HVEM/TNFRSF14 蛋白, Rhesus macaque (HEK293, His)

HVEM (herpes virus entry mediator, TNFRSF14, CD270) is a member of the tumor necrosis factor receptor superfamily (TNFRSF). HVEM is a bidirectional molecular switch that transduces positive and negative signals. HVEM can deliver proinflammatory and survival signals when engaged by BTLA or LIGHT, stimulating lymphocyte proliferation, activation, and inducing inflammatory reactions. While, HVEM binds to CD160 and BTLA, inhibiting T- and B-lymphocyte activation and proliferation^[2][3]. HVEM/TNFRSF14 Protein, Rhesus macaque (HEK293, His) is a recombinant protein with a C-Terminal His label, It consists of 165 amino acids (L39-V203) and is produced in HEK293 cells.

HVEM 广泛表达于多种造血细胞，包括 B 细胞、T 细胞、NK 细胞、单核细胞和未成熟树突状细胞，以及多种非造血细胞和组织，包括肝、肾和肺^{[1]< /sup>.
人HVEM蛋白的氨基酸序列与小鼠HVEM蛋白的同源性较低。
HVEM被称为激活和抑制的“分子开关”模型。HVEM 提供抑制或激活信号并双向调节宿主免疫功能。HVEM与LIGHT或LIGHT-α结合发挥正向刺激作用，刺激淋巴细胞增殖、活化，诱发炎症反应；因此，为 T 细胞激活提供第二刺激信号。此外，HVEM与BTLA和CD160的结合会产生不利的调节作用，促进通过ERK1/2和PI3K（磷脂酰肌醇3激酶）-AKT（蛋白激酶B（PKB））途径的信号转导，导致IFNγ的产生，抑制 T 和 B 淋巴细胞活化和增殖以及 HVEM 与 HSV-gD 的结合，从而促进靶细胞中 HSV 的感染[2][3]。
HVEM 被认为是免疫反应的分子开关，HVEM 诱导 DC 产生 IL-10，并显示出针对肌球蛋白引起的实验性自身免疫性心肌炎 (EAM) 的保护作用[4]。}

Rhesus Macaque

HEK293

C-6*His

F7GSW4 (L39-V203)

/

LPSCKEDEYPVGSECCPKCGPGFHVRQACGEQTGTVCEPCSPGTYIAHFNGLSKCLQCQMCDPAMGLRTSRNCSTTANALCGCSPGHFCIIQDGDHCAACRAYATSSPGQRVQKGGTESQDTLCQNCPPGTFSSNGTLEECQHGTKCSKWLVTEAGPGTSSFRWV

23-36 kDa

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

无菌粉末.

Lyophilized 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]. Ma B, et al. High expression of HVEM is associated with improved prognosis in intrahepatic cholangiocarcinoma. Oncol Lett. 2021 Jan;21(1):69.  [Content Brief]

  [2]. Yu X, et al. BTLA/HVEM Signaling: Milestones in Research and Role in Chronic Hepatitis B Virus Infection. Front Immunol. 2019 Mar 29;10:617.  [Content Brief]

  [3]. Rodriguez-Barbosa JI, et al. HVEM, a cosignaling molecular switch, and its interactions with BTLA, CD160 and LIGHT. Cell Mol Immunol. 2019 Jul;16(7):679-682.  [Content Brief]

  [4]. Cai G, et al. Amelioration of myocarditis by HVEM-overexpressing dendritic cells through induction of IL-10-producing cells. Cardiovasc Res. 2009 Dec 1;84(3):425-33.  [Content Brief]