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4) Check that the AM or GL mutated proteins are indeed deficient for the enzymatic activity.
These results indicate that beta Rac1−/− mice are indeed deficient in RAC1, specifically in pancreatic beta cells.
See explanation in Answer 5 and alternative experiment described in Answer 2. 4) Check that the AM or GL mutated proteins are indeed deficient for the enzymatic activity.
We confirmed by quantitative real-time polymerase chain reaction (qPCR) that BMDCs from myeloid pten -/- were indeed deficient in PTEN (Additional file 1).
If the symbolic system of the DD group is indeed deficient [ 37, 38], as suggested above, then in the symbolic task the DD group should have been more easily influenced by the irrelevant non symbolic dimension (quantity) than the control group.
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Indeed, NER deficient cells (rad14Δ) and DNA damage checkpoint deficient cells (mec1Δ) are not particularly sensitive to the CLUV treatment, contrary to the rad18Δ and rad5Δ cells, deficient in PRR [65], which irreversibly activate Mec1 DNA damage checkpoint and die in the G2 phase.
Indeed, cells deficient in HDAC6 fail to clear misfolded protein aggregates from the cytoplasm, cannot form aggresomes properly, and are hypersensitive to the accumulation of misfolded proteins.
Indeed, FimA deficient strains show reduced biofilm formation [16], while non-encapsulated mutants of P. gingivalis W83 exhibit enhanced biofilm formation [1], [39], [40].
Indeed, mice deficient for TLR2 had less tubular apoptosis as well as an impaired inflammatory response compared to wild type mice.
Indeed, mice deficient in TLR4, TLR2 and MyD88 all have reduced atherosclerosis which establishes that TLR-dependent pathways contribute to disease development.
Indeed, mice deficient in eNOS have reduced GSNO-R activity, and S-nitrosylation increases GSNO-R activity, suggesting that estrogen-dependent increases in eNOS lead to increased GSNO-R activity in the female lung, protecting against excessive S-nitrosylation.
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CEO of Professional Science Editing for Scientists @ prosciediting.com