Abstract: Nucleotide and amino acid sequences are provided for compounds which promote tissue growth, as well as methods for modulating tissue growth, for imaging tissues and organs, and for treating patients.

Abstract: Nucleotide and amino acid sequences are provided for compounds which promote tissue growth, as well as methods for modulating tissue growth, for imaging tissues and organs, and for treating patients. Isolated nucleic acid and amino acid sequences for Ret ligands are disclosed. Ret ligands encoded by the isolated nucleic acid sequences of the invention have a hydrophobic N-terminal signal sequence, a hydrophobic C-terminal sequence and a phosphatidylinositol glycan linkage motif. Vectors and host cells that include Ret ligands encoded by the isolated nucleic acid sequences of the invention are also disclosed.

Abstract: Proteins which are upregulated in injured or regenerating tissues, as well as the DNA encoding these proteins, are disclosed, as well as therapeutic compositions and methods of treatment encompassing these compounds.

Abstract: The invention relates to antibodies which specifically bind to the gc chain of cytokine receptors, as well as to cell lines which produce such antibodies, pharmaceutical compositions, and methods of treating immunological diseases by treating patients with such antibodies.

Abstract: This invention relates to compositions and methods useful for activating LT-&bgr; receptor signaling, which in turn elicits potent anti-proliferative effects on tumor cells. More particularly, this invention relates to lymphotoxin heteromeric complexes formed between lymphotoxin-&agr; and multiple subunits of lymphotoxin-&bgr;, which induce cytotoxic effects on tumor cells in the presence of lymphotoxin-&bgr; receptor activating agents. Also within the scope of this invention are antibodies directed against the lymphotoxin-&bgr; receptor which act as lymphotoxin-&bgr; receptor activating agents alone or in combination with other lymphotoxin-&bgr; receptor activating agents either in the presence or absence of lymphotoxin-&agr;/&bgr; complexes. A screening method for selecting such antibodies is provided.

Abstract: VCAM fusion proteins capable of binding to VLA4, and DNA molecules coding on these fusions.

Abstract: VCAM1 polypeptides and VCAM11/ICAM fusion proteins are disclosed.

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: This invention relates to compositions and methods comprising "lymphotoxin-.beta. receptor blocking agents", which block lymphotoxin-.beta. receptor signalling. Lymphotoxin-.beta. receptor blocking agents are useful for treating lymphocyte-mediated immunological diseases, and more particularly, for inhibiting Th1 cell-mediated immune responses. This invention relates to soluble forms of the lymphotoxin-.beta. receptor extracellular domain that act as lymphotoxin-.beta. receptor blocking agents. This invention also relates to the use of antibodies directed against either the lymphotoxin-.beta. receptor or its ligand, surface lymphotoxin, that act as lymphotoxin-.beta. receptor blocking agents. A novel screening method for selecting soluble receptors, antibodies and other agents that block LT-.beta. receptor signalling is provided.

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: Anti-CD4 antibody homologs, DNA sequences and recombinant DNA molecules encoding them, prophylactic, immunotherapeutic and diagnostic compositions comprising those antibody homologs, and methods for preventing or treating diseases in mammals, including humans, caused by infective agents whose primary targets are CD4.sup.+ lymphocytes. Such diseases include acquired immune deficiency syndrome ("AIDS"), AIDS related complex, and human immunodeficiency virus infection.

Abstract: The present invention relates to uses of mutant proto-oncogenes and oncoproteins expressed by the proto-oncogenes in inhibiting tumor growth and/or inhibiting the transformed phenotype. The preferred oncoprotein is a dominant, interfering mutant of a nuclear E2F transcription factor protein and is preferably a mutant E2F1 transcription factor protein. Methods of treating a target cell are described. Treatment is accomplished by administering to a target cell a dominant interfering mutant of a proto-oncogene in an effective amount. Treatment is also accomplished by administering to a target cell an oncoprotein in an effective amount. Compositions for such use are described as well.

Abstract: This invention relates to delivery of biologically active cargo molecules, such as polypeptides and nucleic acids, into the cytoplasm and nuclei of cells in vitro and in vivo. Intracellular delivery of cargo molecules according to this invention is accomplished by the use of novel transport polypeptides which comprise HIV tat protein or one or more portions thereof, and which are covalently attached to cargo molecules. The transport polypeptides in preferred embodiments of this invention are characterized by the presence of the tat basic region (amino acids 49-57), the absence of the tat cysteine-rich region (amino acids 22-36) and the absence of the tat exon 2-encoded carboxy-terminal domain (amino acids 73-86) of the naturally-occurring tat protein. By virtue of the absence of the cysteine-rich region, the preferred transport polypeptides of this invention solve the potential problems of spurious trans-activation and disulfide aggregation.

Abstract: Polypeptides and proteins comprising the CD2-binding domain of LFA-3 are disclosed. DNA sequences that code on expression for those polypeptides and proteins, methods of producing and using those polypeptides and proteins, and therapeutic and diagnostic compositions are also disclosed. Deletion mutants unable to bind CD2 and methods for their use are also disclosed. In addition, fusion proteins which comprise the CD2-binding domain of LFA-3 and a portion of a protein other than LFA-3, DNA sequences encoding those fusion proteins, methods for producing those fusion proteins, and uses of those fusion proteins are disclosed.

Abstract: The invention is generally directed to methods of promoting normal respiratory tract airflow in subjects with restricted airflow and ciliary clearance caused by the presence of pathological airway contents, and particularly mucoid contents. Actin-binding proteins are administered into the respiratory tract of a subject with a pathological respiratory condition involving the presence of such contents. The actin-binding protein binds to actin polymers in the contents and decreases the viscosity. The actin binding proteins also prevent actin from binding to exogenous or endogenous DNase, thus increasing the degradation of DNA polymers in the contents.