We next analyzed whether in a different HD mouse model expressing endogenous levels of full-length mutant huntingtin (HdhQ111/111) the expression of both receptors was also altered.
Jamie Bascom described a transgenic mouse model, expressing epimorphin (with an IL-2 signal peptide for cell-surface expression) from a mammary-specific WAP (whey acidic protein) promoter.
Together, these results revealed the successful generation of a mouse model expressing bovine CD14 shRNA, and indicated that the inhibition of exogenous CD14 expression altered the expression levels of genes in the TLR4 signaling pathway in vivo.
We confirmed these in vivo data using another TDP-43 Dox-regulatable Tg mouse model expressing hTDP-43NLSm under the control of the neurofilament heavy subunit (NEFH) promoter (rNLS8 27.
A transgenic mouse model expressing the G2019S mutation of LRRK2 is already available and apparently may represent a valuable experimental model for investigating PD pathogenesis and novel treatments.
We previously described a mouse model expressing Rs1, an engineered constitutively active Gs-coupled GPCR, under the control of the 2.3 kb Col I promoter.
Boosting a transgenic mouse model expressing germline VRC01 heavy chains produced broad neutralization of near-native isolates (N276A) and weak neutralization of fully native HIV.
To address this, we have used array tomography to examine an rTgTauEC mouse model expressing a P301L human tau transgene and a transgene labeling cytoplasm red (tdTomato) and presynaptic terminals green (Synaptophysin‐EGFP).
Using a transgenic mouse model expressing the human HHS form of GDH, at least three of these compounds were found to block the dysregulated form of GDH in pancreatic tissue.
Here we have taken advantage of a recently engineered transgenic mouse model expressing enhanced green fluorescence protein (EGFP) under the control of the tyrosine hydroxylase promoter to establish a more effective dopaminergic neuron cell culture model.
Here, we generated a knock-in mouse model expressing a mutation that abolishes the ankyrin-G/GABARAP interaction (Ank3 W1989R) to understand how ankyrin-G and GABARAP regulate GABAergic circuitry in vivo.
