IFN-alpha 4/IFNA4 蛋白, Human (HEK293, His)

IFN-alpha 4 (IFNA4), belongs to type I interferon family, is produced by macrophages with antiviral activities^[1]. IFN-alpha 4/IFNA4 Protein, Human (HEK293, His) contains 166 a.a. (C24-D189), produced in HEK293 cells cells with a C-terminal His-tag.

IFN-α4（IFNA4；IFN-α4）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 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 4是 IFN-α 中占主导地位的亚型，其对 IFNA5、IFNA7 和 IFNA14 的反应占外周血单核细胞 (PBMC) 表达亚型的高达 85%^[3]。
IFN-α 4 受干扰素 (IFN) 调节因子 (IRF)，尤其是 IRF-1 和 IRF-7^[5][6] 的促进。并通过抑制病毒RNA复制发挥作用，增强对病毒的人类自然杀伤细胞毒性^[4][7]。
动物模型中，人IFNA4蛋白的氨基酸序列分别与小鼠（57.07%）和大鼠（57.98）有很大差异。

IFN-alpha 4 exerts function by enhancing human natural killer cytotoxicity in a dose-dependent manner^[4].
IFN-alpha 4 is exclusively activated by IRF-7 and not by IRF-3 in human embryonic kidney 293 cells. IRF-7 is induced by IFN, lipopolysaccharide, and virus infection which has been first described to bind and repress the Qp promoter region of the Epstein-Barr virus (EBV) EBNA-1 gene^[6].
IFN-alpha 4 variant results in significantly decrease of the suppressive effects on HCV RNA replication in HuH-7 cells^[7].

Human

HEK293

C-6*His

P05014 (C24-D189)

3441  [NCBI]

CDLPQTHSLGNRRALILLAQMGRISHFSCLKDRHDFGFPEEEFDGHQFQKAQAISVLHEMIQQTFNLFSTEDSSAAWEQSLLEKFSTELYQQLNDLEACVIQEVGVEETPLMNEDSILAVRKYFQRITLYLTEKKYSPCAWEVVRAEIMRSLSFSTNLQKRLRRKD

Approximately 20 kDa

Greater than 95% as determined by reducing SDS-PAGE.

无菌粉末.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

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]. Li Y, et al. Expression Pattern of Individual IFNA Subtypes in Chronic HIV Infection. J Interferon Cytokine Res. 2017 Dec;37(12):541-549.  [Content Brief]

  [4]. Verhagen A, et al. Comparison of augmentation of human natural killer cell cytotoxicity by interferon-alpha subtypes. Nat Immun Cell Growth Regul. 1990;9(5):325-33.  [Content Brief]

  [5]. Au WC, et al. Identification of a member of the interferon regulatory factor family that binds to the interferon-stimulated response element and activates expression of interferon-induced genes. Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11657-61.  [Content Brief]

  [6]. Lin R, et al. Selective DNA binding and association with the CREB binding protein coactivator contribute to differential activation of alpha/beta interferon genes by interferon regulatory factors 3 and 7. Mol Cell Biol. 2000 Sep;20(17):6342-53.  [Content Brief]

  [7]. Xiao CX, et al. Exome sequencing identifies novel compound heterozygous IFNA4 and IFNA10 mutations as a cause of impaired function in Crohn's disease patients. Sci Rep. 2015 May 22;5:10514.  [Content Brief]