Figure. Schematic illustration on chitotriosidase (CHIT1) regulation of TGF-β pathway. CHIT1 enhances the effect of TGF-β through the induction of TGF-β.

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Figure. Schematic illustration on chitotriosidase (CHIT1) regulation of TGF-β pathway. CHIT1 enhances the effect of TGF-β through the induction of TGF-β receptors expression (both type I and type II) and TGF-β signaling. In the preliminary studies in our laboratory suggest that CHIT1 could bind with a transcription factor such as FoxO3a, or TGF-β receptor associated protein 1 (TGFBRAP1) (unpublished data), modulates TGF-β-stimulated canonical (Smads-dependent) and/or non-canonical MAPK/Erk or Akt signaling. Erk or Akt activation generally increases cell survival or proliferation, that might contribute to the development of tissue fibrosis together with increased expression of profibrotic mediators and extracellular matrix protein accumulation. The exact role and mechanism of CHIT1 in this regulation (such as receptor or interacting proteins of CHIT1) need to be determined in future studies. Figure. Schematic illustration on chitotriosidase (CHIT1) regulation of TGF-β pathway. CHIT1 enhances the effect of TGF-β through the induction of TGF-β receptors expression (both type I and type II) and TGF-β signaling. In the preliminary studies in our laboratory suggest that CHIT1 could bind with a transcription factor such as FoxO3a, or TGF-β receptor associated . . . Allergy Asthma Immunol Res. 2015 Jan;7(1):14-21. http://dx.doi.org/10.4168/aair.2015.7.1.14