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In line with this hypothesis, functional CAR knockout in a murine model led to a dilated intestinal tract (Pazirandeh et al, 2011).
In addition Hes1 is highly expressed in blast-crisis CML and retroviral co-expression of Hes1 with BCR-ABL in a murine model led to an aggressive acute leukemia [ 62].
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Overexpression of SALL4 in a murine model leads to myeloid leukemic development.
In our previous study we have shown that DC-based immunotherapy in this murine model leads to the induction of a strong anti-tumour response [ 28].
The lack of Fc FcR interactions in a subcutaneous murine model leads to poor activation of human Fc-mediated antibody dependent cellular cytotoxicity and complement dependent cytotoxicity-mediated tumor regression and could lead to poor efficacy of chimeric Rituximab.
Iron accumulation in human disease and murine models led to the inference that Cp is important to release iron from the cellular pool, especially mediated by a membrane glycosylphosphatidylinositol-form of this ferroxidase [39].
CR1 is a receptor for complement fragment C4b, whose deficiency in humans and murine models leads to lupus.
The lack of functional Fas signaling in murine models leads to altered endochondral ossification, increase of the bone mass in adult mice, and resistance to ovariectomy-induced bone loss.
Targeted overexpression in the liver in a murine transgenic model led to the development of severe cirrhosis and glomerulonephritis [13], [14].
Furthermore, inhibition of mineralocorticoid receptor expression in a murine conditional knockdown model led to cardiac fibrosis that was fully reversible when mineralocorticoid receptor expression was normalized (1).
Knock-down of c-Myc in a murine lung cancer model led to a reduction in MMP-9 levels and diminished metastasis of lung tumor cells to distant sites [ 46].
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