Pub. Date : 2008 Feb 15
PMID : 18006504
13 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | A MAPK-positive feedback mechanism for BLR1 signaling propels retinoic acid-triggered differentiation and cell cycle arrest. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 2 | MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 3 | MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 4 | In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 5 | In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 6 | In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 7 | Unlike wild-type parental cells, RA-treated BLR1 knock-out cells failed to show RAF and consequential MEK and ERK phosphorylation, failed to accumulate CDK inhibitors that control G(1)/S transition, and failed to differentiate and arrest in response to RA, whereas ectopically overexpressing BLR1 enhanced MAPK signaling and caused accelerated RA-induced differentiation and arrest. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 8 | Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 9 | Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 10 | Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 11 | Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 12 | Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |
| 13 | Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. | Tretinoin | mitogen-activated protein kinase 1 | Homo sapiens |