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However, despite their obvious convenience in basic cancer research and in the testing of experimental therapies, the use of mouse models carries several limitations.
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This shows that mouse models carrying the Cre transgene alone can have significant behavioural phenotypes.
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.
Mouse models carrying mutations commonly found in human tumors provide an opportunity to investigate the mechanisms of tumorigenesis in vivo.
In this report, we present the generation and characterization of two novel knock-in mouse models carrying either HA or Myc-tagged endogenous Polycystin-1.
Accordingly, transgenic mouse models carrying tax have been shown to develop mesenchymal tumors, neurofibromas, arthropathy, and large granular lymphocytic leukemia; however, none of these transgenic mice develops a T-cell leukemia/lymphoma resembling ATL [5].
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.
Finally, mouse models carrying a reduction in Pkd1 expression [9], or transgenic overexpression of the Pkd1 gene [10] all result in renal cystogenesis, suggesting that the expression levels and/or appropriate subcellular localization of PC-1 are critical for its normal function.
Three mouse models carrying heterozygous Dync1h1 mutations mimic the phenotypes observed in humans.
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