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For example, in NIH3T3 mouse fibroblasts, as well as Rat1 fibroblasts, Rac1V12 expression confers growth factor independence, whereas Cdc42V12 expression confers anchorage independent growth [ 8].
With IL-3 in the media, selection for growth factor independence was avoided.
Using a triple mutant of BCR-ABL (Y177F, ΔSH2, and ΔPro), we show that this mutant still confers growth factor independence to 32D cells (Figure 1), but exhibits a profound defect in the transformation of primary hematopoietic cells.
In contrast, the significantly reduced activity of the MAP kinase and PI3-kinase/AKT pathways suggest that they are not required for BCR-ABL to induce growth factor independence in the triple mutant cell lines.
Dicer-null NS cells do not appear to be transformed to an oncogenic phenotype, as they show a marked dependence on growth factor signalling for survival, whereas a classic hallmark of the cancer cell is its growth factor independence [46].
In addition, our previous data indicates that the CA-CSF-1R Y561F is equally competent for signaling as it can induce growth factor independence in MCF-10A cells and promote MCF-10A acini growth similar to CA-CSF-1R [8].
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Growth factor independence-1 (Gfi1), B cell leukemia/lymphoma 11b (Bclysine lysine methyltransferase G9a, and ETS1 are also essential for the development of ILC2s (Spooner et al., 2013; Walker et al., 2015; Yu et al., 2015; Zook et al., 2016).
Growth factor independence-1 (Gfis) is a zinc finger transcriptional repressor that regulates hematopoietic stem cell maintenance, pre-T-cell differentiation, formation of granulocytes, inner ear hair cells, and the development of secretory cell types in the intestine.
The growth factor independence-1 (GFI1) transcription factor is essential for the development of neuroendocrine cells, sensory neurons, and blood.
Immediately upstream of the core promoter, there is a silencer element that contains a putative growth factor independence-1 (GFI-1 -binding GFI-1 -binding
The abnormal SOCS1 expression in psoriatic keratinocytes depended on an alteration of the transcriptional machinery regulating its promoter function, involving growth factor independence-1b and Kruppel-like factor 4 transcription factors.
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