Sentence examples for progression stimulated from inspiring English sources

Overexpression of c-Fos was found to inhibit cell cycle progression, stimulated murine hepatocyte cell death and strongly suppressed tumour formation in vivo (Mikula et al, 2003).

Interestingly, AcSDKP also inhibits cell cycle progression stimulated by serum-derived or platelet-derived growth factor-B in human mesangial cells by inhibiting the degradation of p53, p27kip1 and p21cip1 [ 81].

The current results prompt us to hypothesize that the increase in the levels of expression of TGF-β during tumor progression stimulates the downregulation of TβRs, both in the tumor itself and in stroma (CAFs), which results in the TβR-mediated reduction of apoptosis.

Previously, we demonstrated that TSPY could exert pro-growth properties in enhancing protein synthesis, accelerating cell cycle progression, stimulating cyclin B-CDK1 kinase activities, abbreviating G2/M transition, which potentially could abolish G2/M checkpoints and increasing chromosome nondisjunction and genomic instability [ 29, 30].

Additionally, the potential role of cell fusions as a repair mechanism and the role of cell fusions in cancer development and progression have further stimulated research in this field.

The progression of stimulated sites of the scalp grid followed a spiral sequence, that could be considered a relatively safe method to avoid sequential stimulation of an ordered and topographically organized cortical representation of the muscles.

E2, E3, HPTE, and BPA resulted in increased detection of the marker in uterine epithelial cells, indicating that mitotic progression is stimulated by all three substances.

While Smad-dependent TGF-β signaling primarily functions to inhibit growth, the vast majority of tumors acquire resistance to these effects and tumor progression becomes stimulated by TGF-β in more advanced tumors [ 55].

To test this idea, we used tensor analysis of protein expression profiles, annotated with gene ontologies, to uncover protein expression changes during the progression of stimulated hMSC towards fully differentiated hOST that distinguish distinct intermediary states of OS-hMSC and ECM-hMSC.

Taken together, ASF1A is aberrantly over-expressed in GIC tumors and plays key roles in GIC development and progression by stimulating the transcription of β-catenin target genes.

NF-κB-associated pathways have been widely implicated in oncogenesis and tumor progression by stimulating cell proliferation, inhibiting apoptosis, and promoting metastasis and angiogenesis [35].