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Empirical data show that there is a significant deletion component in the underlying web networks, but the deletion process is not uniform.
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As opposed to the GPCR part of the network, deletion of components of the Ras part is lethal, as is deletion of AC or PKA.
It is unclear why gene deletion of components of the alkaline phosphatase pathway renders cells sensitive to nickel while deletion of components of other transport pathways to the vacuole results in nickel-resistance (discussed below).
It is also unknown why deletion of components of the alkaline phosphatase pathway renders cells sensitive to nickel while deletion of components of other transport pathways to the vacuole results in nickel-resistance.
Similarly, deletion of components of the CDK complexes leads to severe synthetic growth defects when combined with deletion or mutation of factors involved in transcriptional elongation, including TFIIS, the Spt4/5 complex, and the CTD of RNAPII [33], [37], [39], [42] [45].
Following deletion of components of the yeast TCR apparatus, little (RAD16, MET18, RPB4; Table S1) or no (RAD7, RAD23, RAD26, RAD28, RPB9; data not shown) suppression of BRCA1-induced lethality was observed.
TCR-mediated nuclear factor kappa B (NF-κB) activation seems to be involved in differentiation of Treg cells because deletion of components of the NF-κB signaling pathway, as well as of NF-κB transcription factors, leads to markedly decreased Treg cell numbers in thymus and periphery.
In particular deletion of components of the SAGA complex, including Gcn5, confers sensitivity to CG-1521.
According to the "domino-effect" hypothesis [ 28] initial deletion of components such as PsbC and PsbD is expected to lead to mass deletion of other genes involved in photosynthetic light reactions.
To understand how the SCF E3 ligases regulate these cellular processes and embryonic development under in vivo physiological conditions, a number of mouse models with transgenic (Tg) expression or targeted deletion of components of SCF have been established and characterized.
This can be concluded because deletion of components required for heterochromatin formation, i.e., the clrD H3K9 methyltransferase and hepA, encoding heterochromatin protein 1, only partially restores SM production.
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