摘要:
Nucleic acid molecules encoding full length PTP20, PCP-2, BDP1, mCLK2, mCLK3, mCLK4, and SIRP polypeptides, portions of such nucleic acid molecules, nucleic acid vectors containing such nucleic acid molecules, recombinant cells containing such nucleic acid vectors, polypeptides purified from such recombinant cells, antibodies to such polypeptides, and methods of identifying compounds that bind such polypeptides or abrogate their interactions with natural binding partners. Methods for diagnosing abnormal conditions in an organism with PTP20, PCP-2, BDP1, mCLK2, mCLK3, mCLK4, and SIRP related molecules or compounds. PTP20, PCP-2, BDP1, mCLK2, mCLK3, mCLK4, or SIRP polypeptides, nucleic acids encoding such polypeptides, cells, tissues and animals containing such nucleic acids, antibodies to such polypeptides, assays utilizing such polypeptides, and methods relating to all of the foregoing. Methods for treatment, diagnosis, and screening are provided for diseases related to PTP20, PCP-2, BDP1, mCLK2, mCLK3, mCLK4, and SIRP polypeptides or conditions characterized by an abnormal interaction between such a polypeptide and its binding partner.
摘要:
This invention relates to the use a pyruvate-kinase or a nucleic acid coding therefor as a target for the modulation of apoptotic processes, particularly as a target molecule for the diagnosis, prevention or treatment of apoptosis-associated disorders, such as tumours.
摘要:
The present invention relates to the use of a compound which is capable of inhibiting activation of a growth factor receptor of the EGFR-family for the prevention or treatment of processes associated with increased G-protein mediated signal transduction.
摘要:
The present invention relates to the use of ligands for the FLK-1 receptor for the modulation of angiogenesis and vasculogenesis. The invention is based, in part, on the demonstration that Flk-1 tyrosine kinase receptor expression is associated with endothelial cells and the identification of vascular endothelial growth factor (VEGF) as the high affinity ligand of Flk-1. These results indicate a major role for Flk-1 in the signaling system during vasculogenesis and angiogenesis. Engineering of host cells that express Flk-1 and the uses of expressed Flk-1 to evaluate and screen for drugs and analogs of VEGF involved in Flk-1 modulation by either agonist or antagonist activities is described. The invention also relates to the use of FLK-1 ligands, including VEGF agonists and antagonists, in the treatment of disorders, including cancer, by modulating vasculogenesis and angiogenesis.
摘要:
The present invention relates, in general, to an extracellular signal regulated kinase, ERK-5. In particular, the present invention relates to nucleic acid molecules coding for ERK-5; ERK-5 polypeptides; recombinant nucleic acid molecules; cells containing the recombinant nucleic acid molecules; antisense ERK-5 nucleic acid constructs; antibodies having binding affinity to an ERK-5 polypeptide; hybridomes containing the antibodies; nucleic acid probes for the detecting of ERK-5 nucleic acid; a method of detecting ERK-5 nucleic acid or polypeptide in a sample; kits containing nucleic acid probes or antibodies; a method of detecting a compound capable of binding to ERK-5 or a fragment thereof; a method of detecting an agonist or antagonist of ERK-5 activity; a method of agonizing or antagonizing ERK-5 associated activity in a mammal; a method of treating diabetes mellitus, skeletal muscle diseases, Alzheimer's disease, or peripheral neuropathies in a mammal with an agonist or antagonist of ERK-5 activity; and a pharmaceutical composition comprising an ERK-5 agonist or antagonist.
摘要:
The present invention features isolated, purified, or enriched nucleic acid encoding a SIRP polypeptide and isolated, purified, or enriched SIRP polypeptide and uses thereof.
摘要:
The present invention relates to novel cytoplasmic tyrosine kinases isolated from megakaryocytes (megakaryocyte kinases or MKKs) which are involved in cellular signal transduction pathways and to the use of these novel proteins in the diagnosis and treatment of disease. The present invention further relates to specific megakaryocyte kinases, designated MKK1, MKK2 and MKK3, and their use as diagnostic and therapeutic agents.
摘要:
A novel protein tyrosine phosphatase designated PTP-S31 and its subfamily are identified, as are nucleic acid molecule coding therefor. Included in this;family are PTP-S31 proteins or glycoproteins having one, two, or three identified amino acid changes in previously defined consensus sequences in the catalytic phosphatase domains of known protein tyrosine phosphatases. The PTP-S31 proteins or glycoproteins may be produced by recombinant means. Antibodies to PTP-S31 proteins or glycoproteins and nucleic acid constructs coding therefor, and methods for screening molecules which can bind to PTP-S31 proteins or glycoproteins and inhibit or stimulate their enzymatic activity, are provided.
摘要:
For the determination of the activity of a specific protein tyrosine phosphatase (PTPase) in intact cells one incubates intact cells which contain a substrate of the specific PTPase, if desired after stimulating the substrate phosphorylation, with a substance which can penetrate into the intact cells and can selectively inhibit phosphorylation of the substrate, the degree of phosphorylation of the substrate is measured, if desired several times, at various time points and the activity of the specific PTPase is determined from the measured degree of phosphorylation of the substrate. An additional measurement is carried out in the presence of a test substance to determine effectors of the specific PTPase and the effector action of the test substance is determined by comparing the degrees of phosphorylation.
摘要:
The present invention relates to novel modalities of treatment of diabetes, and other diseases caused by dysfunctional signal transduction by insulin receptor type tyrosine kinases (IR-PTK). Applicants discovered that IR-PTK activity may be modified by modulating the activity of a tyrosine phosphatase, and IR-PTK signal transduction may be triggered even in the absence of ligand. Methods for identifying compounds that, by modulating RPTP.alpha. or RPTP.epsilon. activity, elicit or modulate insulin receptor signal transduction are also described.