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Robert F. Dubose

Bio: Robert F. Dubose is an academic researcher from John Wiley & Sons. The author has contributed to research in topics: Semaphorin & Disintegrin. The author has an hindex of 9, co-authored 25 publications receiving 284 citations.

Papers
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Journal ArticleDOI
TL;DR: An ancestral analysis of all known mammalian ADAMs indicates that the zinc-binding motif in the catalytic domain arose once in a common ancestor and was subsequently lost by those members lacking this motif.

66 citations

Patent
05 Oct 2001
TL;DR: In this paper, the authors proposed a method for synthesizing new members of the hematopoietin receptor polypeptide family, including human and murine HPR1 and HPR2.
Abstract: This invention relates to human and murine HPR1 and human and murine HPR2 polypeptides, new members of the hematopoietin receptor polypeptide family; to methods of making such HPR1 and HPR2 polypeptides; to non-human mammals in which the endogenous genomic sequences encoding HPR1 and/or HPR2 polypeptides have been partially or completely inactivated; to methods of using HPR1 or HPR2 polypeptides to identify compounds that alter HPR1 or HPR2 polypeptide activities; and to methods of preparing medicaments for and/or treating conditions associated with hematopoietin receptor function.

53 citations

Journal ArticleDOI
03 Sep 1999-Gene
TL;DR: An ancestral analysis of all known ADAMs indicates that the zinc-binding motif in the catalytic domain arose once in a common ancestor and was lost by those members lacking this motif.

44 citations

Patent
08 Jan 2002
TL;DR: In this article, the B7-H1.2 and Butryophilin 2/3, new members of the human B7 polypeptide family, were described.
Abstract: This invention relates to B7-H1.2 and Butryophilin 2/3, new members of the human B7 polypeptide family, methods of making such polypeptides, and to methods of using them to treat immunological conditions and to identify compounds that alter the activities of these human B7 polypeptides.

30 citations

Patent
26 Jan 2018
TL;DR: In this article, the compositions of conjugates comprising immune-stimulatory compounds are provided, and the methods of preparation and use of the conjugate are also provided, including methods for treating disorders, such as cancer.
Abstract: Various compositions are disclosed. The compositions of conjugates comprising immune-stimulatory compounds are also provided. Additionally provided are the methods of preparation and use of the conjugates. This includes methods for treating disorders, such as cancer.

28 citations


Cited by
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Patent
04 Oct 2006
TL;DR: In this paper, the present invention is directed to secreted and transmembrane polypeptides and to nucleic acid molecules encoding those polyptides, and vectors and host cells comprising those nucleic amino acid sequences.
Abstract: The present invention is directed to secreted and transmembrane polypeptides and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention.

1,267 citations

Journal ArticleDOI
TL;DR: This review will first discuss the properties of each of the domains of the ADAMs, then describe the involvement ofADAMs in selected biological processes, and highlight recent interesting findings suggesting roles for ADams in human disease.
Abstract: The ADAMs family of transmembrane proteins belongs to the zinc protease superfamily. Members of the family have a modular design, characterized by the presence of metalloprotease and integrin receptor-binding activities, and a cytoplasmic domain that in many family members specifies binding sites for various signal transducing proteins. The ADAMs family has been implicated in the control of membrane fusion, cytokine and growth factor shedding, and cell migration, as well as processes such as muscle development, fertilization, and cell fate determination. Pathologies such as inflammation and cancer also involve ADAMs family members. Excellent reviews covering various facets of the ADAMs literature-base have been published over the years and we recommend their examination (Black and White 1998; Schlondorff and Blobel 1999; Primakoff and Myles 2000; Evans 2001; Kheradmand and Werb 2002). In this review, we will first discuss the properties of each of the domains of the ADAMs. We will then go on to describe the involvement of ADAMs in selected biological processes. Then, we will highlight recent interesting findings suggesting roles for ADAMs in human disease. Finally, we look to the future and discuss some of the open issues in ADAMs function and regulation.

1,099 citations

PatentDOI
TL;DR: In this article, the authors present methods of diagnosis by assessing B7-H1 expression in a tissue from a subject that has, or is suspected of having, cancer, methods of treatment with agents that interfere with B7H1-receptor interaction, and methods of selecting candidate subjects likely to benefit from cancer immunotherapy.
Abstract: The invention features methods of diagnosis by assessing B7-H1 expression in a tissue from a subject that has, or is suspected of having, cancer, methods of treatment with agents that interfere with B7-H1-receptor interaction, methods of selecting candidate subjects likely to benefit from cancer immunotherapy, and methods of inhibiting expression of B7-H1.

666 citations

Patent
08 Dec 2009
TL;DR: In this paper, anti-PD-L1 antibodies are used to enhance T-cell function to upregulate cell-mediated immune responses and for the treatment of T cell dysfunctional disorders, including infection (e.g., acute and chronic) and tumor immunity.
Abstract: The present application relates to anti-PD-L1 antibodies, nucleic acid encoding the same, therapeutic compositions thereof, and their use enhance T-cell function to upregulate cell-mediated immune responses and for the treatment of T cell dysfunctional disorders, including infection (e.g., acute and chronic) and tumor immunity.

571 citations

Journal ArticleDOI
01 Jul 2000-Neuron
TL;DR: Reelin inhibits migration of cortical neurons and enables detachment of neurons from radial glia and may arrest neuronal migration and promote normal cortical lamination by binding alpha3beta1 integrin and modulating integrin-mediated cellular adhesion.

545 citations