CD70 Protein, Mouse (HEK293, Fc)

CD70 is the ligand of CD27 in activated T and B lymphocytes, is an important cytokine in CD70-CD27 pathway involving with the generation and maintenance of T cell immunity^[1]. CD70 is a surface antigen, also shows antiviral activity and regulates viability of tumor cells and regulatory T cells^[2][3]. As for CD70 protein in mouse contains TNF_2 domain (60-190 a.a) and transmembrane helix, belonging to the tumor necrosis factor (TNF) family. CD70 Protein, Mouse (HEK293, Fc) is 149 amino acids in length (Q47-P195) and is expressed in the HEK293 cells with N terminal mFc-tag.

CD70 (CD27 Ligand) belongs to the tumor necrosis factor (TNF) family, is the ligand for TNFRSF27/CD27^[1].
CD70 and CD27 are homotrimer type II and homodimer type I transmembrane glycoprotein, expressing on activated and resting T and B lymphocytes, respectively^[3][4].  As for a wildly use of CD70 in animal disease model, the sequence of amino acids in mouse is very different from human (56.25%) and rat (77.20%).
CD70 as one of the most frequently mutated genes in a series of diffuse large B cell lymphomas, especially acts in a crucial Epstein-Barr virus (EBV)-specific T cell immunity and more generally for the immune surveillance of B cells. CD70 inhibits EBV infection by restoring the expansion of EBV-specific T lymphocytes stimulated by the CD70-deficient EBV-infected B cells^[3].
CD70 involves in activation of innate and adaptive immunity, expressing in the mature dendritic cells and being up-regulated upon the triggering of CD40 or Toll-like receptors^[2].
CD70 induces proliferation of costimulated T cells, enhances the generation of cytolytic T cells, and contributes to T cell activation^[4].
CD70 is also reported to play a role in regulating B-cell activation, cytotoxic function of natural killer cells, and immunoglobulin sythesis^[5]. targeting CD70 positive tumors with CAR-T cells induces a potent antitumor response^[6].

Measured by its binding ability in a functional ELISA.

Mouse

HEK293

N-mFc

Q05A52 (Q47-P195)

21948  [NCBI]

QQQRLLEHPEPHTAELQLNLTVPRKDPTLRWGAGPALGRSFTHGPELEEGHLRIHQDGLYRLHIQVTLANCSSPGSTLQHRATLAVGICSPAAHGISLLRGRFGQDCTVALQRLTYLVHGDVLCTNLTLPLLPSRNADETFFGVQWICP

Approximately 43.1 kDa

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

Lyophilized powder.

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]. Bowman MR, et al. The cloning of CD70 and its identification as the ligand for CD27. J Immunol. 1994 Feb 15;152(4):1756-61.  [Content Brief]

  [2]. Jacobs J, et al. CD70: An emerging target in cancer immunotherapy. Pharmacol Ther. 2015 Nov;155:1-10.  [Content Brief]

  [3]. Izawa K, et al. Inherited CD70 deficiency in humans reveals a critical role for the CD70-CD27 pathway in immunity to Epstein-Barr virus infection. J Exp Med. 2017 Jan;214(1):73-89.  [Content Brief]

  [4]. Brown GR, et al. CD27-CD27 ligand/CD70 interactions enhance alloantigen-induced proliferation and cytolytic activity in CD8+ T lymphocytes. J Immunol. 1995 Apr 15;154(8):3686-95.  [Content Brief]

  [5]. Kobata T, et al. CD27-CD70 interactions regulate B-cell activation by T cells. Proc Natl Acad Sci U S A. 1995 Nov 21;92(24):11249-53.  [Content Brief]

  [6]. Jin L, et al. CD70, a novel target of CAR T-cell therapy for gliomas. Neuro Oncol. 2018 Jan 10;20(1):55-65.  [Content Brief]

  [7]. Boursalian TE, et al. Targeting CD70 for human therapeutic use. Adv Exp Med Biol. 2009;647:108-19.  [Content Brief]

  [8]. Arens R, et al. Signaling through CD70 regulates B cell activation and IgG production. J Immunol. 2004 Sep 15;173(6):3901-8.  [Content Brief]