Sentence examples for pathway junctions from inspiring English sources

Thus, SFR could be a general property occurring at signaling pathway junctions.

Thus, SFR can also be used to determine whether competing molecules in vitro are at pathway junctions in vivo.

Thus, we demonstrate that SFR is a novel mechanism for enhanced activation of alternative pathways when molecules at pathway junctions are removed.

To check whether SFR is a general property of signal transduction at pathway junctions, we next analyzed another branch point of the TRAM-dependent component of the TLR4 pathway: TRIF to TBK1, TRAF6 and RIP1 (Figure 1A).

Although we have demonstrated SFR for molecules with common binding domain, SFR might also occur between molecules with different binding domains at pathway junctions from the law of mass flow conservation (Figure 6).

The observation of enhanced alternative pathways when molecules at pathway junction are removed may not be restricted to TLR4 signaling.

That is, when molecules at pathway junction are decreased and increased the activation of alternative pathways enhances and reduces, respectively.

Investigating another TLR4 pathway junction, from TRIF to TRAF6, RIP1 and TBK1, the removal of MyD88-dependent TRAF6 increased expression of TRAM-dependent Cxcl10 and Ifit2.

From in silico MyD88 KO or TRAF6 KO, we simulated enhanced activation of alternative TRAM-dependent pathway through the re-channelling of signal transduction or SFR, which occurs when molecules at pathway junction are removed.

The latter could be supported by the Signaling Flux Redistribution (SFR) concept [52], which indicates that if one pathway is enhanced or impaired at the pathway branches, an alternative pathway is down-regulated or enhanced because the total signaling flux in a pathway junction is conserved.

During the transition from mid to late developmental stages (P15 vs. P21), genes associated with the Wnt signaling pathway, tight junctions, P53 signaling pathway, and focal adhesions showed significant enrichment at P15, while genes belonging to the mitogen-activated protein kinase (MAPK) and calcium signaling pathways were enriched at P21 (Supplementary Fig. 2b).