Patents by Inventor Michael W. Glynn
Michael W. Glynn has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Publication number: 20150018381Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: ApplicationFiled: July 21, 2014Publication date: January 15, 2015Inventors: Leslie B. GORDON, Francis S. COLLINS, Thomas GLOVER, Michael W. GLYNN, Brian C. CAPELL, Adrienne D. COX, Channing J. DER
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Patent number: 8828356Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: GrantFiled: April 4, 2013Date of Patent: September 9, 2014Assignees: Progeria Research Foundation, Inc., The United States of America as represented by the Secretary of the Department of Health and Human Services, The University of North Carolina at Chapel Hill, The Regents of the University of MichiganInventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Patent number: 8691501Abstract: Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies.Type: GrantFiled: August 6, 2012Date of Patent: April 8, 2014Assignees: Progeria Research Foundation, Inc., The United States of America as represented by the Secretary of the Department of Health and Human Services, The Universitry of North Carolina at Chapel Hill, The Regents of the University of MichiganInventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Publication number: 20120329066Abstract: Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies.Type: ApplicationFiled: August 6, 2012Publication date: December 27, 2012Inventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Patent number: 8257915Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: GrantFiled: October 15, 2010Date of Patent: September 4, 2012Assignees: Progeria Research Foundation, Inc., The United States of America as represented by the Secretary of the Department of Health and Human Services, The University of North Carolina at Chapel Hill, The Regents of the University of MichiganInventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Publication number: 20110027806Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: ApplicationFiled: October 15, 2010Publication date: February 3, 2011Inventors: LESLIE B. GORDON, FRANCIS S. COLLINS, THOMAS GLOVER, MICHAEL W. GLYNN, BRIAN C. CAPELL, ADRIENNE D. COX, CHANNING J. DER
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Patent number: 7838531Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: GrantFiled: July 25, 2007Date of Patent: November 23, 2010Assignees: The United States of America as represented by the Department of Health and Human Services, The Regents of the University of Michiga, Progeria Research Foundation, Inc., The University of North Carolina at Chapel HillInventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Publication number: 20080131375Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.Type: ApplicationFiled: July 25, 2007Publication date: June 5, 2008Inventors: Leslie B. Gordon, Francis S. Collins, Thomas Glover, Michael W. Glynn, Brian C. Capell, Adrienne D. Cox, Channing J. Der
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Patent number: 5716628Abstract: Disclosed herein is an antimicrobial composition characterized by synergistic antibacterial and antifungal efficacy and comprising a pyrithione salt or pyrithione acid, and at least one compound selected from the group consisting of benzyl and lower alkyl esters of para-hydroxybenzoic acid, salts thereof, carboxylic acids, salts thereof, and combinations thereof. Also disclosed is a method of imparting antimicrobial activity to a composition comprising water or an organic solvent which comprises adding thereto an antimicrobially effective amount of the above-described antimicrobial composition.Type: GrantFiled: July 29, 1996Date of Patent: February 10, 1998Assignee: The University of ConnecticutInventors: Robert T. Vinopal, John D. Nelson, Jr., Michael W. Glynn, Robert W. Coughlin, Robert F. Vieth, Jon R. Geiger
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Patent number: 5540920Abstract: Disclosed herein is an antimicrobial composition characterized by synergistic antibacterial and antifungal efficacy and comprising a pyrithione salt or pyrithione acid, and at least one compound selected from the group consisting of benzyl and lower alkyl esters of para-hydroxybenzoic acid, salts thereof, carboxylic acids, salts thereof, and combinations thereof. Also disclosed is a method of imparting antimicrobial activity to a composition comprising water or an organic solvent which comprises adding thereto an antimicrobially effective amount of the above-described antimicrobial composition.Type: GrantFiled: November 22, 1994Date of Patent: July 30, 1996Assignee: Olin CorporationInventors: Robert T. Vinopal, John D. Nelson, Jr., Michael W. Glynn, Robert W. Coughlin, Robert F. Vieth, Jon R. Geiger