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(a) Strategy for generating mESC models, or mESC-derived cellular models, and mouse models carrying a chromosomal translocation.
This shows that mouse models carrying the Cre transgene alone can have significant behavioural phenotypes.
Studies of mouse models carrying ALS mutations (e.g., SOD1, TARDP-43, and FUS) have significantly expanded our understanding of ALS over the last 20 years.
Knock-in mouse models carrying such mutations showed an increased susceptibility to cortical spreading depression, the likely underlying mechanism of migraine aura [46, 47].
Knockin (KI) mouse models carrying FHM1 or FHM2 mutations show a lower threshold for CSD induction and a higher velocity of CSD propagation.
This hypothesis was confirmed by monitoring B cell development in knockin (KI) mouse models carrying V (D) J rearrangements identical to those of the mature bNAbs 2F5 and 4E10.
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Both mouse models carry CAG repeats that cause childhood disease in humans, and therefore, inclusion pathology may be a feature of the childhood rather than the adult forms of HD.
However, despite their obvious convenience in basic cancer research and in the testing of experimental therapies, the use of mouse models carries several limitations.
To date, mouse models carry Fbxw7 null alleles, but these do not faithfully recapitulate the mutations most commonly present in human cancers.
This study presents a new coisogenic mouse model carrying a point mutation in Ffar1 with functional consequence.
In the new mouse model carrying HBV cccDNA, injection of sgRNA Cas9 plasmids via rapid tail vein resulted in the low level of cccDNA and HBV protein.
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