PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9141522-9 1997 IGF-I (100 ng/mL) had similar effects as IGF-II and significantly (P < 0.001) increased ACTH-, forskolin-, and cAMP-stimulated production of cortisol by 2.8-, 3.9-, and 3.1-fold, respectively, and that of DHEA-S by 1.3-, 1.6-, and 1.4-fold, respectively. Colforsin 98-107 insulin like growth factor 1 Homo sapiens 0-5 22484028-9 2012 The effects of hCG and forskolin on caspase-3/7 were attenuated by co-treatment with NVP-AEW54, an IGF1 receptor antagonist. Colforsin 23-32 insulin like growth factor 1 Homo sapiens 99-103 11120746-8 2001 IGF-I inhibited both basal and forskolin-stimulated cAMP levels. Colforsin 31-40 insulin like growth factor 1 Homo sapiens 0-5 10650934-10 2000 In contrast, increasing intracellular cAMP with forskolin resulted in abrogation of IGF-I-induced JNK activity. Colforsin 48-57 insulin like growth factor 1 Homo sapiens 84-89 9165004-5 1997 This effect of IGF-I and EGF was not inhibited by increased intracellular cAMP generated by pretreatment of the cells with 10 microM forskolin. Colforsin 133-142 insulin like growth factor 1 Homo sapiens 15-20 9165004-10 1997 Pretreatment of cells with 10 microM forskolin decreased IGF-I- and EGF-stimulated luciferase activity by approximately 75%. Colforsin 37-46 insulin like growth factor 1 Homo sapiens 57-62 16177565-4 2005 Forskolin also inhibited Akt phosphorylation stimulated by other growth factors such as IGF-1, epidermal growth factor, and insulin. Colforsin 0-9 insulin like growth factor 1 Homo sapiens 88-93 9405735-10 1998 Forskolin (10(-8) M) and dibutyryl cAMP (10(-3) M) increased IGF-I mRNA levels sixfold, and cotreatment with E2 did not affect these changes, consistent with a possible mediation of the estrogen effect on IGF-I gene expression by cAMP. Colforsin 0-9 insulin like growth factor 1 Homo sapiens 61-66 9405735-10 1998 Forskolin (10(-8) M) and dibutyryl cAMP (10(-3) M) increased IGF-I mRNA levels sixfold, and cotreatment with E2 did not affect these changes, consistent with a possible mediation of the estrogen effect on IGF-I gene expression by cAMP. Colforsin 0-9 insulin like growth factor 1 Homo sapiens 205-210 8848250-1 1995 The purpose of this study was to determine whether the loss of protein kinase C (PKC) from adrenal chromaffin cells affected the enhancement of high K(+)- and forskolin-stimulated tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) activity observed in cells treated with insulin-like growth factor-I (IGF-I). Colforsin 159-168 insulin like growth factor 1 Homo sapiens 282-310 8848250-1 1995 The purpose of this study was to determine whether the loss of protein kinase C (PKC) from adrenal chromaffin cells affected the enhancement of high K(+)- and forskolin-stimulated tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) activity observed in cells treated with insulin-like growth factor-I (IGF-I). Colforsin 159-168 insulin like growth factor 1 Homo sapiens 312-317 7749503-2 1995 We investigated IGF-I mRNA expression during treatment with thyrotropin (TSH), forskolin and potassium iodide (KI) in intact porcine thyroid follicles ex vivo. Colforsin 79-88 insulin like growth factor 1 Homo sapiens 16-21 7749503-5 1995 In untreated follicles no IGF-I mRNA was found, whereas in follicles stimulated with TSH an IGF-I mRNA of 7.0 kb was detected after 24 h, which persisted for another 24 h. Forskolin treatment mimicked the TSH effect, indicating that IGF-I mRNA expression may be stimulated by the adenylate cyclase pathway. Colforsin 172-181 insulin like growth factor 1 Homo sapiens 92-97 7749503-5 1995 In untreated follicles no IGF-I mRNA was found, whereas in follicles stimulated with TSH an IGF-I mRNA of 7.0 kb was detected after 24 h, which persisted for another 24 h. Forskolin treatment mimicked the TSH effect, indicating that IGF-I mRNA expression may be stimulated by the adenylate cyclase pathway. Colforsin 172-181 insulin like growth factor 1 Homo sapiens 92-97 7532580-11 1995 Increased IGFBP-3 and -6 production in response to RA + forskolin was accompanied by a decrease in IGF-stimulated thymidine incorporation into DNA; by contrast, the bioactivity of an IGF analog that does not bind with IGFBPs, [Gln3, Ala4, Tyr15, Leu16]IGF-I, was unchanged under these conditions. Colforsin 56-65 insulin like growth factor 1 Homo sapiens 252-257 7734622-6 1995 The interaction of forskolin and PMA with IGF-I was then determined. Colforsin 19-28 insulin like growth factor 1 Homo sapiens 42-47 7734622-8 1995 It is concluded that forskolin and, to a lesser extent, PMA exert their effect at the G1 phase of the cycle to enhance IGF-I effects in cell proliferation. Colforsin 21-30 insulin like growth factor 1 Homo sapiens 119-124 8027214-6 1994 In contrast to the inhibitory actions of EGF, FGF, and TGF beta on 17 alpha-hydroxylase expression, insulin and insulin-like growth factor-I enhanced forskolin-stimulated 17 alpha-hydroxylase activity. Colforsin 150-159 insulin like growth factor 1 Homo sapiens 112-140 7864902-3 1995 However, in human osteoblast-like cells both TGF-beta and forskolin increased IGF-I mRNA levels in a time- and dose-dependent manner. Colforsin 58-67 insulin like growth factor 1 Homo sapiens 78-83 21153151-6 1995 Concurrent treatment with IGF-I (50 ng/mL) enhanced forskolin-stimulated aromatase activity in PCOS granulosa-lutein cultures. Colforsin 52-61 insulin like growth factor 1 Homo sapiens 26-31 8788308-7 1995 Dibutyryl-cAMP, isobutyl-methyl-xanthine (inhibitor of cAMP catabolism) or forskolin (stimulator of cAMP production) inhibited IGF-I output at these doses. Colforsin 75-84 insulin like growth factor 1 Homo sapiens 127-132 1714831-9 1991 B-chain IGF-I (decreased affinity for IGFBP) increased cell number and enhanced forskolin"s effects on IGFBP-3 secretion and mRNA abundance to the same extent as insulin, whereas [Leu24,1-62]IGF-I (decreased affinity for the type I IGF receptor) did not. Colforsin 80-89 insulin like growth factor 1 Homo sapiens 8-13 1659515-1 1991 The effects of hCG, 8-bromo-cAMP, 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, and forskolin on insulin-like growth factor-I (IGF-I) receptor gene expression of Leydig cells were studied. Colforsin 89-98 insulin like growth factor 1 Homo sapiens 102-130 1659515-6 1991 In conclusion, IGF-I receptors can be up-regulated by hCG, 8-bromo-cAMP, and forskolin. Colforsin 77-86 insulin like growth factor 1 Homo sapiens 15-20 8058064-8 1994 Forskolin (50 microM), isobutylmethylxanthine (0.5 mM), and forskolin/isobutylmethylxanthine in combination attenuated IGF-1-induced ERK activity in WT cells by 54, 55, and 75% respectively. Colforsin 0-9 insulin like growth factor 1 Homo sapiens 119-124 8058064-8 1994 Forskolin (50 microM), isobutylmethylxanthine (0.5 mM), and forskolin/isobutylmethylxanthine in combination attenuated IGF-1-induced ERK activity in WT cells by 54, 55, and 75% respectively. Colforsin 60-69 insulin like growth factor 1 Homo sapiens 119-124 7505278-7 1994 Forskolin and a group of candidate growth factors, including platelet-derived growth factor, epidermal growth factor, and acidic and basic fibroblast growth factor, modestly increased IGFBP secretion when compared to untreated cells, but these effects were small when compared to IGF-I treatment. Colforsin 0-9 insulin like growth factor 1 Homo sapiens 280-285 2538338-8 1989 An increase in intracellular Ca2+ concentration by treatment with A23187, a calcium ionophore, or an increase in intracellular cAMP level by treatment with dibutyryl cAMP or forskolin almost completely inhibited the insulin-, IGF-I-, or EGF-induced formation of ruffling membranes. Colforsin 174-183 insulin like growth factor 1 Homo sapiens 226-231