摘要:
Human MINR genes are identified as modulators of INR signaling and thus are therapeutic targets for disorders associated with defective INR signaling. Methods for identifying modulators of MINR, comprising screening for agents that modulate the activity of MINR are provided.
摘要:
Human GALK1 genes are identified as modulators of the PTEN/AKT pathway, and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT, comprising screening for agents that modulate the activity of GALK1 are provided.
摘要:
Human EEF2K genes are identified as modulators of the PTEN/AKT pathway and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT comprising screening for agents that modulate the activity of EEF2K are provided.
摘要:
The invention encompasses methods and compositions for increasing or decreasing collagen 1A1 expression and/or α-smooth muscle actin expression in lung fibroblasts using SERPINE2 and antagonists of SERPINE2. The invention also encompasses methods and compositions for increasing or decreasing the formation of myofibroblasts. The invention further provides methods and compositions for treatment of lung diseases, such as idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease.
摘要:
Human CDC6 genes are identified as modulators of the PTEN/AKT pathway, and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT, comprising screening for agents that modulate the activity of CDC6 are provided.
摘要:
Human MPTENAKT genes are identified as modulators of the PTEN/AKT pathway, and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT, comprising screening for agents that modulate the activity of MPTENAKT are provided.
摘要:
Human EEF2K genes are identified as modulators of the PTEN/AKT pathway and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT comprising screening for agents that modulate the activity of EEF2K are provided.