Therapeutic insights into the treatment of Idiopathic Pulmonary Fibrosis: Tumor suppressor p53 and its homologues TAp73β and TAp63γ function as antifibrotic mediators via up regulation of ARPC2, 01/October/2014, 08.37 am

Therapeutic insights into the treatment of Idiopathic Pulmonary Fibrosis: Tumor suppressor p53 and its homologues TAp73β and TAp63γ function as antifibrotic mediators via up regulation of ARPC2, 01/October/2014, 08.37 am

Therapeutic insights into the treatment of Idiopathic Pulmonary Fibrosis: Tumor suppressor p53 and its homologues TAp73β and TAp63γ function as antifibrotic mediators via up regulation of ARPC2, 01/October/2014, 08.37 am 150 150 Dr Boomi's Genom-2-Discovery Center

Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, Therapeutic insights into the treatment of Idiopathic Pulmonary Fibrosis: Tumor suppressor p53 and its homologues TAp73β and TAp63γ function as antifibrotic mediators via up regulation of ARPC2, 01/October/2014, 08.37 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Web: http://genomediscovery.org

Courtesy: When you cite drop us a line at info@genomediscovery.org

Significance: This study suggests that  p53 and its homologues TAp73β and TAp63γ, by increasing the expression of their target genes, they may function as antifibrotic mediators. Thereby, they may inhibit the progression of Idiopathic pulmonary fibrosis. Thus, this study suggests that pharmacological formulations encompassing “p53/TAp73β/TAp63γ activators” may be used to inhibit the progression of idiopathic fibrotic diseases.