Sentence examples for mice with global from inspiring English sources

Exercise-dependent regulation of bone structure and functions was compared in mice with global Fstl3 gene deletion (Fstl3 −/−) and their age-matched Fstl3 +/+ littermates.

We examined OA development, chondrocyte and osteoblast behavior, and β-catenin signaling after ligament and meniscus damage in mice with global heterozygous deletion of Lrp6.

Upon left ventricular pressure overload, cardiac function was only preserved in mice with miR-21 deficiency in nonmyocyte cardiac cells, but not in mice with global or cardiac myocyte-specific ablation.

Knockout mice with global deficiency of ZnT8 showed normal glucose homeostasis and insulin production under normal conditions (Lemaire et al., 2009).

Using mice with global and cardiomyocyte conditional deletion of β-arrestin2, we show that under conditions of in vivo pressure overload the cellular source of the exocytosis of exosomes containing AT1R is the cardiomyocyte.

To provide a deeper and more granular understanding of the metabolic impact of the SRC family members, we performed targeted metabolomic analyses of key metabolic byproducts of glucose, fatty acid, and amino acid metabolism in mice with global knockouts (KOs) of SRC-1, SRC-2, or SRC-3.

In contrast, it was reported that mice with a global deletion of sirt1 are more prone to develop autoimmunity [13]; [13].

However, the use of mice with Arl6ip5 global deficiency compromised the findings.

The biological role of this interaction was investigated in vitro and in vivo in the postnatal hearts of mice with a global KLF15 functional deletion.

In contrast, mice with a global deficiency of NOX2 were reported to have an unaltered BP response to angiotensin II [ 116], suggesting that this isoform is less important.

A role for the NRP1 cytoplasmic domain in arteriogenesis has been demonstrated in mice with a global knock-in of NRP1 lacking its cytoplasmic region.