载脂蛋白1重组兔单抗

bsm-54473R

重组兔单抗

CD95/FAS Recombinant Rabbit mAb

载脂蛋白1重组兔单抗

ALPS1A; APO-1; APT1; CD95; FAS1; FASTM; TNFRSF6; APO1; TNFR6; lpr; FasR; TNR6_HUMAN; FAS; Apo-1 antigen; Apoptosis-mediating surface antigen FAS; FASLG receptor; TNR6_MOUSE; TNR6_RAT;

Rabbit

Recombinant protein human CD95/FAS

IgG

Liquid

affinity purified by Protein A

Recombinant

6F9

45 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

FAS(也称作Apo-1;CD95;FasL receptor;TNFR)是一个含有死亡结构域的受体，是一型膜蛋白，属于TNF-R家族成员，具有诱导细胞凋亡的功能，广泛分布于许多不同类型的细胞，主要用于各种恶性肿瘤（包括：乳腺癌、肾细胞癌、胃癌、肺癌以及肝病等）的研究。分子量为：40-50kDa。

FAS的凋亡信号主要是通过与其胞浆区相关的死亡结构域蛋白FADD介导的。FAS与FasL结合后，FADD一方面通过C端的DD结合FAS, 另一方面通过N端的DED与Caspase-8 N端DED结合，通过Caspase-8诱导效应性Caspase 蛋白酶的激活，并最终导致细胞凋亡的发生。FAS主要表达于活化淋巴细胞、单核细胞、中性粒细胞和成纤维细胞等。

Fas又称作APO-1/CD95，属TNF受体家族。Fas基因编码产物为分子量45KD的跨膜蛋白，分布于胸腺细胞，激活的T和B淋巴细胞，巨噬细胞，肝、脾、肺、心、脑、肠、睾丸和卵巢细胞等。
Fas蛋白与Fas配体结合后，会激活caspase，导致靶细胞走向凋亡

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq, Mar 2011]