Sentence examples for mutant cooperates with from inspiring English sources

Our results suggest that the constitutively active FGFR2K569E mutant cooperates with forced Myc expression in oncogenic transformation in part by suppressing Myc-dependent apoptosis.

aPKC-dependent signalling in scrib mutants cooperates with JNK to significantly enhance oncogene-mediated tumour overgrowth.

Brumby AM, Richardson HE. scribble mutants cooperate with oncogenic Ras or Notch to cause neoplastic overgrowth in Drosophila.

For example, Scrib-deficient mutants cooperate with oncogenes to mediate transformation in Drosophila.

Similarly, clarification is needed of how scrib mutants cooperate with oncogenes in mediating transformation in Drosophila.

We have also identified distinct JNK and aPKC-dependent modes by which scrib mutants cooperate with oncogenes in tumourigenic overgrowth and this has the potential to impact upon our understanding of how loss of human Scrib can also promote oncogene-mediated transformation.

We found that the mutant KRAS cooperates with p53 in the induction of Noxa, but not other pro-apoptotic p53 target genes.

As p53 has been established as a SMAD2/3 transcriptional co-factor downstream of TGF- β, we suggest a model in which mutant p53 cooperates with SMAD3 to enhance Nox4 transcription to promote subsequent Nox4 oxidase activity that participates in redox regulation of FAK activation and cell motility.

We found that the expression of the C. elegans lipase LIPL-4, which is overexpressed in the glp-1 germline less mutant and cooperates with the autophagic pathway to extend its lifespan (Lapierre et al., 2011; Wang et al., 2008), is dramatically reduced by frh-1 RNAi.

As scrib mutants also cooperate with NACT to produce non-differentiated tumours that invade and fuse with the brain lobes, we also investigated whether JNK was essential for N-driven tumourigenesis.

Thus, blocking both JNK and aPKC signalling completely suppressed the ability of scrib mutants to cooperate with oncogenic N signalling and overcame the aPKCCAAXDN-dependent restraint in scrib- + NACT tissue overgrowth.