The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) IL10R and/or a human or chimeric (e.g., humanized) IL10, and methods of use thereof.

The object of the present invention is to provide a polynucleotide which can be inserted into an expression vector and can enhance the transcriptional activity of a predetermined promoter under heart failure.

The object is achieved by an enhancer polynucleotide comprising a polynucleotide consisting of a sequence having 80% or more identity with a sequence represented by SEQ ID NO: 1, or a polynucleotide consisting of a sequence having 80% or more identity with a sequence represented by SEQ ID NO: 2, wherein the enhancer polynucleotide responds to heart failure (where the enhancer polynucleotide excludes a polynucleotide having the same sequence as a sequence represented by SEQ ID NO: 13 and a polynucleotide having the same sequence as a sequence represented by SEQ ID NO: 12).

Provided is a method of producing a genome-edited bird having resistance to avian influenza viruses. A method according to an aspect may enable precise inhibition of interaction between virus proteins while maintaining the original function of an ANP32A gene in a host by substituting only key amino acids of the ANP32A gene. When the method is used, by including cell lines having resistance to avian influenza viruses, new poultry and bird breeds that may not pose any biological safety issues may be efficiently developed. Thus, it is expected that the potential for industrial application is high.

Described herein are methods of prolonging or reactivating organogenesis in a subject in need thereof (e.g., a subject that has impaired organ function such as a prematurely born infant). The methods comprise increasing the expression or activity of Lin28A or Lin28B proteins, inhibiting the expression or activity of let-7 family microRNAs, and/or inhibiting the expression or activity of Dis3L2 exonuclease.

Provided is a method for preparing a diabetic dog model by means of gene editing technology, a diabetic dog model prepared therefrom, as well as cells and issues thereof. The method comprises the following steps: (1) obtaining a dog fertilized egg cell, which comprises a point mutation in GCK gene, for a diabetic dog model by means of gene editing; and (2) transplanting the dog fertilized egg cell into one fallopian tube of a female dog, in which both fallopian tubes have been flushed, to prepare a diabetic dog model comprising a point mutation in GCK gene.

Transgenic mammals that express bovine-based immunoglobulins are described herein, including transgenic rodents that express bovine-based immunoglobulins for the development of bovine therapeutic antibodies.

The present disclosure provides methods and compositions for high frequency mouse transgenesis using, for example, a Bxb1 landing pad.

The present invention relates to compositions, methods, uses and kits for the treatment of renal cystogenesis. In particular, the compositions, methods, uses and kits are particularly useful, but not limited to, the treatment or prevention of Polycystic Kidney Disease. In one aspect, the prevent invention provides a method of minimising or delaying renal cystogenesis in a subject in need thereof, the method comprising inhibiting AKT in the subject, or reducing the level of Aurora kinase in the subject, thereby minimising or delaying renal cystogenesis.

A nerve in a mammal is optogenetically transduced, wherein the nerve is susceptible to stimulus by selective application of transdermal light, and a light source is applied to dermis of the mammal at or proximate to the optogenetically transduced nerve, to thereby stimulate the nerve. A wearable device for optogenetic motor control and sensation restoration of a mammal includes a wearable support, a power source at the wearable support, a controller at the wearable support and in electrical communication with a power source, and a transdermal light source coupled to the controller.

Nonsense-mediated mRNA decay (NMD) polypeptides, nucleic acids encoding NMD polypeptides, and methods of using such polypeptides and nucleic acids in the treatment of ALS and in screening for agents for the treatment of ALS are described.