摘要:
The present invention relates to C. elegans insulin-like genes and methods for identifying insulin-like genes. The methods provide nucleotide sequences of C. elegans insulin-like genes, amino acid sequences of their encoded proteins, and derivatives (e.g., fragments) and analogs thereof. The invention further relates to fragments (and derivatives and analogs thereof) of insulin-like proteins which comprise one or more domains of an insulin-like protein. Antibodies to an insulin-like protein, and derivatives and analogs thereof, are provided. Methods of production of an insulin-like protein (e.g., by recombinant means), and derivatives and analogs thereof, are provided. Further, methods to identify the biological function of a C. elegans insulin-like gene are provided, including various methods for the functional modification (e.g., overexpression, underexpression, mutation, knock-out) of one or more genes simultaneously. Still further, methods to identify a C. elegans gene which modifies the function of, and/or functions in a downstream pathway from, an insulin-like gene are provided.
摘要:
Drosophila melanogaster and C. elegans that have been genetically modified to express or mis-express proteins involved in the sterol regulatory element binding protein (SREBP) pathway are described. These genetically modified animal models have identifiable phenotypes that make them useful in assays for studying lipid metabolism, other genes implicated in lipid metabolism, and compounds capable of modulating lipid metabolism pathways. Methods for studying lipid metabolism in living nematodes using fluorescently-labelled fatty acid conjugates, such BODITY™ fatty acid conjugates, are also described. Novel SREBP pathway nucleic acid and protein sequences are also described.
摘要:
Human VIPR1 genes are identified as modulators of the E2F/RB pathway, and thus are therapeutic targets for disorders associated with defective E2F/RB function. Methods for identifying modulators of E2F/RB, comprising screening for agents that modulate the activity of VIPR1 are provided.