96 results about "Neuroblastoma cell" patented technology

Genetically engineered, CE7-specific redirected immune cells expressing a cell surface protein having an extracellular domain comprising a receptor which is specific for CE7, an intracellular signaling domain, and a transmembrane domain, and methods of use for such cells for cellular immunotherapy of CE7+ neuroblastoma are disclosed. In one embodiment, the immune cell is a T cell and the cell surface protein is a single chain FvFc:ζ receptor where Fv designates the VH and VL chains of a single chain monoclonal antibody to CE7 linked by peptide, Fc represents a hinge-CH2—CH3 region of a human IgG1, and ζ represents the intracellular signaling domain of the zeta chain of human CD3. DNA constructs encoding a chimeric T-cell receptor and a method of making a redirected T cell expressing a chimeric T cell receptor by electroporation using naked DNA encoding the receptor are also disclosed.

PL37 (RAARISLGPRCIKAFTE [SEQ ID NO: 2]) is an Antisense Homology Box peptide composed of amino acids 37 to 53 of C5a-anaphylatoxin. Complementary peptides, ASGAPAPGPAGPLRPMF (Pep-A [SEQ ID NO: 1]) and ASTAPARAGLPRLPKFF (Pep-B [SEQ ID NO: 3]) were designed and characterized. Pep-A bound to PL37 and to C5a with very slow dissociation, whereas Pep-B failed to bind at all. C5a was inactivated by 7 nM or more of Pep-A and this concentration of Pep-A inhibited induction of intracellular Ca++ influx in neutrophils. Patch clamp studies also showed the effectiveness of Pep-A in C5a-receptor-expressing neuroblastoma cells. Pep-A administration prevented rats from C5a-mediated rapid lethal shock. A-Pep-A (Pep-A acetylated with alanine at the amino-terminus) was more stable in vivo and showed stronger inhibition of inflammatory reactions in mice and rats. Chemical modification of Pep-A (e.g., acetylation, or single or multiple amino acid replacement, insertion, or deletion within the native Pep-A sequence) will yield effective inhibitors, and will often improve inhibitory function on C5a anaphylatoxin. In such modified constructs it will often be desired to conserve some or all 5 prolines found in Pep-A to preserve inhibitory function on C5a.

The present invention relates to host cells that can function as neurons which are obtained by introducing and expressing von Hippel-Lindau gene in cancer cells, such as neuroblastoma cells and anaplastic oncocytes derived from the nerve system, or embryonic stem cells. The obtained hosts that have grown in vitro are grafted to the central nerve system or peripheral nerves to take so as to allow the host cells to function as neurons, thereby treating intractable neuronal diseases associated with neurological functional disorder, such as Parkinson's disease, amyotrophic lateral sclerosis, Huntington's chorea, Alzheimer's disease, brain infarction, spinal cord injury, brain contusion or malignant tumor.

The invention relates to a new purpose of protein kinase Mnk2a. According to the invention, the Mnk2a can be identified by a western means, the phosphorylation of Alpha-synuclein129 site serine through an extracellular signal-regulated kinase (ERK) signal passage, and at the same time, the effect that in human neuroblast oncocyte (SH-5Y-5Y) nucleuses, Mnk2a can intensify the formation of Alpha-synuclein granular aggregates similar to Lewy bodies is detected by a cell immunofluorescence means. The further basis and the action mechanism can be provided for the full study of disease generation pathogenesis of parkinson's diseases (PD).