (ATRX) to regulate chromatin deposition at telomeres. In addition, it also acts as a pro-apoptotic molecule that can specifically enhance Fas-induced apoptosis by activating the Jun N-terminal kinase (JNK) signaling pathway, through its interaction with the apoptosis signal-regulating kinase 1 (ASK1).