Abstract:
A IFN-.beta. mutein in which phe (F), tyr (Y), trp (W) or his (H) is substituted for val (V) at position 101, when numbered in accordance with wild type IFN-.beta., DNA sequences encoding these IFN-.beta. muteins, recombinant DNA molecules containing those DNA sequences operatively linked to expression control sequences and capable of inducing expression of an IFN-.beta. mutein, hosts transformed with those recombinant DNA molecules, pharmaceutical compositions containing IFN-.beta. muteins and methods of using those compositions to treat viral infections, cancer or tumors or for immunomodulation.
Abstract:
A IFN-.beta. mutein in which phe (F), tyr (Y), trp (W) or his (H) is substituted for val (V) at position 101, when numbered in accordance with wild type IFN-.beta., DNA sequences encoding these IFN-.beta. muteins, recombinant DNA molecules containing those DNA sequences operatively linked to expression control sequences and capable of inducing expression of an IFN-.beta. mutein, hosts transformed with those recombinant DNA molecules, pharmaceutical compositions containing IFN-.beta. muteins and methods for treating viral infections, cancer or tumors, undesired cell proliferation, or for immunomodulation.
Abstract:
This invention relates to cleaved dimers of Mullerian inhibiting substance-like polypeptides. More particularly, this invention relates to such dimers, methods of producing them and methods of using them in the treatment of cancer and tumors, especially those of the female genital tract. The dimers of this invention are also useful in compositions and methods for contraception.
Abstract:
Endogenous Sp35 is a negative regulator for neuronal survival, axon regeneration, oligodendrocyte differentiation and myelination. Molecules that block endogenous Sp35 function, such anti-Sp35 antibodies can be used as therapeutics for the treatment of neuron and oligodendrocyte dysfunction. The present invention provides antibodies specific for Sp35, and methods of using such antibodies as antagonists of endogenous Sp35 function. The invention further provides specific hybridoma and phage library-derived monoclonal antibodies, nucleic acids encoding these antibodies, and vectors and host cells comprising these antibodies. The invention further provides methods of promoting oligodendrocyte survival and myelination in a vertebrate, comprising administering to a vertebrate in need of such treatment an effective amount of an anti-Sp35 antibody.
Abstract:
Endogenous LINGO-1 is a negative regulator for neuronal survival, axon regeneration, oligodendrocyte differentiation and myelination. Molecules that block endogenous LINGO-1 function, such anti-LINGO-1 antibodies can be used as therapeutics for the treatment of neuron and oligodendrocyte dysfunction. The present invention provides antibodies specific for LINGO-1, and methods of using such antibodies as antagonists of endogenous LINGO-1 function. The invention further provides specific hybridoma and phage library-derived monoclonal antibodies, nucleic acids encoding these antibodies, and vectors and host cells comprising these antibodies. The invention further provides methods of promoting oligodendrocyte survival and myelination in a vertebrate, comprising administering to a vertebrate in need of such treatment an effective amount of an anti-LINGO-1 antibody.
Abstract:
Variant Neublastin polypeptides having substitutions at selected amino acid residues are disclosed. Substitution at one or more selected amino acid residues decreases heparin binding and increases serum exposure of variant Neublastin polypeptides. Also disclosed are methods of using variant Neublastin polypeptides to treat disorders and activate the RET receptor in a mammal.
Abstract:
Compositions and methods for folding proteins belonging to the transforming growth factor beta superfamily are disclosed. The compositions and methods allow for the folding of such proteins when produced in an expression system that does not yield a properly folded, biologically active product.
Abstract:
Endogenous LINGO-1 is a negative regulator for neuronal survival, axon regeneration, oligodendrocyte differentiation and myelination. Molecules that block endogenous LINGO-1 function, such anti-LINGO-1 antibodies can be used as therapeutics for the treatment of neuron and oligodendrocyte dysfunction. The present invention provides antibodies specific for LINGO-1, and methods of using such antibodies as antagonists of endogenous LINGO-1 function. The invention further provides specific hybridoma and phage library-derived monoclonal antibodies, nucleic acids encoding these antibodies, and vectors and host cells comprising these antibodies. The invention further provides methods of promoting oligodendrocyte survival and myelination in a vertebrate, comprising administering to a vertebrate in need of such treatment an effective amount of an anti-LINGO-1 antibody.
Abstract:
Endogenous LINGO-1 is a negative regulator for neuronal survival, axon regeneration, oligodendrocyte differentiation and myelination. Molecules that block endogenous LINGO-1 function, such anti-LINGO-1 antibodies can be used as therapeutics for the treatment of neuron and oligodendrocyte dysfunction. The present invention provides antibodies specific for LINGO-1, and methods of using such antibodies as antagonists of endogenous LINGO-1 function. The invention further provides specific hybridoma and phage library-derived monoclonal antibodies, nucleic acids encoding these antibodies, and vectors and host cells comprising these antibodies. The invention further provides methods of promoting oligodendrocyte survival and myelination in a vertebrate, comprising administering to a vertebrate in need of such treatment an effective amount of an anti-LINGO-1 antibody
Abstract:
Nogo receptor 1 (NgR1) is a leucine rich repeat protein that forms part of a signaling complex that modulates axon regeneration. Previous studies have shown that the entire LRR region of Nogo receptor-1, including the C-terminal cap of LRR, LRRCT, is needed for ligand binding, and that the adjacent CT stalk of the Nogo receptor-1 contributes to interaction with its co-receptors. The present invention is directed to the use of certain Nogo receptor-1 and Nogo receptor-2 polypeptides and polypeptide fragments for promoting neurite outgrowth, neuronal survival, and axonal regeneration in CNS neurons. The invention features molecules and methods useful for inhibiting neurite outgrowth inhibition, promoting neuronal survival, and/or promoting axonal regeneration in CNS neurons.