Kumar B V S Suneel, Malik Siddharth, Grandhi Pradeep, Dayam Raveendra, Sarma J A R P
GVK Biosciences Pvt. Ltd, Phase1, Technocrats Industrial Estate, Balanagar, Hyderabad-500037, Andhra Pradesh, India.
Curr Top Med Chem. 2014;14(17):1977-89. doi: 10.2174/1568026614666140929120231.
Anthrax Lethal Factor (LF) is a zinc-dependent metalloprotease, one of the virulence factor of anthrax infection. Three forms of the anthrax infection have been identified: cutaneous (through skin), gastrointestinal (through alimentary tract), and pulmonary (by inhalation of spores). Anthrax toxin is composed of protective antigen (PA), lethal factor (LF), and edema factor (EF). Protective antigen mediates the entry of Lethal Factor/Edema Factor into the cytosol of host cells. Lethal factor (LF) inactivates mitogen-activated protein kinase kinase inducing cell death, and EF is an adenylyl cyclase impairing host defenses. In the past few years, extensive studies are undertaken to design inhibitors targeting LF. The current review focuses on the small molecule inhibitors targeting LF activity and its structure activity relationships (SAR).
炭疽致死因子（LF）是一种锌依赖性金属蛋白酶，是炭疽感染的毒力因子之一。已确定三种炭疽感染形式：皮肤型（通过皮肤）、胃肠型（通过消化道）和肺型（通过吸入孢子）。炭疽毒素由保护性抗原（PA）、致死因子（LF）和水肿因子（EF）组成。保护性抗原介导致死因子/水肿因子进入宿主细胞的细胞质。致死因子（LF）使丝裂原活化蛋白激酶激酶失活，从而诱导细胞死亡，而EF是一种腺苷酸环化酶，会损害宿主防御功能。在过去几年中，人们进行了广泛的研究以设计针对LF的抑制剂。本综述重点关注靶向LF活性的小分子抑制剂及其构效关系（SAR）。
