NKX-2.2 and NKX-6.1 transgenic mouse models for diabetes, depression, and obesity

US6127598A · kind A · utility

Assignee

• The Regents of the University of California · US

Inventors

• Michael German · San Francisco, US
• John L. R. Rubenstein · San Francisco, US
• Lori Sussel · San Francisco, US
• Maike Sander · San Francisco, US
• Dennis J. Hartigan-O'Connor · Ann Arbor, US
• Roger Pedersen · Cambridge, GB
• Juanito Meneses · Palo Alto, US

Key dates

• Filing date: Jul 25, 1997
• Grant date: Oct 3, 2000
• Expiry date: Jul 25, 2017

Classification

• Technology area (CPC A): Human Necessities
• CPC primary: A61K48/00
• WIPO field: Pharmaceuticals
• WIPO sector: Chemistry

Abstract

The present invention features mouse models for Nkx-2.2 gene function and for Nkx-6.1 gene function, wherein the transgenic mouse is characterized by having a defect in Nkx-2.2 gene function or a defect in Nkx-6.1 gene function (where, because Nkx-2.2 acts upstream of Nkx-6.1, a defect in Nkx-2.2 gene function affects Nkx-6.1 gene function) and by having a decreased number of insulin-producing cells relative to a normal mouse. Where the transgenic mouse contains a defect in Nkx-2.2 gene function, the mouse is further characterized by a decreased number of serotonin-producing cells relative to a normal mouse. The transgenic mice may be either homozygous or heterozygous for the Nkx-2.2 or Nkx-6.1 defect.