TNFAIP1 (tumor necrosis factor, a-induced protein 1) was first discovered as an interleukin-6 (IL-6) and tumor necrosis factor (TNF) a-inducible protein. It is a highly conserved protein and is conserved across humans, rat and C. elegans. It is highly expressed in brain and heart, and its expression is determined by the developmental stage. Its N-terminal contains the conserved BTB/POZ (BR-C, ttk and bab/ Pox virus and Zinc finger) domain. This gene is located on human chromosome 17q22-q23, and codes for a protein with predicted 316-amino acids
Synonyms: Anti-B12; Anti-B61; Anti-BTBD34; Anti-EDP1; Anti-MGC2317
Storage: -20C
Application: All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry. The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: TNFAIP1 (tumor necrosis factor, a-induced protein 1) is expressed according to the developmental stage, and is highly expressed in brain and heart. Therefore, it might play an essential role in the development of brain and heart. In endothelial cells, its expression is induced by TNFa, by the transcription factor Sp1 (specificity protein 1). TNFAIP1 is thus involved in inflammation-related angiogenesis. It acts as a ligand for Eck receptor protein tyrosine kinase (RPTK), when stimulated by TNFa under inflammatory conditions, and hence, promotes angiogenesis and resulting chronic inflammation. It is pro-apoptotic in nature, and when induced by RhoB, it induces apoptosis via the SAPK/JNK (Stress-activated protein kinase/c-Jun NH2-terminal kinase)-mediated signal pathway. It also suppresses the activation of nuclear factor ? B (NF-?B) and activating protein-1 reporters, by interacting with and degrading potassium channel tetramerisation domain containing 10 (KCTD10).
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