IFN-alpha 5/IFNA5 Protein, Mouse (HEK293, Fc)

IFN-alpha 5 (IFNA5), belongs to type I interferon family, is produced by macrophages with antiviral activities^[1]. IFN-alpha 5/IFNA5 Protein, Mouse (HEK293, Fc) contains 189 a.a. (M1-E189), produced in HEK293 cells with a C-terminal hFc-tag.

IFN-alpha 5 (IFNA5; IFN-α5), belongs to the alpha/beta interferon (IFN) family, is produced by the macrophages with antiviral activities. Interferon (IFN) is originally identified as a substance ‘interfering’ with viral replication in vitro. IFN-α/β and related molecules are classified as type I IFNs, as for the other two types of type II IFN (IFN-γ) and type III IFNs (IFN-λ), respectively^[1].
Interferon stimulates the production of two enzymes: a protein kinase and an oligoadenylate synthetase. Interferon alpha (IFNa) shows significant biological activity in various cancers, paticularly haematological malignancies such as hairy cell leukaemia and chronic myelogenous leukaemia^[2].
IFN-alpha 5 involves in innate immunity, and is one of the genes associated with acute viral bronchiolitis (AVB) caused by respiratory syncytial virus (RSV), determining susceptibility to RSV bronchiolitis^[3][4].
The excessively expressed interferon-α (IFN-α) might contribute to the uncontrolled inflammatory responses, causing pathological damage during influenza virus infection. However IFN-alpha 5 is dominantly expressed in respiratory epithelial cells from the patients infected with less pathogenic infectious bronchitis virus (IBV)^[5].
As for a wildly use of IFN in animal model, the sequence of amino acids in IFNA5 protein of mouse is very different from human (60.32%).

IFN-α subtype shows dominance in mouse lungs infected with influenza viruses. IFN-α1, IFN-α5, and IFN-α9 are dominantly expressed in the lungs of the mice infected with H1N1 influenza viruses accompanied with the high-level production of CXCL1, more infiltrated neutrophils and more severe damage in mouse lungs^[5].

Type I interferons (IFNs) are produced early in response to viral infection and modulate adaptive immunity. Thus IFNA5 enhances the replication of murine cytomegalovirus (MCMV) and helps little about systemic murine cytomegalovirus (MCMV) infection and myocarditis^[6].

Mouse

HEK293

C-hFc

Q810G2 (M1-E189)

15968  [NCBI]

Approximately 48.8 kDa.

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Zhang SY, et al. Inborn errors of interferon (IFN)-mediated immunity in humans: insights into the respective roles of IFN-alpha/beta, IFN-gamma, and IFN-lambda in host defense. Immunol Rev. 2008 Dec;226:29-40.  [Content Brief]

  [2]. Raj NB, et al. Identification of a novel virus-responsive sequence in the promoter of murine interferon-alpha genes. J Biol Chem. 1991 Jun 15;266(17):11360-5.  [Content Brief]

  [3]. Hirankarn N, et al. Genetic association of interferon-alpha subtypes 1, 2 and 5 in systemic lupus erythematosus. Tissue Antigens. 2008 Dec;72(6):588-92.  [Content Brief]

  [4]. Janssen R, et al. Genetic susceptibility to respiratory syncytial virus bronchiolitis is predominantly associated with innate immune genes. J Infect Dis. 2007 Sep 15;196(6):826-34.  [Content Brief]

  [5]. Yang L, et al. Diversity of locally produced IFN-α subtypes in human nasopharyngeal epithelial cells and mouse lung tissues during influenza virus infection. Appl Microbiol Biotechnol. 2020 Jul;104(14):6351-6361.  [Content Brief]

  [6]. Cull VS, et al. Type I interferon gene therapy protects against cytomegalovirus-induced myocarditis. Immunology. 2002 Jul;106(3):428-37.  [Content Brief]