Abstract: The present invention provides a mutant protein of activation-induced cytidine deaminase, wherein hsAID is mutated with the following mutations: T82I, K10E, K34E, E156G, 181*, S38, H130, V152, R174, T100. The present invention also provides a High-efficiency Base Editor, including the mutant protein of activation-induced cytidine deaminase of the present invention and a DNA-specific binding protein, which are linked sequentially via a linking sequence. The present invention also provides a single-base locus-directed editing system, including single-base locus-directed editing proteins and target Hyper Mutation Fragment. Compared with the existing activation-induced cytidine deaminase (AID)-based single-base editing system, the mutant protein inducing system of the present invention has a smaller molecular weight and higher mutation efficiency.

Abstract: An application of dipeptide as an ACE enzyme activity inhibitor. Virtual screening is performed on 400 types of dipeptide based on ACE inhibiting effects thereof according to a detected ACE enzyme crystal structure by using self-developed software and adopting a molecular docking method, experiments are conducted to verify the ACE inhibitory activity of the dipeptide obtained by virtual screening, and it finds out that the dipeptide with the N terminal as cysteine has better ACE inhibitory activity.

Abstract: An application of dipeptide as an ACE enzyme activity inhibitor. Virtual screening is performed on 400 types of dipeptide based on ACE inhibiting effects thereof according to a detected ACE enzyme crystal structure by using self-developed software and adopting a molecular docking method, experiments are conducted to verify the ACE inhibitory activity of the dipeptide obtained by virtual screening, and it finds out that the dipeptide with the N terminal as cysteine has better ACE inhibitory activity.

Abstract: The present invention discloses target point, preparation and method for treating human ADSL deficiency. The present invention established an ADSL deficiency retrieval model in nematode through RNA interference technique, and found that the sole RNA interference with PAICS gene could increase the expression of ADSL gene. Based on the conclusion of nematode model study, it can be foreseen that through interference with PAICS gene expression in ADSL deficient patient, accumulation of SAICAR in patient body fluid will be decreased and thereby reducing damage to cells, achieving the object of treating human ADSL deficiency or relieving symptoms.