PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9507016-0 1998 All-trans-retinoic acid inhibits Jun N-terminal kinase-dependent signaling pathways. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 33-54 9507016-4 1998 In this study, we examined MAP kinase-dependent pathways as potential targets of retinoid signaling and the role of MAP kinases in retinoid-induced c-fos gene regulation. Retinoids 131-139 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 148-153 9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 41-62 9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 64-67 9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 25-29 mitogen-activated protein kinase 8 Homo sapiens 41-62 9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 25-29 mitogen-activated protein kinase 8 Homo sapiens 64-67 9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-146 9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 retinoic acid receptor alpha Homo sapiens 220-229 9507016-11 1998 In light of the growth activation induced by JNK/SEK-dependent pathways in a variety of cells, these data support further investigation into the role of JNK-dependent signaling in the growth-suppressive effects of retinoids. Retinoids 214-223 mitogen-activated protein kinase 8 Homo sapiens 45-48 9507016-11 1998 In light of the growth activation induced by JNK/SEK-dependent pathways in a variety of cells, these data support further investigation into the role of JNK-dependent signaling in the growth-suppressive effects of retinoids. Retinoids 214-223 EPH receptor A4 Homo sapiens 49-52 9507016-11 1998 In light of the growth activation induced by JNK/SEK-dependent pathways in a variety of cells, these data support further investigation into the role of JNK-dependent signaling in the growth-suppressive effects of retinoids. Retinoids 214-223 mitogen-activated protein kinase 8 Homo sapiens 153-156