Interestingly, a miR-155/Akt2 positive feedback loop may exist, as Akt2 is required for complete miR-155 up-regulation [51].
Sample text:```Intriguingly, using MPRs-deficient MEF cells, mouse and human CLN5 have been shown to reach lysosomes in an MPRindependent manner [12].```
Sample intent: background
Sample text:```Previous studies described that ectopic miR-99a expression slowed keratinocyte growth and liver cancer cell growth by blocking the cell cycle at the G1/S transition [10,29].```
Sample intent: method



Sample text:```ly), which have been originally identified as molecules activated by growth factor-stimulation of fibroblusts, are key kinases in the intracellular signal transduction pathways (1-6).```
Sample intent: method



Sample text:```Overexpression of miR-218 inhibits cancer cell proliferation, migration and invasion [24, 26, 27], and promotes colon cancer cell apoptosis [28].```
Sample intent: method



Sample text:```c-Jun-N-Terminal inhibitory kinase JIK and TRAF2 to the stimulated ER stress sensor IRE-1, where TRAF2 can activate ASK-1, an upstream activating kinase of JNK (2) activation of caspase 12, which is released from its```
Sample intent: method



Sample text:```germination stimulatory activity by germination bioassays with Striga hermonthica as previously described by Jamil et al. (2010).```
Sample intent: background
Sample text:```In line with previous results (3, 19, 20, 30), we found that during muscle contraction ERK1/2 phosphorylation was increased and was not affected by CaMKII inhibition.```
Sample intent: result



Sample text:```c-Jun-N-Terminal inhibitory kinase JIK and TRAF2 to the stimulated ER stress sensor IRE-1, where TRAF2 can activate ASK-1, an upstream activating kinase of JNK (2) activation of caspase 12, which is released from its```
Sample intent: method



Sample text:```In addition, consistent with the result of our preclinical study, recent clinical study showed that alectinib was also highly active against ALK-positive NSCLC patients after treatment with crizotinib [21].```
Sample intent: result



Sample text:```ly), which have been originally identified as molecules activated by growth factor-stimulation of fibroblusts, are key kinases in the intracellular signal transduction pathways (1-6).```
Sample intent: method



Sample text:```Previous studies described that ectopic miR-99a expression slowed keratinocyte growth and liver cancer cell growth by blocking the cell cycle at the G1/S transition [10,29].```
Sample intent: method



Sample text:```Several studies have shown that a major function of PP2A is downregulation of the Ras/MAP kinase pathway (2, 3, 22, 30, 50, 51, 53).```
Sample intent: method



Sample text:```germination stimulatory activity by germination bioassays with Striga hermonthica as previously described by Jamil et al. (2010).```
Sample intent: background



Sample text:```Overexpression of miR-218 inhibits cancer cell proliferation, migration and invasion [24, 26, 27], and promotes colon cancer cell apoptosis [28].```
Sample intent: method



Sample text:```Intriguingly, using MPRs-deficient MEF cells, mouse and human CLN5 have been shown to reach lysosomes in an MPRindependent manner [12].```
Sample intent: background



Sample text:```In line with our results, several previous studies demonstrated the anti-proliferative effect of PPARs agonists in several cell types [11-15].```
Sample intent: result