The present disclosure relates to compositions, nucleic acid constructs, methods and kits thereof for cell induction or reprogramming cells to the dendritic cell state or antigen presenting cell state, based, in part, on the surprisingly effect described herein of novel use and combinations of transcription factors that permit induction or reprogramming of differentiated or undifferentiated cells into dendritic cells or antigen presenting cells. Such compositions, nucleic acid constructs, methods and kits can be used for inducing dendritic cells in vitro, ex vivo, or in vivo, and these induced dendritic cells or antigen presenting cells can be used for immunotherapy applications.

Early vascular cells (EVCs), including endothelial cells and pericytes, are generated from hiPSCs. Unlike the isolated endothelial progenitor cells, the differentiated ECs mature and are functional. When encapsulated in synthetic hydrogel, EVCs respond to matrix cues and self-assembled to form three-dimensional EVCs. Moreover, these EVCs respond to hypoxic microenvironment and undergo vasculogenesis to form complex 3D networks.

A culture medium is provided for establishing expanded potential stem cell (EPSC) lines for mammals. Methods are provided using the medium for the in vitro conversion and maintenance of cells, including pluripotent cells into EPSCs.

The present disclosure provides an in vitro method for preparation of human pluripotent stem cells (HPSCs) from human adipocyte-derived stem cells (ADSCs) without any genetic engineering techniques and without involving any exogenous gene elements, plasmid or transcription factors and the so obtained HPSCs are referred to as directly-generated human pluripotent stem cells (dgHPSCs). The present invention further provides an in vitro method for insulin production from the dgHPSCs by means of single- or co-transduction with human estrogen-related receptor gamma (ERRγ) gene by the lentivirus vector pWPI/ERRγ encoding the human ERRγ gene and/or with human insulin (INS) gene by a lentivirus vector, pWPI/INS encoding the human INS gene, where the insulin secreted by such co-transduced cells is higher than singly transduced cells. The present invention also provides an in vitro method for insulin production in a glucose-concentration responsive manner involving single transduction of the dgHPSCs with the human ERRγ gene.

Extracellular vesicles, their manufacture, and methods of treatment are described. Generally, extracellular vesicles can be generated by applying sulfhydryl blocking reagents on animal cells. Extracellular vesicles can be loaded with compounds for an intended use, such as, for example, loading an extracellular vesicle with a medicament to treat an animal. As described here, extracellular vesicles can be generated in a large scale and used for personalized treatments.

The present invention relates in part to nucleic acids encoding proteins, nucleic acids containing non-canonical nucleotides, therapeutics comprising nucleic acids, methods, kits, and devices for inducing cells to express proteins, methods, kits, and devices for transfecting, gene editing, and reprogramming cells, and cells, organisms, and therapeutics produced using these methods, kits, and devices. Methods for inducing cells to express proteins and for reprogramming and gene-editing cells using RNA are disclosed. Methods for producing cells from patient samples, cells produced using these methods, and therapeutics comprising cells produced using these methods are also disclosed.

Provided are a medium composition for culturing animal cells for producing a recombinant extracellular matrix protein, a method of producing the recombinant extracellular matrix protein with high purity, and a method of assaying a monomer of the recombinant extracellular matrix protein.

The disclosure provides methods for the production of induced cellular vesicles from natural killer cells and uses thereof, including as a cancer therapy.

The present invention relates to oligonucleotides that are capable of inducing expression of ubiquitin-protein ligase E3A (UBE3A) from the paternal allele in animal or human neurons. The oligonucleotides target the suppressor of the UBE3A paternal allele by hybridization to SNHG14 long non-coding RNA downstream of SNORD109B. The present invention further relates to pharmaceutical compositions and methods for treatment of Angelman syndrome.

The present invention relates in part to nucleic acids encoding proteins, nucleic acids containing non-canonical nucleotides, therapeutics comprising nucleic acids, methods, kits, and devices for inducing cells to express proteins, methods, kits, and devices for transfecting, gene editing, and reprogramming cells, and cells, organisms, and therapeutics produced using these methods, kits, and devices. Methods for inducing cells to express proteins and for reprogramming and gene-editing cells using RNA are disclosed. Methods for producing cells from patient samples, cells produced using these methods, and therapeutics comprising cells produced using these methods are also disclosed.