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IGF1 — PEPD

Text-mined interactions from Literome

Karna et al., Mol Cell Biochem 2008 : Since insulin-like growth factor ( IGF-I ) is the most potent stimulator of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta ( 1 ) integrin signaling, the effect of PEP on IGF-I receptor (IGF-IR) and beta ( 1 ) integrin receptor expressions were evaluated ... Since insulin-like growth factor ( IGF-I ) is the most potent stimulator of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta ( 1 ) integrin signaling, the effect of PEP on IGF-I receptor (IGF-IR) and beta ( 1 ) integrin receptor expressions were evaluated ... The hypothetical mechanism of the role of prolidase in IGF-IR , beta ( 1 ) integrin receptor expressions, and clinical significance of the process are discussed
Karna et al., Pharmazie 2010 : Since insulin-like growth factor receptor ( IGF-IR ) is the most potent regulator of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta1 integrin signaling, the effect of CAP on IGF-IR and beta1 integrin receptor expressions was evaluated
Karna et al., Nat Prod Res 2011 : Since the IGF-I receptor (IGF-IR) is the most potent regulator of both collagen biosynthesis and prolidase activity, and prolidase is regulated by ß1 integrin signalling, the effect of SCUT on IGF-IR and ß1 integrin receptor expressions were evaluated
Miltyk et al., Mol Cell Biochem 1998 : We have found that insulin-like growth factor-I (IGF-I) , potent stimulator of collagen biosynthesis, induces prolidase activity in cultured human skin fibroblasts ... Thus we conclude that prolidase activity is regulated by IGF-I in confluent fibroblasts