|Tested species reactivity||Human, Non-human primate|
|Published species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide corresponding to residues 497-510 and 298-311 of human RIP3.|
|Purification||Antigen affinity chromatography|
|Contains||0.05% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||10 µg/ml|
|Western Blot (WB)||3-7 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Western Blot (WB)||See 1 publications below|
RIP3 is a novel member of RIP Ser/Thr kinase family. It is a potent inducer of apoptosis and is an important component of TNFR1 signaling complex. RIP3 consists of an N-terminal RIP-like-Kinase domain and a unique, non-homologous C-terminus responsible for caspase activation and apoptosis induction. RIP3 is expressed in multiple tissues including hematopoietic cells and plays a functional role in the regulation of apoptosis and NF-kB signaling. It is recruited to the TNFR1 signaling complex in a RIP-dependant manner where it induces apoptosis by activating caspases and/or inhibiting TNFR1-induced NF-kB activation. RIP3 negatively regulates the TLR3-Trif-mediated NF-kB signaling pathway by competing with the binding of Trif to RIP1. The human RIP3 gene is localized in the chromosomal region 14q11.2.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Ubiquitination and degradation of the FADD adaptor protein regulate death receptor-mediated apoptosis and necroptosis.
PA1-41533 was used in western blot to study the role of FADD adaptor protein degradation in death receptor-mediated apoptosis and necroptosis
|Lee EW,Kim JH,Ahn YH,Seo J,Ko A,Jeong M,Kim SJ,Ro JY,Park KM,Lee HW,Park EJ,Chun KH,Song J||Nature communications (3:null)||2012|