Abstract: This disclosure relates to DNA aptamer specifically binding to periostin, which is cancer-related protein, a composition for inhibiting cancer and/or cancer metastasis and/or a composition for diagnosis of cancer and/or cancer metastasis, comprising the same as an active ingredient, wherein the aptamer has different binding mechanism from the existing antibodies, and thus, may inhibit and diagnose cancer/cancer metastasis more effectively.

Abstract: The present invention relates to a pharmaceutical composition for preventing or treating diabetes or a complication of diabetes, which includes a TENC1 (tensin like C1 domain-containing phosphatase) expression or activity suppressor, and, more specifically, relates to a pharmaceutical composition for preventing or treating diabetes or a complication of diabetes, which either suppresses the degradation of IRS-1 (insulin receptor substrate-1) or suppresses the phosphorylation of IRS-1 due to the PTPase activity of TENC1.

Abstract: This disclosure relates to DNA aptamer specifically binding to periostin, which is cancer-related protein, a composition for inhibiting cancer and/or cancer metastasis and/or a composition for diagnosis of cancer and/or cancer metastasis, comprising the same as an active ingredient, wherein the aptamer has different binding mechanism from the existing antibodies, and thus, may inhibit and diagnose cancer/cancer metastasis more effectively.

Abstract: The present invention relates to a pharmaceutical composition for preventing or treating diabetes or a complication of diabetes, which includes a TENC1 (tensin like C1 domain-containing phosphatase) expression or activity suppressor, and, more specifically, relates to a pharmaceutical composition for preventing or treating diabetes or a complication of diabetes, which either suppresses the degradation of IRS-1 (insulin receptor substrate-1) or suppresses the phosphorylation of IRS-1 due to the PTPase activity of TENC1.

Abstract: This disclosure relates to an angiogenesis-related pharmaceutical composition using connective tissue growth factor, more particularly to a pharmaceutical composition for promoting angiogenesis containing the connective tissue growth factor or a pharmaceutical composition for inhibiting angiogenesis containing at least one selected from the group consisting of polypeptide, antibody and a compound binding to connective tissue growth factor.

Abstract: This disclosure relates to an angiogenesis-related pharmaceutical composition using connective tissue growth factor, more particularly to a pharmaceutical composition for promoting angiogenesis containing the connective tissue growth factor or a pharmaceutical composition for inhibiting angiogenesis containing at least one selected from the group consisting of polypeptide, antibody and a compound binding to connective tissue growth factor.

Abstract: The present invention relates to a method of regulating mammalian target-of-rapamycin (mTOR) by regulating a phospholipase D (PLD) activity that generates a complex with mTOR. Further, the present invention also relates to a method of screening inhibitors of mTOR, and a method and a composition for treating mTOR-related metabolic diseases by inhibiting mTOR.

Abstract: The present invention relates to method of regulating mammalian target-of-rapamycin (mTOR) based on a novel finding of a regulating mechanism of mTOR by a phospholipase D (PLD), and Ras homolog enriched in brain (Rheb). Further, the present invention also relates to a method of screening inhibitors of mTOR, and a method and a composition for treating mTOR-related metabolic diseases by inhibiting mTOR.

Abstract: Disclosed are peptides having SEQ ID NOs: 1 to 24 that induce superoxide generation by human monocytes or neutrophils; that induce an intracellular calcium increase by human peripheral blood monocytes or neutrophils; binds to formyl peptide receptor or formyl peptide receptor-like 1; that induce chemotactic migration of human monocytes or neutrophils in vitro; that induce degranulation in formyl peptide receptor expressing cells or formyl peptide receptor-like 1 expressing cells; that stimulate extracellular signal regulated protein kinase phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1; or that stimulate Akt phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1.

Abstract: The present invention relates to a method of protecting cells against damage caused at least in part by apoptosis, comprising administering to subjects a therapeutic dose of leumorphin having cytoprotective activity, and a pharmaceutical composition comprising an effective amount of leumorphin having a cytoprotective activity.

Abstract: The present invention relates to a ligand to regulate immune response, i.e., PACAP27 which is one of pituitary adenylate cyclase-activating polypeptides and Serum amyloid A (SAA), and their novel use in treating or preventing diseases associated with immune response. More specifically, the present invention relates to a complex of PACAP27-FPRL1 having a regulatory effect on immune response, and a use thereof in regulating immune response. In another aspect, the present invention relates to a complex of SAA and FPRL1, and a use thereof in inhibiting synoviocyte hyperplasia and angiogenesis and treating or preventing inflammatory diseases including Rheumatoid arthritis (RA).

Abstract: The present invention relates to a method of regulating mammalian target-of-rapamycin (mTOR) by regulating a phospholipase D (PLD) activity that generates a complex with mTOR. Further, the present invention also relates to a method of screening inhibitors of mTOR, and a method and a composition for treating mTOR-related metabolic diseases by inhibiting mTOR.

Abstract: The present invention relates to an glucose uptake modulator, a pharmaceutical composition comprising the glucose uptake modulator, and a method of treating a diabetes or diabetic complications in a mammal in need thereof, which comprises administering to said mammal an effecting amount of a glucose uptake modulator.

Abstract: The present application discloses W-rich peptide that is useful for inhibiting FPR class receptor activity.

Abstract: The present inventors show that a brief exposure to EGF stimulates insulin secretion glucose-independently via a Ca2+ influx- and PLD2-dependent mechanism. Furthermore, the present invention shows that EGF is a novel secretagogue that lowers plasma glucose levels in normal and diabetic mice, suggesting the potential for EGF treatment in diabetes.

Abstract: The present invention relates to method of regulating mammalian target-of-rapamycin (mTOR) based on a novel finding of a regulating mechanism of mTOR by a phospholipase D (PLD), and Ras homolog enriched in brain (Rheb). Further, the present invention also relates to a method of screening inhibitors of mTOR, and a method and a composition for treating mTOR-related metabolic diseases by inhibitin mTOR.

Abstract: The present application describes peptides that stimulate arachidonic acid release in target cells. The application also discloses peptides that cause intracellular calcium release. The application also discloses methods of using the disclosed peptides.

Abstract: Disclosed are peptides having SEQ ID NOs: 1 to 24 that induce superoxide generation by human monocytes or neutrophils; that induce an intracellular calcium increase by human peripheral blood monocytes or neutrophils; binds to formyl peptide receptor or formyl peptide receptor-like 1; that induce chemotactic migration of human monocytes or neutrophils in vitro; that induce degranulation in formyl peptide receptor expressing cells or formyl peptide receptor-like 1 expressing cells; that stimulate extracellular signal regulated protein kinase phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1; or that stimulate Akt phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1.

Abstract: Disclosed are peptides having SEQ ID NOs: 1 to 24 that induce superoxide generation by human monocytes or neutrophils; that induce an intracellular calcium increase by human peripheral blood monocytes or neutrophils; binds to formyl peptide receptor or formyl peptide receptor-like 1; that induce chemotactic migration of human monocytes or neutrophils in vitro; that induce degranulation in formyl peptide receptor expressing cells or formyl peptide receptor-like 1 expressing cells; that stimulate extracellular signal regulated protein kinase phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1; or that stimulate Akt phosphorylation via activation of formyl peptide receptor or formyl peptide receptor-like 1.

Abstract: The present application discloses W-rich peptide that is useful for inhibiting FPR class receptor activity.