To test whether oncogenic Ras mutation would lead to UCC, we utilised mice carrying the constitutively active H-Ras Q61L oncogene ('low-copy').
To investigate the role of TNF, we utilised mice with a targeted disruption of the TNF gene (TNF−/−) or of the TNF receptor 1 gene (TNFR−/−).
To achieve this, we utilised mice bearing a conditional Apc allele on either a wild type or p53 deficient background [ 10, 11] and determined if any p53 dependent feedback loops have a functional consequence immediately following Apc loss.
In addition, we utilised primary mouse neurons taken from mice and a widely used human dopaminergic neuroblastoma cell line (SHSY5Y), which allowed cross-validation in three complementary cellular systems.
We utilised a mouse model to investigate how trisomy 21 might affect gene regulatory networks and adult neurogenesis.
We utilised two mouse models, each manifesting distinct AD-related pathologies: the K3 tau transgenic model, which develops NFTs [ 21, 22]; and the APP/PS1 transgenic model, which develops amyloid plaques [ 23].
Based on these observations, we utilised the mouse CIA model to investigate the functional capillary density in the inflamed synovium and to analyse genes that are involved in synovial angiogenesis during arthritis.
Therefore, to accurately evaluate the effect of reduced NPC2 expression at later stages when senescent levels are higher, we utilised Braf +/LSL−V600E /AdCre mice on the Npc2 +/hypo background, most of which survived for more than 10 weeks after AdCre delivery.
To investigate the route of metabolism of 24S,25-epoxycholesterol 24S,25-epoxycholesterolo dinferent knockout mouse models, Cyp27a1−/− and Cyp7brain weere the expression of the Cyp enzyme sterol 27-hydroxylase (Cyp27a1) or oxysterol 7α-hydroxylase (Cyp7b1) is eliminated respectively.
We utilised a unique set of mouse knockout cell lines, GTPase pulldowns, gentamicin protection assays and high-resolution scanning electron microscopy.
