Exact(52)
To evaluate the role of Ihh in OA development, Ihh was specifically deleted in murine cartilage using an Ihh conditional deletion construct (Col2a1-CreER T2 ; Ihhfl/fl).
By characterizing mice that have the Traf3 gene specifically deleted in B lymphocytes (B-TRAF3-/ mice), we found that TRAF3 deletion causes vastly prolonged survival of mature B cells independent of BAFF, which eventually leads to B lymphoma development in mice [ 4, 14].
To control for unexpected effects from the lack of Lrp5 in noncartilage tissues, we generated chondrocyte-specific conditional KO mice (Lrp5 fl/fl ; Col2a1-cre), whereby the cre recombinase gene specifically deleted the Lrp5 gene from cartilage, but not other tissues, such as brain, heart and bone.
Unlike germline knockouts, mice specifically deleted for Rb in the developing telencephalon survived until birth.
To this end, we specifically deleted the HIF-1α isoform in periosteal progenitor cells and show that activation of HIF-1α signaling in these cells is critical for bone repair by modulating angiogenic and metabolic processes.
Aim of this study was to investigate if [11C]erlotinib PET is sensitive enough to measure a reduction of Abcg2 expression in the liver using a transgenic mouse model, in which the epidermal growth factor receptor (EGFR) was cell-type specifically deleted in hepatocytes of the liver leading to a down-regulation of Abcg2.
Similar(7)
To analyze this we used a method to specifically delete antigen-specific CD8+ T cells in vivo.
To investigate which domains of LEDGF/p75 are involved in the nuclear FRET increase, we generated a series of LEDGF/p75 mutant constructs, specifically deleting or altering domains involved in chromatin binding (Supplementary Fig. S8) and reintroduced these to complement LEDGF/p75KD cells.
A mesenchymal-specific Cbfβ CKO mouse model was generated by using the Dermo1-Cre mouse line to specifically delete Cbfβ in mesenchymal stem cells, which give rise to osteoblasts and chondrocytes.
We will specifically delete miR-155, Apoe and Trem2 in microglia of AD mouse models; 2) restoration of M0-homeostatic microglia via Mertk pathway in humanized APOE4 and AD mice.
In the current study, we have verified the functionality of our episomal CRIPSR/Cas9 system first by inactivating visible reporter gene, and further by specifically deleting a single genomic region and editing multiplex genes in a transgene-free manner.
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