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AGENCY:

National Institutes of Health, Public Health Service, DHHS.

ACTION:

Notice.

SUMMARY:

The inventions listed below are owned by agencies of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing.

ADDRESSES:

Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: (301) 496-7057; fax: (301) 402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

Recombinant SUMO-1 Isopeptidase Substrates for FRET Assays

Mary Dasso and Jun Hang (NICHD).

DHHS Reference No. E-086-02/0—Research Tool.

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@od.nih.gov.

The NIH announces a new Fluorescence Resonance Energy Transfer (FRET) assay for peptidases that regulate the processing of SUMO-1 and its removal from conjugation. SUMO-1 is an ubiquitin-like protein that becomes covalently linked to other proteins, which in turn may participate in events leading to cancer and viral infection. The inventors have created a FRET substrate that fuses unprocessed SUMO-1 at its N- and C-termini with different Green Fluorescence Protein (GFP) derivatives. The FRET assay may be used to identify pharmacological agents that can regulate the SUMO-1 peptidases or to monitor their activities.

Human Gene Critical to Fertility

Lawrence Nelson and Zhi-bin Tong (NICHD).

DHHS Reference No. E-239-00/1 filed 04 Apr 2001 (PCT/US01/10981).

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@od.nih.gov.

Some molecular pathways are unique to the reproductive process. Illuminating such processes would be expected to lead the way to the most specific molecular contraceptive targets. The Mater gene is essential for embryonic development beyond the two-cell stage. Mater expression is specific to the oocyte. Thus, Mater appears to qualify as a player in a unique molecular pathway that is specific to the reproductive process.

The human MATER gene was identified through research investigating autoimmune premature ovarian failure. Premature ovarian failure (POF) is a term used to describe a condition associated with female sex hormone deficiency and infertility in women younger than age 40. As many as 1% of all women in the United States are thought to be afflicted with POF. Autoimmunity is a well-established mechanism of premature ovarian failure.

The NIH announces a new technology that encompasses the MATER gene, protein and MATER-specific antibodies. These molecules can be used in diagnosing and/or treating infertility, and in developing contraceptives.

Anti-Inflammatory Actions of Cytochrome P450 Epoxygenase-derived Eicosanoids

Drs. Darryl C. Zeldin (NIEHS), James Liao (EM).

DHHS Reference Nos. E-252-1999/0-US-02 filed 09 Aug 2000 and E-252-1999/0-PCT-03 filed 10 Aug 2000.

Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; shinnm@od.nih.gov.

Cytochrome P450s catalyze the NADPH-dependent oxidation of arachidonic acid to various eicosanoids found in several species including humans. The eicosanoids are biosynthesized in numerous tissues including pancreas, intestine, kidney, heart, and lung where they are involved in many different biological activities.

The NIH announces a new therapy wherein epoxyeicosatrienoic acid (EET) compositions have been found to be useful in preventing endothelial cell death due to hypoxia-reoxygenation. Given that endothelial injury is an important early event in the development of the atherosclerotic plaque and is associated with myocardial dysfunction in ischemic heart disease, reduced EET levels are speculated to be involved in the pathogenesis of these cardiovascular disorders.

This research is described in Yang et al., Molecular Pharmacology 60: 310-320, 2001.

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