Patents by Inventor Wilfried Ellmeier

Wilfried Ellmeier 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).

  • Patent number: 7129055
    Abstract: Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the ?-chemokines RANTES, MIP-1?, and MIP-1?.
    Type: Grant
    Filed: December 11, 2000
    Date of Patent: October 31, 2006
    Assignee: New York University
    Inventors: Dan R. Littman, Hongkui Deng, Wilfried Ellmeier, Nathaniel R. Landau, Rong Liu
  • Publication number: 20030096221
    Abstract: Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the &bgr;-chemokines RANTES, MIP-1&agr;, and MIP-1&bgr;.
    Type: Application
    Filed: December 11, 2000
    Publication date: May 22, 2003
    Inventors: Dan R. Littman, Hongkui Deng, Wilfried Ellmeier, Nathaniel R. Landau, Rong Liu
  • Patent number: 6258527
    Abstract: Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the &bgr;-chemokines RANTES, MIP-1&agr;, and MIP-1&bgr;.
    Type: Grant
    Filed: May 21, 1997
    Date of Patent: July 10, 2001
    Assignees: The Aaron Diamond Aids Research Center, New York University
    Inventors: Dan R. Littman, Hongkui Deng, Wilfried Ellmeier, Nathaniel R. Landau, Rong Liu
  • Patent number: 5939320
    Abstract: Entry of HIV-1 into target cells requires cell surface CD4 as well as additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T cell lines was recently identified and named fusin. Fusin, however, does not promote entry of macrophage-tropic viruses that are believed to be the key pathogenic strains in vivo. It has now been determined that the principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR5, a receptor for the .beta.-chemokines RANTES, MIP-1.alpha., and MIP-1.beta..
    Type: Grant
    Filed: June 19, 1996
    Date of Patent: August 17, 1999
    Assignees: New York University, The Aaron Diamond Aids Research Center
    Inventors: Dan R. Littman, Hongkui Deng, Wilfried Ellmeier, Nathaniel R. Landau, Rong Liu
  • Patent number: 5683878
    Abstract: Disclosed is a gene situated in the region of the neuroblastoma consensus deletion 1p36.2-p36.1 which codes for a helix-loop-helix protein with the designation HEIR-1. The loss of this gene is significantly correlated with allelic tumor deletions in neuroblastomas and expression of this correlates inversely both N-myc overexpression in tumors and with N-myc expression in normal development. The cDNA and antibodies coding for HEIR-1 are used for the diagnosis of pathological conditions associated with aberration in the region of the neuroblastoma consensus deletion.
    Type: Grant
    Filed: June 6, 1995
    Date of Patent: November 4, 1997
    Assignees: Boehringer Ingelheim International GmbH, Genentech, Inc.
    Inventors: Wilfried Ellmeier, Andreas Weith
  • Patent number: 5654188
    Abstract: Described is a gene situated in the region of the neuroblastoma consensus deletion 1p36.2-p36.1 and which codes for a helix-loop-helix protein with the designation HEIR-1. The gene is affected significantly by allelic tumor deletions in neuroblastomas and correlates inversely both N-myc overexpression in tumors and with N-myc expression in normal development. The cDNA and antibodies coding for HEIR-1 are used for the diagnosis of pathological conditions associated with aberration in the region of the neuroblastoma consensus deletion.
    Type: Grant
    Filed: June 23, 1994
    Date of Patent: August 5, 1997
    Assignee: Boehringer Ingelheim International GmbH
    Inventors: Wilfried Ellmeier, Andreas Weith