IFN-alpha 5/IFNA5 蛋白, Mouse (P.pastoris, His)

IFN-alpha 5 (IFNA5), belongs to type I interferon family, is produced by macrophages with antiviral activities^[1]. IFN-alpha 5/IFNA5 Protein, Mouse (P.pastoris, His) contains 168 a.a. (C24-E189), produced in P. pastoris yeast cells with a C-terminal His-tag.

干扰素-α5（IFNA5；IFN-α5）属于α/β干扰素（IFN）家族，由巨噬细胞产生，具有抗病毒活性。干扰素（IFN）最初被认为是一种在体外“干扰”病毒复制的物质。IFN-α/β及相关分子被归类为I型干扰素，其他两类分别为II型干扰素（IFN-γ）和III型干扰素（IFN-λ）^[1]。
干扰素刺激两种酶的产生：蛋白激酶和寡腺苷酸合成酶。干扰素 α (IFNa) 在多种癌症中显示出显着的生物活性，特别是血液系统恶性肿瘤，如毛细胞白血病和慢性粒细胞白血病^[2]。
IFN-α 5 参与先天免疫，并且是与呼吸道合胞病毒 (RSV) 引起的急性病毒性细支气管炎 (AVB) 相关的基因之一，决定了对 RSV 细支气管炎的易感性^[3][4]。
流感病毒感染过程中，过度表达的干扰素-α（IFN-α）可能会导致炎症反应失控，造成病理损伤。而IFN-α 5主要表达于低致病性传染性支气管炎病毒(IBV)感染者的呼吸道上皮细胞^[5]。
至于IFN在动物模型中的广泛使用，小鼠IFNA5蛋白的氨基酸序列与人类差异很大（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

P. pastoris

C-His

Q810G2 (C24-E189)

15968  [NCBI]

Approximately 20.3 kDa.

Greater than 90% as determined by reducing SDS-PAGE.

无菌粉末.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [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]