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13, 14 The REV7 protein is involved in TLS and homologous recombination repair, 16– 28, 28 and Rev7-deficient mice show numerous apoptotic cells and accumulation of DNA damage in both germ cells and somatic cells, 29 suggesting that REV7 dysfunction enhances cellular sensitivity to DNA damage.
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The results showed that compared with the brains from WT mice those of the Ppt1-KI and Ppt1 −/− (Fig. 4N) mice showed numerous TUNEL-positive cells.
On the other hand, some Purkinje cells in Atxn1-KI mice showed numerous fine and short dendrites reminiscent of a loss of pruning or abnormal sprouting; such changes were not found in Atxn1-KI HMGB1 mice (Supplementary Fig S7A and B).
Likewise, 80% of aberrations detected by array CGH in tumour cells of the mouse model for epithelial ovarian cancer are conserved in human epithelial ovarian cancer [281] and epithelial carcinomas in mice with telomere dysfunction show numerous copy number changes in regions syntenic to those in human cancers [282].
As in the human disease counterpart, MMs from Ink4a-, and-, and Ink4a Arf-deficient mInk4a Arf-deficientd numiceus chromosome altypically.
Tumor sections from these mice also showed numerous dark brown-colored apoptotic cells.
In the Harderian gland of GFP-LC3 transgenic control mice about 25% (n = 3) of ductal cells, identified by their large round nuclei, show numerous GFP- puncta" (FiGFP- puncta1B, S2B).
Pkd1 -/- mutant embryos show numerous large renal cysts at E17.5.
These mouse groups showed numerous T-cell clusters in hippocampus and rostral neocortex, consisting of CD3-immunoreactive cells in areas rich in amyloid plaques.
Rac1-deficient mice show cell death in numerous locations, particularly in embryonic mesodermal cells.
Additionally, although both rely broadly on intact corticostriatal circuitry function, numerous studies in rats and mice show that PIT and conditioned reinforcement are dissociable at the systems, receptor and molecular levels [5], [35], [36].
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