Abstract: The present invention provides peptidic TGF-? antagonists capable of inhibiting TGF-? signaling and disrupting the biochemical events that promote fibrosis and the epithelial-mesenchymal transition. The peptidic TGF-? antagonist may contain from 11 to 28 amino acid residues (for instance, may consist of from 12 to 16 amino acid residues) and may have the following structure (II): NH2?ETWIWLDTNMG-Xaa1-Y?COOH??(II) wherein Xaa1 is any amino acid and Y is a peptide having from 0 to 9 amino acids. The peptidic TGF-? antagonists can advantageously be used for the prevention, treatment, and/or alleviation of the symptoms of a condition associated with an increase in TGF-? activity, including fibrosis (such as fibrosis of the skin, liver, lungs, and heart, among others) and cancer (including various carcinomas, such as squamous cell carcinoma, sarcomas, and metastatic cancers).

Abstract: The present invention provides peptidic TGF-? antagonists capable of inhibiting TGF-? signaling and disrupting the biochemical events that promote fibrosis and the epithelial-mesenchymal transition. The peptidic TGF-? antagonist may contain from 11 to 28 amino acid residues (for instance, may consist of from 12 to 16 amino acid residues) and may have the following structure (II): NH2?ETWIWLDTNMG-Xaa1-Y?COON??(II) wherein Xaa1 is any amino acid and Y is a peptide having from 0 to 9 amino acids. The peptidic TGF-? antagonists can advantageously be used for the prevention, treatment, and/or alleviation of the symptoms of a condition associated with an increase in TGF-? activity, including fibrosis (such as fibrosis of the skin, liver, lungs, and heart, among others) and cancer (including various carcinomas, such as squamous cell carcinoma, sarcomas, and metastatic cancers).

Abstract: The present invention provides peptidic TGF-? antagonists capable of inhibiting TGF-? signaling and disrupting the biochemical events that promote fibrosis and the epithelial-mesenchymal transition. The peptidic TGF-? antagonist may contain from 11 to 28 amino acid residues (for instance, may consist of from 12 to 16 amino acid residues) and may have the following structure (II): NH2? ETWIWLDTNMG-Xaa1-Y?COOH (II) wherein Xaa1 is any amino acid and Y is a peptide having from 0 to 9 amino acids. The peptidic TGF-? antagonists can advantageously be used for the prevention, treatment, and/or alleviation of the symptoms of a condition associated with an increase in TGF-? activity, including fibrosis (such as fibrosis of the skin, liver, lungs, and heart, among others) and cancer (including various carcinomas, such as squamous cell carcinoma, sarcomas, and metastatic cancers).

Abstract: The present invention provides peptidic TGF-? antagonists capable of inhibiting TGF-? signaling and disrupting the biochemical events that promote fibrosis and the epithelial-mesenchymal transition. The peptidic TGF-? antagonist may contain from 11 to 28 amino acid residues (for instance, may consist of from 12 to 16 amino acid residues) and may have the following structure (II): NH2? ETWIWLDTNMG-Xaa1-Y?COOH (II) wherein Xaa1 is any amino acid and Y is a peptide having from 0 to 9 amino acids. The peptidic TGF-? antagonists can advantageously be used for the prevention, treatment, and/or alleviation of the symptoms of a condition associated with an increase in TGF-? activity, including fibrosis (such as fibrosis of the skin, liver, lungs, and heart, among others) and cancer (including various carcinomas, such as squamous cell carcinoma, sarcomas, and metastatic cancers).

Abstract: The invention concerns compounds, compositions and methods for the treatment of skin cells. Described herein are CD109 polypeptides and uses thereof for the in vivo treatment of various skin disorders, including skin fibrosis, skin scarring, wound healing and psoriasis.

Abstract: The present invention relates to a TGF-?1 binding protein called r150. This protein has a GPI-anchor contained in r150 itself and not on a tightly associated protein and that it binds TGF-?1 with an affinity comparable to those of the signaling receptors. Furthermore, the released (soluble) form of this protein binds TGF-?1 independent of the types I and II receptors. Also, the soluble form inhibits the binding of TGF-? to its receptor. In addition, evidence that r150 is released from the cell surface by an endogenous phospholipase C is provided. Also, the creation of a mutant human keratinocyte cell line with a defect in GPI synthesis which displays reduced expression of r150 is described. Our results using these mutant keratinocytes suggest that the membrane anchored form of r150 is a negative modulator of TGF-beta responses.

Abstract: The present invention relates to a TGF-&bgr;1 binding protein called r150. This protein has a GPI-anchor contained in r150 itself and not on a tightly associated protein and that it binds TGF-&bgr;1 with an affinity comparable to those of the signaling receptors. Furthermore, the released (soluble) form of this protein binds TGF-&bgr;1 independent of the types I and II receptors. Also, the soluble form inhibits the binding of TGF-&bgr; to its receptor. In addition, evidence that r150 is released from the cell surface by an endogenous phospholipase C is provided. Also, the creation of a mutant human keratinocyte cell line with a defect in GPI synthesis which displays reduced expression of r150 is described. Our results using these mutant keratinocytes suggest that the membrane anchored form of r150 is a negative modulator of TGF-beta responses.