Sentence examples for mouse models suggests from inspiring English sources

Experimental evidence in mouse models suggests that the degradation of the extracellular matrix by matrix metalloproteinases (MMPs) plays an important role in infarct rupture.

However, evidence from mouse models suggests that Tregs may have other anti-inflammatory properties in addition to suppressing T cell activation [1], [3].

Experimental evidence in mouse models suggests that Factor XIII might play a key role in wound healing, and low persistent values lead to increased incidence of cardiac rupture following myocardial infarction.

Taken together, the data from mouse models suggests that ADPKD is recessive at the molecular level and that embryonic loss of either Pkd1 or Pkd2 is incompatible with viability.

Moreover, the analysis of AD transgenic mouse models suggests an altered ganglioside metabolism in AD.

The therapeutic activity of the nutlins in mouse models suggests that activating WT p53 by inhibiting Mdm2 may produce such an outcome.

As an example, ciliopathies like BBS are associated with diabetes mellitus and obesity, and mouse models suggest a role for cilia in controlling hyperphagia [25].

Studies on human samples indicate that the cell-of-origin is likely a cone photoreceptor [35, 36] whereas studies in mouse models suggest a horizontal cell [37], or a Müller glia cell [38].

These observations along with experimental evidence in cellular and mouse models suggest that TG2 can contribute to the abnormal aggregation of disease causing proteins and consequently to neuronal damage.

However, chronic gastrointestinal dysfunction suffered by a subset of patients after surgery as well as studies in HSCR mouse models suggest that aberrant NC segregation and differentiation may be occurring in ganglionated regions of the intestine.

Studies of mouse models suggest that IL-2 signalling is critical for Treg homeostasis in vivo [13], [14].