Merck + Co., Inc.

Other

Howard Y Chen

Leonardus H T Van Der Ploeg

Hui Zheng

Myrna E Trumbauer

Airu S Chen

John W Hess

Catherine D Strader

Leonardus H Van Der Ploeg

Kathryn J Hofmann

Joseph A Borkowski

Gurparlash Singh

David W Smith

Dalip J S Sirinathsinghji

Aurawan Vongs

Guy Seabrook

Dalip Sirinathsinghji

Robert P Heavens

Cells and non-human transgenic animals have been engineered to be deficient in the gene encoding the melcanocortin-3 receptor protein (MC-3R). MC-3R deficient transgenic animals have increased fatmass and reduced lean body mass, showing that the MC-3R protein is involved in the regulation of body fat and muscle mass. These MC-3R deficient transgenic animals can be used to select for and test potential modulators of MC-3R. This data allows for methods of screening for MC-3R modulators which effect body weight and associated methods of treating various disorders associated with inappropriate regulation of body weight. The disclosure also relates to a MC-3R/MC-4R double knockout mouse which can be used to select for and test potential modulators (e.g., agonists or antagonists) of MC-3R and/or MC-4R. It is shown that MC-3R serves a non-redundant role, when compared to MC-4R, in the regulation of energy homeostasis.

Melanocortin-3 receptor deficient cells, non-human transgenic animals and methods of selecting compounds which regulate body weight

Melanocortin-3 receptor deficient cells, non-human trangenic animals and methods of selecting compounds which regulate body weight

Transgenic non-human mammals which express in their brains a nucleic acid construct comprising a DNA sequence encoding a human amyloid precursor protein FAD variant where at amino acid position 717 valine is substituted by isoleucine. These transgenic non-human mammals can be assays systems for determining compounds which are effective in modulating production of human amyloid precursor protein in brain and in isolated neuronal cells. Specifically exemplified are transgenic mice whose genome comprises a DNA sequence encoding a human amyloid precursor protein FAD variant where at amino acid position 717 valine is substituted by isoleucine operably linked to a Thy-1 promoter. The mice are shown to produce the APP-FAD variant in their brains by mRNA and protein assays.

Transgenic mouse expressing a familial form of human amyloid precursor protein

The present invention relates to a transgenic nonhuman animal lacking native amyloid precursor protein. The transgenic mouse of the invention may be used in the study of Alzheimer's Disease and disorders involving the central nervous system.

Transgenic mouse having a disrupted amyloid precursor protein gene

Expression of human interleukin-1.beta. in a transgenic animal

A transgenic non-human animal with alterations in a bradykinin B2 receptor gene is prepared by introduction of a gene encoding an altered bradykinin B2 receptor into a host non-human animal.

Bradykinin B2 receptor modified transgenic non-human animals

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Westfield, NJ, United States of America

Howard Y Chen