IFN-alpha/beta R2 蛋白, Human (217a.a, HEK293, His)

IFN-alpha/beta R2, one of the subunit of IFN-α/β receptor, is a type I IFN receptor. IFN-alpha/beta R2 forms the heterodimeric receptor with IFNAR1, and binds to type I IFNs^[1]. IFN-alpha/beta R2 also interacts with JAK1 and leads to tyrosine phosphorylation of the IFNARs and STAT proteins^[2]. Upon activation by these IFNs, IFNAR1 and IFN-alpha/beta R2 undergo a conformational change to promote a cascade of downstream signaling events, including the phosphorylation of Tyk2 and JAK1, STAT1 and STAT2^[3]. IFN-alpha/beta R2 Protein, Human (217a.a, HEK293, His) is a recombinant human IFN-alpha/beta R2 (I27-K243) with C-terminal 6*His tag, which is produced in HEK293 cells.

IFN-α/β R2是IFN-α/β受体的亚基之一，是I型干扰素受体。IFN-α/β R2 在外周血 B 细胞和单核细胞上表达，介导这些细胞的分化和活化^[4]。
IFN-α/β R2 形成异二聚体受体（ IFN-α/β 受体）与 IFNAR1 一起。IFN-α/-β 等 IFN 可以诱导 IFNAR1 和 IFN-α/β R2 结合，从而使 JAK1 和 TYK2 形成功能性信号传导单元^[1]。被这些 IFN 激活后，IFNAR1 和 IFN-α/β R2 会发生构象变化，促进一系列下游信号传导事件。信号转导事件包括 Tyk2 和 JAK1（转录 STAT1 和 STAT2 的信号转导子和激活子）的磷酸化，以及由磷酸化 STAT1 和 STAT2 以及 IRF9 组成的 IFN 刺激基因因子 3 (ISGF3) 复合物的形成。3]。IFNAR2 对于抗病毒免疫至关重要^[5]。
人 IFN-α/β R2 由胞外结构域 (I27-K243)、螺旋结构域 (I244-L264) 和胞浆结构域组成域（K265-R515）。IFN-α/β R2 的氨基酸序列在不同物种中有所不同。人 IFN-α/β R2 与小鼠的氨基酸序列同一性<50%。
IFN-α/β R2 介导 IFN 诱导的 IFNAR 和 STAT 蛋白酪氨酸磷酸化，并激活 JAK-STAT 信号级联反应^[1]

IFN-alpha/beta R2 (human, 30 μg/mL, 4 h) down-regulates the production of IL-17 and IFN-γ in PBMCs^[6].
IFN-alpha/beta R2 (human, 100 ng/mL, 40 h) reduces the cell proliferation rate in PBMCs^[6].

1.Immobilized Human IFNA2 at 10 μg/mL (100 μL/well) can bind IFNAR2. The ED₅₀ for this effect is 568.9 ng/mL.
2.Measured by its ability to inhibit rh IFNβ mediated protection of WISH Human amnion cells infected with vesicular stomatitis virus (VSV) to viral lysis.The EC₅₀ for this effect is typically 1-4 μg/mL.

Human

HEK293

C-His

P48551 (I27-K243)

3455  [NCBI]

ISYDSPDYTDESCTFKISLRNFRSILSWELKNHSIVPTHYTLLYTIMSKPEDLKVVKNCANTTRSFCDLTDEWRSTHEAYVTVLEGFSGNTTLFSCSHNFWLAIDMSFEPPEFEIVGFTNHINVMVKFPSIVEEELQFDLSLVIEEQSEGIVKKHKPEIKGNMSGNFTYIIDKLIPNTNYCVSVYLEHSDEQAVIKSPLKCTLLPPGQESESAESAK

33-50 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 or 50 mM Tris-HCL, 300 mM NaCL, 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]. Zanin N, et al. Interferon Receptor Trafficking and Signaling: Journey to the Cross Roads. Front Immunol. 2021 Jan 20;11:615603.  [Content Brief]

  [2]. Shemesh M, et al. IFNAR1 and IFNAR2 play distinct roles in initiating type I interferon-induced JAK-STAT signaling and activating STATs. Sci Signal. 2021 Nov 23;14(710):eabe4627.  [Content Brief]

  [3]. Jun Zou, et al. Chapter 7 - Antiviral Immunity: Origin and Evolution in Vertebrates. The Evolution of the Immune System. 2016,Pages 173-204.

  [4]. Pogue SL, et al. The receptor for type I IFNs is highly expressed on peripheral blood B cells and monocytes and mediates a distinct profile of differentiation and activation of these cells. J Interferon Cytokine Res. 2004 Feb;24(2):131-9.  [Content Brief]

  [5]. Duncan CJ, et al. Human IFNAR2 deficiency: Lessons for antiviral immunity. Sci Transl Med. 2015 Sep 30;7(307):307ra154.  [Content Brief]

  [6]. Hurtado-Guerrero I, et al. Immunomodulatory and Antiproliferative Activities of Recombinant Soluble IFNAR2 without IFN-β Mediation. J Clin Med. 2020 Mar 31;9(4):959.  [Content Brief]