Nicholas E.S. Sibinga

TL;DR: This model consists of individual networks constructed using molecular data generated from intestinal samples isolated from three populations of patients with IBD at different stages of disease, and provides the integrated circuits of genetic, molecular, and clinical traits that can be directly queried to interrogate and refine the regulatory framework defining IBD.

TL;DR: In this paper, the authors show that recessive mutations in fat1 cause a distinct renal disease entity in four families with a combination of Steroid-resistant nephrotic syndrome (SRNS), tubular ectasia, haematuria and facultative neurological involvement.

TL;DR: It is indicated that Ang II regulates Fat1 expression and activity and induces Fat1-dependent VSMC migration via activation of AT1R, ERK1/2, and Nox1-derived ROS, suggesting a role for Fat1 downstream of Ang II signaling that leads to vascular remodeling.

TL;DR: It is shown that the atypical Fat1 cadherin acts as a molecular ‘brake’ on mitochondrial respiration that regulates vascular smooth muscle cell (SMC) proliferation after arterial injury and suggests that Fat1 controls mitochondrial activity to restrain cell growth during the reparative, proliferative state induced by vascular injury.

TL;DR: Reporter gene analyses identified sequences between −902 and −789, including consensus Ets and interferon regulatory factor elements, required for macrophage-specific andinterferon γ-inducible transcriptional activity.