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Under certain conditions EGF induces morphological transformation and adhesion independent growth of mouse cells.
In preclinical stages, microglial cells that highly reacted towards focal lesions acquired over the course of the disease an ameboid shape indicating morphological transformation and consequent cellular activation.
Therefore, activation of autocrine TGF-β signaling, following ICN stable expression, is predominantly responsible for suppressing v-Src-induced transformation of QNR cells, as defined by the loss of both morphological transformation and anchorage-independent growth capacity.
In this work, we have identified autocrine TGF-β3 signaling activation as a major effector of Notch-induced phenotypic changes, sufficient to induce transition in differentiation markers expression, suppress morphological transformation and significantly inhibit anchorage-independent growth.
The readily loss of GATA4 expression through changes in chromatin conformation suggests a potential non-phenotypic initiating event, leading to subsequent loss of GATA6, morphological transformation, and ultimate tumorigenesis.
I presented an assessment of physiological components that drive morphological transformation and solid tumor progression arising from the self-propagating tumor microenvironment.
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Foci were determined from the edges using morphological transformations and optimal thresholding.
We show that the combination of well-resolved phylogenies obtained by phylogenomic analyses and well-documented extensive morphological datasets is an appropriate basis for reconstructing complex morphological transformations and for the inference of evolutionary histories.
In this review, we discuss the necessity for control over the assembly and morphological transformation of peptides and peptide conjugates, the critical role of these properties for their ultimate biological application, as well as the methods by which this can be programmed into the molecular structure.
Nuclear localisation of active ERK is necessary for the correct control of gene expression by growth-factors, and for morphological transformation of fibroblasts and PC12 [19]–[22].
Re-expression of SSeCKS to physiologic levels in Src- or Ras-transformed fibroblasts or epithelial prostate cancer cells suppresses morphological transformation, anchorage- and growth factor-independent proliferation, and metastatic potential, while restoring normal actin-based cytoskeletal architecture and cell-cycle controls on cyclin D1 expression [ 4, 6, 7].
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Since I tried Ludwig back in 2017, I have been constantly using it in both editing and translation. Ever since, I suggest it to my translators at ProSciEditing.

Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com