Disclosed is an isolated or purified T cell receptor (TCR), wherein the TCR has antigenic specificity for a mutated human RAS amino acid sequence with a substitution of glycine at position 12 with aspartic acid presented by a human leukocyte antigen (HLA) Class I molecule. Related polypeptides and proteins, as well as related nucleic acids, recombinant expression vectors, host cells, populations of cells, and pharmaceutical compositions are also provided. Also disclosed are methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal.

The present disclosure provides DNA molecules and constructs, including their nucleotide sequences, useful for expressing proteins in plants to promote formation of nodule-like structures in the presence of Rhizobia. The present disclosure also provides DNA molecules and constructs, including their nucleotide sequences, useful for expressing proteins in plants to increase drought resistance. The present disclosure also provides plants and plant cells transgenic plants, plant cells, plant parts, seeds, and commodity products comprising the DNA molecules, along with methods of their use.

The present invention relates to in situ glycosylated MHC II/CII peptide complexes, i.e., complexes naturally glycosylated during recombinant protein expression in the host cell. The invention further relates to methods of producing glycosylated MHC II/CII peptide complexes in mammalian cells. Furthermore the invention relates to the use of such post-translationally modified, preferably glycosylated MHC II/CII complexed for use in treating rheumatoid arthritis, preferably in humans.

According to one aspect and example, a method for facilitating cellular interactions in biological tissue provides controllable activation of a selected type of stem cell among a plurality of cell types present in the tissue. The method includes various steps including the introduction of a microbial opsin into a region of the tissue that includes a selected type of stem cell, by expressing the microbial opsin in the stem cell. A light source is then introduced near the stem cell, and the light source is used to controllably activate the light source to direct pulses of illumination from the light source to the selected type of stem cell, for selectively controlling the growth and development of the stem cell in a manner that is independent of the growth and development of the other types of cells.

The present invention provides a novel virus-like particle expression vector pTMSCA2C, which is constructed as follows: firstly, using plasmid pTrcHis-MS2 as a starting vector and mutating the base T at position 5 of the gene sequence of MS2 bacteriophage 19mer packaging site on the plasmid pTrcHis-MS2 into C through genetic mutation technologies to obtain a plasmid pTMSC; then, mutating valine which is a amino acid corresponding to the initiation codon on the plasmid pTMSC for encoding the maturase protein of MS2 bacteriophage into methionine to obtain a plasmid pTMSCA; and finally, the gene sequence coding wild type MS2 bacteriophage coat protein, after the removal of the terminator, is linked in series with the gene sequence coding MS2 bacteriophage coat protein comprising histidine-tag which is from a pseudovirus vector pTrcMS, and the gene sequence obtained after linking in series is linked to the plasmid pTMSCA to give pTMSCA2C. When the virus-like particle is prepared by using the expression vector pTMSCA2C of the present invention, the yield and purity of the virus-like particle may be improved while the workload for preparation of virus-like particles may be greatly reduced.

This disclosure relates to vectors, isolated cells, compositions, and methods for the treatment of critical limb ischemia and associated disorders. One aspect of the disclosure relates to a vector comprising a nucleic acid encoding a 165A isoform VEGF protein and a promoter that regulates expression of the nucleic acid encoding the VEGF.

According to one aspect and example, a method for facilitating cellular interactions in biological tissue provides controllable activation of a selected type of stem cell among a plurality of cell types present in the tissue. The method includes various steps including the introduction of a microbial opsin into a region of the tissue that includes a selected type of stem cell, by expressing the microbial opsin in the stem cell. A light source is then introduced near the stem cell, and the light source is used to controllably activate thejight source to direct pulses of illumination from the light source to the selected type of stem cell, for selectively controlling the growth and development of the stem cell in a manner that is independent of the growth and development of the other types of cells.

One aspect of the present application relates to a recombinant cell comprising a chimeric antigen receptor and shRNA targeted to inhibit the life cycle of HIV. Another aspect of the present application relates to a chimeric antigen molecule, the extracellular region of which is from or comprising the extracellular region of human CD4 molecule, the transmembrane region of which is from or comprising the transmembrane domain of CD8, and a recombinant cell comprising the above chimeric antigen molecule. The above recombinant cell can be used to treat HIV infection, and have stronger comprehensive killing efficacy, longer effective time, and less risk of causing cytokine storm in the environment of HIV infection.

This disclosure relates to vectors, isolated cells, compositions, and methods for the treatment of critical limb ischemia and associated disorders. One aspect of the disclosure relates to a vector comprising a nucleic acid encoding a 165A isoform VEGF protein and a promoter that regulates expression of the nucleic acid encoding the VEGF.

Described herein is an in vitro genetic rescue assay for identifying a functionally defective DDX41 variant which includes identifying a DEAD-Box Helicase 41 (DDX41) variant of uncertain significance (VUS), infecting a first Ddx41.sup.+/ cell with a retrovirus expressing the DDX41-VUS, infecting a second Ddx41.sup.+/ cell with a retrovirus expressing a wild type control DDX41, growing the first and second infected cells in culture for a period of time and quantitating mRNA expression of a DDX41-regulated transcript in both the first and second infected cells after the period of time, calculating a differential expression of the DDX41-regulated transcript for the first infected cell compared the second infected cell, and identifying the DDX41-VUS as the functionally defective DDX41 variant wherein a change in the differential expression is 1.5-fold or greater. The identified functionally defective DDX41 variants can be used in methods of monitoring a patient for the development/progression of myeloid malignancy.