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In addition, the biological activity of recombinant scgIL-12 (rscgIL-12) are demonstrated for its stimulation of PBL proliferation, chemotactic migration, induction of TNF-α gene expression and a plausible adjuvant effect of prolonged protection against parasite infection in fish.
VEGF produces may biological effects such as endothelial cell mitogenesis, migration, induction of proteinases leading to remodeling of the extracellular matrix, increased vascular permeability, and maintenance of the survival of newly formed blood vessels [42].
In vitro studies indicate that TGF-β1 is activated upon contact between endothelial and mesenchymal cells [2] and that it mediates a variety of actions associated with vessel maturation including, inhibition of EC proliferation and migration, induction of pericyte differentiation, and production of basement membrane [2] [4].
NO plays a role in cellular proliferation, migration, induction of epithelial-mesenchymal transition, angiogenesis, and apoptosis of cancer cells.
Indeed, germ cell and trophoblast differentiation shares many of the phenotypic hallmarks observed in cancer cells including immortalisation, tissue invasion, stimulation of cell migration, induction of angiogenesis and downregulation of the major histocompatibility complex resulting in immune evasion.
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The normal suppression of angiogenesis by TSP-1 and -2 involves multiple mechanisms including direct interaction with vascular endothelial cell growth factor (VEGF), inhibition of matrix metalloproteinase 9 (MMP9) activation, inhibition of endothelial cell migration and induction of endothelial cell apoptosis.
It promotes angiogenesis through indirect effects, such as through monocyte migration or induction of angiogenic factors such as VEGF and MMP9 [27], [28], [28], or by directly functioning on endothelial cells [22].
I will discuss the role of ErbB receptors in tumor cell proliferation, migration, and induction of tumor vasculature.
Second, studies in zebrafish show that commensal microbiota stimulate neutrophil migration through induction of SAA (Kanther et al., 2013).
Note that this inhibition effect might due to either inhibition of cell migration or induction of cell death after KT-NB treatment.
administration of ex vivo modified DCs in patients with advanced melanoma, evaluating both migration and induction of tumor antigen-specific immune responses.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com