DcR3/TNFRSF6B 蛋白, Human (sf9, hFc)

DcR3 is a secreted member of the Tumor Necrosis Factor (TNF) receptor superfamily, recognized as a significant anti-apoptotic factor with prominent involvement in various inflammatory and neoplastic conditions. DcR3 can neutralize the cytotoxic ligands TNFS14/LIGHT, TNFSF15 and TNFSF6/FASL against apoptosis^[1][2][3]. DcR3 has been associated with tumorigenesis and metastasis, via DcR3/STAT1/IRF1 feedback loop^[4][5]. DcR3/TNFRSF6B Protein, Human (sf9, hFc) has a full length of 300 amino acids (M1-H300), produced in sf9 insect cells with C-terminal hFc-tag.

诱饵受体 3 (DcR3) 是肿瘤坏死因子 (TNF) 受体超家族的分泌成员，可中和三种不同的 TNF 配体/促凋亡分子：FasL、LIGHT 和 TL1A。这些配体中的每一个都与独特的信号受体结合，指导独特且关键的免疫反应。DCr3 与相应细胞因子的功能受体（FasL 的 Fas、TL1A 的 DR3、LIGHT 的 LTbR 和疱疹病毒进入介质/HVEM）竞争性结合，从而阻止下游促凋亡信号传导。DcR3 由 Tnfrsf6b 基因编码，该基因不编码细胞质或跨膜片段，从而产生包括信号肽在内的 300 个氨基酸的专性分泌蛋白。然而，小鼠和大鼠基因组缺少 Tnfrsf6b 基因^[1][2]。DcR3 在多种恶性肿瘤中过度表达，并与肿瘤发生和进展相关。因此，它被认为是预测癌症侵袭和炎症进展的潜在生物标志物。具体而言，DcR3 通过激活人结直肠癌 (CRC)^[3][4] 中的 TGF-β3/SMAD 信号通路诱导上皮间质转化。此外，它还能增加 PI3K/AKT/GSK-3β/β-catenin 信号通路的多个组件的表达水平，例如 p-AKT、GSK-3β、p-GSK-3β 和 β-catenin。此外，DcR3 还可增强 N-cadherin 和 Vimentin 的表达，并降低 E-cadherin^[3] 的表达。DcR3 还通过 DcR3/STAT1/IRF1 反馈环促进胰腺癌的增殖和侵袭。它促进信号转导子和转录激活子 1 (STAT1) 的磷酸化，导致干扰素调节因子 1 (IRF1) 急剧增加。随后，IRF1 会增加 DcR3 的转录活性，形成正反馈环以强化 DcR3 的表达^[5]。人DcR3蛋白与其他动物的同源性较低，与大鼠、小鼠和猪的序列相似性分别为20.49%、20.82%和20.00%。

Measured by its ability to inhibit Fas Ligand induced apoptosis of Jurkat human acute T cell leukemia cells and the ED₅₀ for this effect is typically ≤25 μg/mL in the presence of 200 ng/mL human Fas ligand.

Human

Sf9 insect cells

C-hFc

O95407 (V30-H300)

8771  [NCBI]

Approximately 65 kDa

Greater than 85% as determined by reducing SDS-PAGE.

溶液

Supplied as a 0.2 μm filtered solution of 100 mM Glycine, 10 mM NaCl, pH 7.0.

<1 EU/μg, determined by LAL method.

N/A.

Stored at -80°C for 1 year. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Zhan C, et al. Decoy strategies: the structure of TL1A:DcR3 complex. Structure. 2011 Feb 9;19(2):162-71.  [Content Brief]

  [2]. Lagou S, et al. The Role of Decoy Receptor DcR3 in Gastrointestinal Malignancy. Cancer Diagn Progn. 2022 Jul 3;2(4):411-421.  [Content Brief]

  [3]. Ge H, et al. DcR3 induces proliferation, migration, invasion, and EMT in gastric cancer cells via the PI3K/AKT/GSK-3β/β-catenin signaling pathway. Onco Targets Ther. 2018 Jul 19;11:4177-4187.  [Content Brief]

  [4]. Liu YP, et al. DcR3 induces epithelial-mesenchymal transition through activation of the TGF-β3/SMAD signaling pathway in CRC. Oncotarget. 2016 Nov 22;7(47):77306-77318.  [Content Brief]

  [5]. Gao L, et al. DcR3, a new biomarker for sepsis, correlates with infection severity and procalcitonin. Oncotarget. 2017 Dec 28;9(13):10934-10944.  [Content Brief]