TNF-alpha/TNFSF2 蛋白, Mouse (P. pastoris)

Tumour Necrosis Factor alpha (TNF alpha) is a potent pro-inflammatory cytokine^[1]. TNF alpha binds to its receptors, mainly TNFR1 and TNFR2, and then transmits molecular signals for biological functions such as inflammation and cell death^[2]. TNF alpha stimulates NF-κB pathway via TNFR2 promotes cancer growth, invasion, and metastasis. Anti-TNF-α MAb significantly suppresses the tumor development in colitis-associated cancer (CAC) mouse^[3]. TNF alpha as a proneurogenic factor activates the SAPK/JNK Pathway and can facilitate neuronal replacement and brain repair in response to brain injury^[4]. TNF-alpha/TNFSF2 Protein, Mouse (P. pastoris) is a recombinant protein and is produced in P. pastoris.

TNF α 由巨噬细胞、单核细胞、中性粒细胞、T 细胞和 NK 细胞等多种细胞产生^[2]。
人 TNF α 蛋白的氨基酸序列同源性较低小鼠、大鼠、牛、食蟹猴之间的 TNF α 蛋白。而人TNFα与食蟹猴TNFα蛋白的氨基酸序列一致性为94.85%，小鼠TNFα与大鼠TNFα蛋白的氨基酸序列一致性为94.47%。
TNFα以两种形式存在；II 型跨膜蛋白 (tmTNF-α) 和成熟可溶性蛋白 (sTNF-α)。TNF-α与其受体（主要是TNFR1和TNFR2）结合，然后传递分子信号以实现炎症和细胞死亡等生物学功能。sTNF-α 和 tmTNF-α 均激活 TNFR1，并处理与 TNFR1 相关死亡结构域 (TRADD) 接头蛋白相互作用的死亡结构域 (DD)。TNFR2信号通路主要由tmTNF-α激活。TNFR1 信号传导往往具有促炎和凋亡作用。TNFR2 会导致 NF-κB 和 MAPK 以及 AKT 激活，TNFR2 激活与组织再生、细胞增殖和细胞存活以及宿主防御和炎症等稳态生物活性相关^[1]。
TNF-α 对正常免疫反应至关重要，异常分泌 TNF-α 激活滑膜成纤维细胞、角质形成细胞、破骨细胞，诱发类风湿性关节炎、炎症性肠病、银屑病关节炎 (PsA) 和非感染性葡萄膜炎 (NIU)^[3]。TNF α 独立于 Pgp 外排活性正向调节内源 TNF-α 表达水平，诱导 IHF 细胞增殖^[4]。组织中的 TNF α 可能促进癌症生长、侵袭和转移。此外，TNF α 通过 TNFR2 刺激 NF-κB 通路，而抗 TNF-α MAb 显着抑制结肠炎相关癌 (CAC) 小鼠的肿瘤发展^[5]。TNF α 作为一种原神经生成因子，可激活 SAPK/JNK 通路，并可促进脑损伤后的神经元替换和脑修复^[6]。

TNF alpha (小鼠) (0, 2.5, 5, 10, 20, 40 ng/ml; 5 min) 以剂量依赖性方式刺激 NF-κB 通路并上调 CT26 细胞中 p65 和 IκBα 的磷酸化水平 ^[3].
TNF alpha (小鼠) (1, 10 ng/mL; 7 days) 通过 TNFR1 激活诱导 SVZ 细胞的神经元分化^[4]。
TNF alpha (小鼠) (1, 10; 100 ng/mL; 48 h) 在 1 ng/mL 和高浓度 (10 和 100 ng/ml) 下诱导细胞增殖，在 SVZ 细胞中诱导细胞凋亡 ^[4].

The ED₅₀ is <0.01 ng/mL as measured by L929 cells, corresponding to a specific activity of >1 × 10⁸ units/mg.

Mouse

P. pastoris

Tag Free

P06804 (S84-L235)

21926  [NCBI]

SQNSSDKPVAHVVANHQVEEQLEWLSQRANALLANGMDLKDNQLVVPADGLYLVYSQVLFKGQGCPDYVLLTHTVSRFAISYQEKVNLLSAVKSPCPKDTPEGAELKPWYEPIYLGGVFQLEKGDQLSAEVNLPKYLDFAESGQVYFGVIAL

Approximately 17 kDa

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

无菌粉末.

Lyophilized after extensive dialysis against PBS.

<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]. Horiuchi T, et al. Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents. Rheumatology (Oxford). 2010 Jul;49(7):1215-28.  [Content Brief]

  [2]. Zelová H, et al. TNF-α signalling and inflammation: interactions between old acquaintances. Inflamm Res. 2013 Jul;62(7):641-51.  [Content Brief]

  [3]. El-Tahan RR, et al. TNF-α gene polymorphisms and expression. Springerplus. 2016 Sep 7;5(1):1508.  [Content Brief]

  [4]. Jang DI, et al. The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics. Int J Mol Sci. 2021 Mar 8;22(5):2719.  [Content Brief]

  [5]. Berguetti T, et al. TNF-α Modulates P-Glycoprotein Expression and Contributes to Cellular Proliferation via Extracellular Vesicles. Cells. 2019 May 24;8(5):500.  [Content Brief]

  [6]. Onizawa M, et al. Signaling pathway via TNF-alpha/NF-kappaB in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis. Am J Physiol Gastrointest Liver Physiol. 2009 Apr;296(4):G850-9.  [Content Brief]

  [7]. Bernardino L, et al. Tumor necrosis factor-alpha modulates survival, proliferation, and neuronal differentiation in neonatal subventricular zone cell cultures. Stem Cells. 2008 Sep;26(9):2361-71.  [Content Brief]

  [8]. Matsuno H, et al. The role of TNF-alpha in the pathogenesis of inflammation and joint destruction in rheumatoid arthritis (RA): a study using a human RA/SCID mouse chimera. Rheumatology (Oxford). 2002 Mar;41(3):329-37.  [Content Brief]