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To determine whether miR-17-5p mediatumorigenesisesin in MYCN-amplified neuroblastoma cells, we evaluated the effect of miR-17-5p knockdown in LAN-5 cell line, which expresses miR-17-5p at elevated level (Figure 1B).
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While mutations in Wnt genes have been linked to several human diseases (http://www.stanford.edu/~rnusse/diseases/Humangeneticdis.htm), further identification of specific Wnt isoforms mediating tumorigenesis in different cancer types, skeletal diseases, and stem cell maintenance will clearly be critical for realizing the therapeutic potential of Wnt coreceptor antibodies.
In this study, we have dissected the contribution of the RhoGEF2 pathway in Ras-mediated tumorigenesis in Drosophila epithelial tissues.
We are currently examining the pathways required for IGF-IR and IRS-mediated tumorigenesis in the mammary gland.
Consistent with the importance of RhoGEF2 in Rho-family activation being important for Ras-mediated tumorigenesis, in the genetic screen we also identified Rac1 and an activated allele of Rho1 as cooperating genes with Ras ACT (Brumby et al., 2011).
p110α is essential for signaling and growth of tumors driven by PIK3CA mutations, RTKs, and/or mutant Ras, whereas p110β lies downstream of G-protein-coupled receptors and has been shown to mediate tumorigenesis in PTEN-deficient cells [ 9].
p110α is essential for signaling and growth of tumors driven by PIK3CA mutations, RTKs, and/or mutant Ras, whereas p110β lies downstream of GPCRs and has been shown to mediate tumorigenesis in PTEN-deficient cells.
In order to identify other genes that contribute to Ras-mediated tumorigenesis in Drosophila, we carried out a dominant modifier genetic screen to identify genes that, when overexpressed, would act like scrib mutants and cooperate with Ras ACT (Brumby et al., 2011).
c-Myc has recently been demonstrated to mediate nuclear β-catenin-mediated tumorigenesis in the APC-deficient mouse model of intestinal neoplasia [46].
Increased expression of CD44, which was considered in this study to be a cancer stem cell marker, was also observed in inflammation and mediates tumorigenesis (Heldin et al, 2008).
In addition to its critical involvement in angiogenesis, Notch pathway also mediates tumorigenesis and progression through tumor cell proliferation, apoptosis, and self-renewal 10, 11.
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