Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: The present invention provides molecules including Pin2 and telomerase binding polypeptides, polynucleotides encoding such polypeptides, and antibodies specifically immunoreactive to said polypeptides. The invention also provides methods for screening agents which modulate the function or expression of said Pin2 and telomerase binding polypeptides. Methods are provided for disease diagnosis and treatment using said agents, said antibodies and oligonucleotides derived from the above polynucleotides.

Abstract: An animal model for neurodegenerative disorders, e.g., a transgenic model in which the Pin1 gene is misexpressed is described. The animal is useful for identifying and monitoring treatments and agents for a number of neurodegenerative disorders. Accordingly, also provided are methods for preventing, treating and/or delaying the onset of neurodegenerative disorders by administering to a subject in need thereof and agent that increases Pin1 biological activity in neuronal tissues and fluids.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: Inhibitors of phosphoserine- or phosphothreonine-specific pepidyl prolyl isomerases are described.

Abstract: This invention provides a method for treating a Pin1-associated state in a subject including administering to a subject an effective amount of a fredericamycin A compound such that the Pin1-associated state is treated. In another aspect, this invention includes the above described method, wherein the Pin1-associated state is a cyclin D1 elevated state, neoplastic transformation, and/or tumor growth. In an embodiment, this invention provides the above described methods, wherein the Pin1-associated state is colon cancer, breast cancer, a sarcoma, a malignant lymphoma, and/or esophageal cancer. This invention also provides a method for treating cyclin D1 overexpression in a subject including administering to a subject an effective amount of a combination of a fredericamycin A compound and a hyperplastic inhibitory agent such that the cyclin D1 overexpression is treated.

Abstract: The invention relates to methods and compositions of WW-domains as phosphoserine and phosphothreonine binding modules. The WW-domain containing polypeptides of the invention can be used, for example, to regulate cell growth; to treat neurodegenerative diseases; to screen for substances that modulated interactions between WW-domain containing polypeptides and phosphorylated ligands; as drug targeting vehicles; to direct protein degradation; and in the treatment of certain diseases or conditions characterized by aberrant WW-domain containing polypeptides or their ligands.

Abstract: The invention relates to methods and compositions of WW-domains as phosphoserine and phosphothreonine binding modules. The WW-domain containing polypeptides of the invention can be used, for example, to regulate cell growth; to treat neurodegenerative diseases; to screen for substances that modulated interactions between WW-domain containing polypeptides and phosphorylated ligands; as drug targeting vehicles; to direct protein degradation; and in the treatment of certain diseases or conditions characterized by aberrant WW-domain containing polypeptides or their ligands.

Abstract: Inhibitors of phosphoserine- or posphothreonine-specific peptidyl prolyl isomerases are described. Such inhibitors include molecules that mimic the structure and conformation of the pSer/pThr-Pro peptide moiety of the isomerase substrate when the substrate is bound into the active site of the isomerase. For example, a protein, peptide or peptide mimetic including xSer/ThrY where x is a negatively charged tetra or pentavalent moiety and Y is a Pro or a Pro analog. Methods of inhibiting cell growth and methods of identifying phosphoserine- or phosphothreonine-proline specific peptidyl-prolyl isomerase inhibitors are also included in the invention.

Abstract: Methods for the use of Pin1 as a marker of abnormal cell growth are disclosed. In one embodiment, the method includes detecting a level of Pin1 to stage an abnormal cell growth, such as breast or prostate cancer. In another embodiment, the method includes evaluating the efficacy of a treatment of an abnormal cell growth, such as cancer, by monitoring the levels of Pin1. In another embodiment, the method includes evaluating the extent of metastasis of abnormal cell growth, such as cancer. The levels of Pin1 can be protein levels or nucleic acid levels.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.

Abstract: A novel class of NIMA interacting proteins (PIN), exemplified by Pin1, is provided. Pin1 induces a G2 arrest and delays NIMA-induced mitosis when overexpressed, and triggers mitotic arrest and DNA fragmentation when depleted. Methods of identifying other Pin proteins and Pin-interacting proteins and identifying compositions which affect Pin activity or expression are also provided.