Sentence examples for mouse models suggest from inspiring English sources

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.

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].

Recent advances in the molecular biology and physiology of water transport have yielded new insights into how and why water moves across cell membranes, and studies on aquaporin knockout mouse models suggest that aquaporins are involved in the development of some diseases and they may be useful targets of research into selective-inhibitor drugs.

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

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].

The immunosuppressive properties of mTOR inhibitors, coupled with their efficacy for tumor prevention in mouse models, suggested that modulation of the immune system is important for mutant K-Ras mediated lung tumorigenesis.

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.