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EGF — PTH

Text-mined interactions from Literome

Cole et al., Endocrinology 1999 : EGF and PTH caused time- and AG1478-sensitive phosphorylation of the EGFR, but EGFR desensitization did not affect MAPK activation by PTH
González et al., Kidney Int 2002 : Mechanisms of the regulation of EGF receptor gene expression by calcitriol and parathyroid hormone in UMR 106-01 cells
González et al., Calcif Tissue Int 2002 : Studies from our laboratory in osteoblast-like cells have shown that the increase in EGF receptor expression in response to PTH was cyclic AMP mediated and was blocked by treatment with retinoic acid ( RA )
Ahmed et al., Mol Endocrinol 2003 : To further examine the mechanism of PTH stimulated EGF receptor transactivation, we employed COS-7 cells expressing the rat PTH receptor
Xian et al., Endocr Rev 2007 : In addition, EGF-like ligands, particularly amphiregulin, can be strongly regulated by PTH , an important regulatory factor in bone modeling and remodeling
Alsat et al., J Clin Endocrinol Metab 1991 : Parathyroid hormone increases epidermal growth factor receptors in cultured human trophoblastic cells from early and term placenta ... This PTH induced effect on EGF receptors was associated with an augmented functional response of trophoblastic cells to EGF ... These results demonstrate that PTH increases the number of biologically active EGF receptors during the in vitro differentiation of human trophoblast cells
Breyer et al., Am J Physiol 1990 : Kinetic studies ( 0 degrees C ) revealed an association t1/2 of 20.7 min and a dissociation t1/2 of 27 min. Competition studies revealed that 125I-EGF binding was inhibited by unlabeled EGF or its homologue transforming growth factor-alpha, but not by parathyroid hormone or insulin
Ohta et al., Endocrinology 1989 : The effects of PTH on the binding and mitogenic activity of epidermal growth factor (EGF) were studied in clonal, PTH- and EGF-responsive mouse osteoblastic cell line, MC3T3-E1 ... The PTH induced decrease in EGF binding was time dependent, requiring at least 4 h of PTH treatment at 37 C for a maximal effect, completely reversible after cessation of PTH exposure and specific only to biologically active PTH ... Scatchard analysis of saturation binding data revealed that the PTH induced reduction of EGF binding was accounted for by a proportional decrease in the available EGF binding sites without an alteration in binding affinity ( Kd = 0.7-0.8 nM ) ... Addition of either colchicine or cytochalasin-B during PTH treatment completely abolished the PTH induced reduction of EGF binding
Rodan et al., J Endocrinol 1989 (Osteosarcoma) : The production of PTH-LP was stimulated by 12-O-tetradecanoyl-phorbol-13-acetate ( TPA ; 150 nmol/l ) and epidermal growth factor ( EGF ; 10 ng/ml )
Drake et al., Endocrinology 1994 (Second Messenger Systems) : PTH , in a dose- and time dependent manner, increased the number of EGF receptors 2-fold ... In the presence of cyclohexamide, the effect of PTH on EGF binding was abolished, suggesting that new protein synthesis was required to increase the number of EGF receptors ... These data suggest that the proliferative effects of PTH on the osteoblast may be mediated indirectly by a PTH induced increase in the number of EGF receptors
González et al., Calcif Tissue Int 1996 : These data are consistent with our previous studies which showed that the effect of PTH on the induction of EGF receptors was mediated by a cAMP dependent mechanism ... These data indicate that EGF receptors in UMR 106-01 cells are up-regulated by PTH and calcitriol and that this process can be modulated by retinoids