Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free free
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll "Myc ed messages": myc induces transcription of E2F1 while inhibiting its translation via a microRNA polycistron Coller HA; Forman JJ; Legesse-Miller APLoS Genet 2007[Aug]; 3 (8): e146The recent revelation that there are small, noncoding RNAs that regulate the expression of many other genes has led to an exciting, emerging body of literature defining the biological role for these molecules within signaling networks. In a flurry of recent papers, a microRNA polycistron induced by the oncogenic transcription factor c-myc has been found to be involved in an unusually structured network of interactions. This network includes the seemingly paradoxical transcriptional induction and translational inhibition of the same molecule, the E2F1 transcription factor. This microRNA cluster has been implicated in inhibiting proliferation, as well as inhibiting apoptosis, and promoting angiogenesis. Consistent with its seemingly paradoxical functions, the region of the genome in which it is encoded is deleted in some tumors and overexpressed in others. We consider the possibility that members of this polycistronic microRNA cluster help cells to integrate signals from the environment and decide whether a signal should be interpreted as proliferative or apoptotic.|Animals[MESH]|Apoptosis/genetics[MESH]|Down-Regulation/*genetics[MESH]|E2F1 Transcription Factor/*antagonists & inhibitors/*biosynthesis/genetics[MESH]|Genes, myc/genetics/*physiology[MESH]|Growth Inhibitors/genetics[MESH]|Humans[MESH]|MicroRNAs/genetics/*physiology[MESH]|Multigene Family[MESH]|Transcriptional Activation/*genetics[MESH]|Up-Regulation/*genetics[MESH] |