DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 58 (DDX58) (N-Term) antibody

Antigen: DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 58 (DDX58)

Synonyms: RIG-I, FLJ13599, DKFZp434J1111, DKFZp686N19181, C330021E21, 6430573D20Rik, DDX58, RHIV-1

Binding Site: N-Term

Clonality: Polyclonal

Host: Rabbit

Reactivity: Human

Conjugate: Un-conjugated

Application: Immunohistochemistry (IHC)

Catalog no.: ABIN965985

Additional Information

Alternative name: DDX58

Immunogen: Polyclonal antibody produced in rabbits immunizing with a synthetic peptide corresponding to N-terminal residues of human DDX58 (Probable ATP-dependent RNA helicase DDX58)

Description: DDX58 (Probable ATP-dependent RNA helicase DDX58) is involved in innate immune defense against viruses. Upon interaction with intracellular dsRNA produced during viral replication, triggers a transduction cascade involving MAVS/IPS1, which results in the activation of NF-kappa-B, IRF3 and IRF7 and the induction of the expression of antiviral cytokines such as IFN-beta and RANTES (CCL5). Essential for the production of interferons in response to RNA viruses including paramyxoviruses, influenza viruses, Japanese encephalitis virus and HCV. DDX58 (Probable ATP-dependent RNA helicase DDX58) is maintained as a monomer in an autoinhibited state. Upon viral dsRNA binding and conformation shift, homomultimerizes and interacts with MAVS. Interacts with DHX58/LGP2, IKBKE, TBK1 and TMEM173/STING. DDX58 (Probable ATP-dependent RNA helicase DDX58) is present in vascular smooth cells at protein level. DDX58 belongs to the helicase family and contains 2 CARD domains, 1 helicase ATP-binding domain and 1 helicase C-terminal domain.
Synonyms: DEAD-box protein 58, RIG-1 (Retinoic acid-inducible gene 1 protein)

Application Details

Research Area: Immunology, Chromatin Binding Proteins, DNA/RNA, Transcription Factors

Restrictions: For Research Use only

Publications

Product: Imaizumi, Aratani, Nakajima et al.: "Retinoic acid-inducible gene-I is induced in endothelial cells by LPS and regulates expression of COX-2." in: Biochemical and biophysical research communications, Vol. 292, Issue 1, pp. 274-9, 2002 (PubMed).

Cui, Imaizumi, Yoshida et al.: "Retinoic acid-inducible gene-I is induced by interferon-gamma and regulates the expression of interferon-gamma stimulated gene 15 in MCF-7 cells." in: Biochemistry and cell biology = Biochimie et biologie cellulaire, Vol. 82, Issue 3, pp. 401-5, 2004 (PubMed).

Yoneyama, Kikuchi, Natsukawa et al.: "The RNA helicase RIG-I has an essential function in double-stranded RNA-induced innate antiviral responses." in: Nature immunology, Vol. 5, Issue 7, pp. 730-7, 2004 (PubMed).

Sumpter, Loo, Foy et al.: "Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I." in: Journal of virology, Vol. 79, Issue 5, pp. 2689-99, 2005 (PubMed).

Seth, Sun, Ea et al.: "Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3." in: Cell, Vol. 122, Issue 5, pp. 669-82, 2005 (PubMed).

Huang, Liu, Xu et al.: "SIKE is an IKK epsilon/TBK1-associated suppressor of TLR3- and virus-triggered IRF-3 activation pathways." in: The EMBO journal, Vol. 24, Issue 23, pp. 4018-28, 2005 (PubMed).