Abstract: The present invention relates to nucleic acids that encode novel basic helix-loop-helix polypeptides. The present invention also relates to novel basic helix-loop-helix polypeptides, in particular, rat Relax and human ngn3 polypeptides. The invention also relates to methods for the detection of nucleic acids and polypeptides according to the invention. The invention also relates to methods for the detection of activators or inhibitors of the polypeptides of the invention. Finally, the present invention relates to methods of prevention and/or treatment of pathologies, dysfunctions, disorders or conditions affecting the nervous system.
Type:
Grant
Filed:
June 16, 2000
Date of Patent:
February 14, 2006
Assignee:
Centelion SAS
Inventors:
Christine Icard-Liepkalns, Jacques Mallet, Philippe Ravassard
Abstract: The present invention relates to variants of TRAF2 which demonstrate the ability to inhibit the TNF ? signaling path-way. In particular, applicants have isolated a splice variant of TRAF2 referred to hereinafter as “TRAF2 truncated” or “TRAF2TR” and a TRAF2 expression construct with enhanced dominant negative properties, hereafter referred to as “TRAF2 truncated-deleted” or “TRAF2TD”. Both TRAF2TR and TRAF2TD have the ability to inhibit the TNF ? signaling pathway and in TRAF2TD, this ability is greatly enhanced, greatly reducing the response to TNF ? binding.
Type:
Grant
Filed:
April 6, 2000
Date of Patent:
February 14, 2006
Assignee:
Centelion SAS
Inventors:
George H. Searfoss, III, Marco F. Pagnoni, Yuri D. Ivashchenko, Kun Guo, Kenneth L. Clark
Abstract: The present invention relates to the use of a plasmid encoding a fibroblast growth factor as therapeutic agent for the prevention and treatment of hypercholesterolemia or diabetes associated myocardial or skeletal angiogenic defects. The present invention also relates to a method for enhancing formation of both collateral blood vessels and arterioles in myocardial or skeletal ischemic tissues in a mammalian subject suffering from hypercholesterolemia or diabetes. The present invention further relates to a method of promoting collateral blood vessels in ischemic myocardial or skeletal tissues without inducing VEGF-A factor expression and causing edema in the treated muscles.