IFI35 Rabbit Polyclonal Antibody

CAT#: TA377334

IFI35 Rabbit polyclonal Antibody

Specifications

Product Data

• Applications: IF, WB
• Recommended Dilution: WB,1:500 - 1:2000
  IF,1:50 - 1:100
• Reactivities: Human, Mouse
• Modifications: Unmodified
• Host: Rabbit
• Isotype: IgG
• Clonality: Polyclonal
• Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 1-288 of human IFI35 (NP_005524.2).
• Formulation: Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3.
• Concentration: lot specific
• Purification: Affinity purification
• Conjugation: Unconjugated
• Stability: Shelf life: one year from despatch.
• Predicted Protein Size: 31kDa
• Gene Name: interferon induced protein 35
• Database Link:
  Entrez Gene 3430 Human
  UniProt ID P80217
• Background: Acts as a signaling pathway regulator involved in innate immune system response. In response to interferon IFN-alpha, associates in a complex with signaling pathway regulator NMI to regulate immune response; the complex formation prevents proteasome-mediated degradation of IFI35 and correlates with IFI35 dephosphorylation. In complex with NMI, inhibits virus-triggered type I interferon/IFN-beta production. In complex with NMI, negatively regulates nuclear factor NF-kappa-B signaling by inhibiting the nuclear translocation, activation and transcription of the NF-kappa-B subunit p65/RELA, resulting in the inhibition of endothelial cell proliferation, migration and re-endothelialization of injured arteries. Beside its role as an intracellular signaling pathway regulator, also functions extracellularly as damage-associated molecular patterns (DAMPs to promote inflammation when actively released by macrophage to the extracellular space during cell injury and pathogen invasion. Macrophage-secreted IFI35 activates NF-kappa-B signaling in adjacent macrophages through Toll-like receptor 4/TLR4 activation, thereby inducing NF-kappa-B translocation from the cytoplasm into the nucleus which promotes the release of proinflammatory cytokines.