Sentence examples for binding we hypothesized that from inspiring English sources

Because Wss1 was reported to be Ub/SUMO isopeptidase (Mullen et al., 2010) and the WLM domain contributes to SUMO binding, we hypothesized that WLM might bind the carboxy-terminus of SUMO.

Because these two motifs suggest the possibility of intramolecular binding, we hypothesized that the C-terminus of Dvl/Dsh binds intrinsically to the Dvl PDZ domain.

Based on observations that Ad infection of clonal cell populations show cell-to-cell variability in the extent of capsid binding, we hypothesized that the cell cycle may influence the outcome of Ad infection.

Since 3' deletion mutant showed reduced PTB binding, we hypothesized that this might also affect the IRF2-IRES activity.

Because of the similarities between apoE and apoA in receptor binding, we hypothesized that the apoE receptor domain is also associated with angiogenesis and tumor growth.

Since parkin ubiquitination activity is further enhanced through phosphoubiquitin binding, we hypothesized that this basic patch is the phosphoubiquitin-binding site.

Assuming that HR+ve tumors attract higher estrogen levels in and around the tumor due to an increased tendency of estrogen binding, we hypothesize that this estrogen-rich environment leads to higher Adenosine Deaminase Gene expression, which in turn is responsible for the degradation of Adenosine (ADO), a potent anti-inflammatory agent [ 29, 30].

We hypothesized that binding of ser phosphorylated HSP20 to the thin filament was responsible for relaxation without MRLC dephosphorylation.

We hypothesized that binding of ser-phosphorylated HSP20 to the thin filament may "turn off" thin filaments so that phosphorylated myosin does not interact with the thin filament (i.e. a model similar to skeletal muscle troponin I).

Since DC migration is directed by CCL21 binding to CCR7 on DCs and we observed direct binding of CCL21 to sialic acids, we hypothesized that polySia on mDCs might promote DC migration towards CCL21.

We hypothesized that PtdInsP3 binding and membrane localization is not required for AKT phosphorylation and activation by PDK1 if the two proteins could be brought into proximity as stable complex with proper conformation by alternative mechanisms.