Sentence examples for mouse strains deficient from inspiring English sources

Using mouse strains deficient in TLR4 protein or signaling, we hypothesized that TLR4 would be important for development of systemic inflammation and hepatic injury after HS/R.

The analysis of mouse strains deficient for CD83 [8], [8] revealed that thymic CD83 expression is crucial for the maturation of double positive thymocytes to single CD4 positive T cells.

Inbred C57BL/6 (B6), and mouse strains deficient for gzmA (gzmA−/−), and gzmA×B (gzmA×B−/−), bred on the B6 background were maintained at the John Curtin School of Medical Research, Canberra and analysed for their genotypes as described [18].

In the present study, acatalasemic mouse strains deficient in catalase activity were used as an animal model.

To confirm the potential involvement of PAR1 or PAR2 in the MMP-1-dependent survival in sepsis, we used mouse strains deficient in either Par1 or Par2.

A similar phenotype is observed in mouse strains deficient in LTB4 biosynthesis enzymes such as 5-LO and LTA4H, which collectively highlight the significance of LTB4 in inflammatory arthritis and osteoclastogenesis [ 16, 17].

A mouse strain deficient for RIPK1 specifically in liver parenchymal cells (Ripk1LPC-KO) and their controls (Ripk1fl/fl littermates) were inoculated with low quantities of viruses.

And, we recently reported [7] that microinjection of Rad51 into oocytes of AKR/J mice, a mouse strain deficient in DNA repair, not only reduced the extent of DDSBs, but also suppressed apoptosis; thus strengthening the relationship between the activation of Rad51 and oocyte resistance to cell death.

KO C57/BL6 mice strains deficient in TNF-R1 (TNF-R1-KO) or in TLR4-KO and female athymic Swiss nude mice, all 8 10 weeks of age (Charles River Laboratories), were maintained in laminar flow rooms keeping temperature and humidity constant.

In addition, from our studies, crossing the Id2gfp mice with strains deficient in various transcription factors has opened the capacity to identify the checkpoints in DC lineage development both in vitro and in vivo that have not been readily resolved using knockout models.

Here, we have used in vitro and in vivo analysis of wild type mice and of two Lrp4 mutant mouse strains, one fully deficient (null mutant, Lrp4-/- Lrp4-/- Dietrich, in pretalation) and a functional hypomorph (Lrp4-ECD; [18]) to show that Lrp4 is an osteoblast expressed receptor for Dkk1 and sclerostin and regulates bone growth and bone turnover in vivo.