Fas/CD95 蛋白, Rat (HEK293, Fc)

Fas receptor is a cell surface death receptor, can bind to Fas ligand to form death-inducing signaling complexes, such as Fas associated death domain proteins (FADD)^[1][2]. Fas receptor participates in the caspase cascade and regulate the activation of JNK and p38-K downstream. It is also involved in the signaling cascade of ERK/JNK MAPKs, activating MAPK3/ERK1, MAPK8/JNK and NF-κB, which has been implicated in the pathogenesis of various malignant tumors and immune system diseases^[3][4]. Rat Fas receptor contain a death domain (219-303 a.a.) that plays a key role in regulating programmed death. Fas/CD95 Protein, Rat (HEK293, Fc) produced in HEK293 cells with C-terminal hFc tag.

Fas受体是TNFSF6/FASLG的受体，又称凋亡介导表面抗原FAS和Apo-1抗原。它是一种细胞表面蛋白，与 Fas 配体连接后介导细胞凋亡。Fas受体属于肿瘤坏死因子受体超家族，通过选择性剪接产生7种亚型，其中一些亚型是无义介导的mRNA衰减（NMD）的候选亚型。Fas 基因在人和小鼠的多种组织中表达，包括胸腺、脾脏、卵巢和心脏，以及多种细胞类型，包括活化的 T 淋巴细胞和 B 淋巴细胞。异构体 1 和异构体 6 在静息外周血单核细胞中表达水平相同。激活后，同工型 1 的水平会增加，同工型 6 的水平会降低^[1]。Fas 受体含有死亡结构域。它已被证明在程序性细胞死亡的生理调节中发挥核心作用，并与免疫系统的各种恶性肿瘤和疾病的发病机制有关。它与其配体相互作用，形成死亡诱导信号复合物，其中包括 Fas 相关死亡结构域蛋白 (FADD)、caspase 8 和 caspase 10^[2]。具体来说，复合物中 caspase 的自蛋白水解过程触发下游 caspase 级联，包括酸性鞘磷脂酶的激活、鞘磷脂的消耗、神经酰胺的释放以及随后的 JNK 和 p38-K 的激活。因此，Fas 受体通过 caspase 的调节发挥作用，导致细胞凋亡^[3]。此外，Fas 引发的信号传导由丝裂原激活蛋白激酶 (MAPK) 介导，包括细胞外信号调节激酶 (ERK) 和 c-Jun N 末端激酶 (JNK)，它们诱导 NF-κB 的后续激活。同时，Fas 的刺激会诱导基质金属蛋白酶 (MMP)-9 和 IL-8^[4] 等促炎介质的表达。人Fas蛋白的氨基酸序列与大鼠和小鼠的氨基酸序列同源性较低，相似率分别为49.54%和48.93%。

Fas (CD95) shows an increase expression in adult rat brain after kainate-induced seizures in rats^[5].

Rat

HEK293

C-hFc

Q63199 (Q22-K170)

246097  [NCBI]

MLWIMAVLPLVLAGPELNVRMQGTDSIFEGLELKRSVRETDNNCSEGLYQVGPFCCQPCQPGERKVKDCTTSGGAPTCHPCTEGEEYTDRKHYSDKCRRCAFCDEGHGLEVETNCTRTQNTKCRCKENFYCNASLCDHCYHCTSCGLEDILEPCTRTSNTKCKKQSSNYK

Approximately 57&36 kDa

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Liu C, et al. Differential expression of human Fas mRNA species upon peripheral blood mononuclear cell activation. Biochem J. 1995 Sep 15;310 ( Pt 3)(Pt 3):957-63.  [Content Brief]

  [2]. Screaton RA, et al. Fas-associated death domain protein interacts with methyl-CpG binding domain protein 4: a potential link between genome surveillance and apoptosis. Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5211-6.  [Content Brief]

  [3]. Brenner B, et al. Fas/CD95/Apo-I activates the acidic sphingomyelinase via caspases. Cell Death Differ. 1998 Jan;5(1):29-37.  [Content Brief]

  [4]. Lee SM, et al. Stimulation of Fas (CD95) induces production of pro-inflammatory mediators through ERK/JNK-dependent activation of NF-κB in THP-1 cells. Cell Immunol. 2011;271(1):157-62.  [Content Brief]

  [5]. Tan Z, et al. Increased expression of Fas (CD95/APO-1) in adult rat brain after kainate-induced seizures. Neuroreport. 2001 Jul 3;12(9):1979-82.  [Content Brief]