Exact(3)
Functional studies that dissect PIK3CA and BRAF somatic mutations have established the oncogenic nature of these RAS effector genes [9] [11].
In vitro and in vivo studies of the most common germline and somatic RET mutations have established their role in oncogenesis [ 10– 13].
Analyses of sequence neighborhoods of human mutations have established, for this species at least, that a mutagenic influence of neighboring nucleotides on mutation rates is not restricted to CpG dinucleotides [ 5].
Similar(57)
Mutation analyses have established acidic residues essential for activity in other RNase H family proteins.
Despite infrequent inactivation in many cancers, mutation and functional data have established that KDM6A is a bona fide tumor suppressor gene.
Recent discoveries have established that mutations in EPAS1, the gene encoding hypoxia-inducible factor (HIF -2α transcription factor, are causative of familial and sporadic instances of polycytHIF -2αas well as various neuroendocrine transcription
We have established that mutations in the gltA gene encoding citrate synthase (CS) were critical for both potentiating the evolution of aerobic citrate utilization in the Lenski LTEE and for the subsequent refinement of this new metabolic capability.
Studies have established that mutations, dysregulations or dysfunction of miRNA biogenesis and their targets led to the blockage of physiological and biochemical pathways that influenced various diseases in human [ 5].
Previous investigations, using either mutation analyses or structural studies, have established the importance of the residues within loops LL,1, L6,7, and Lα,β of DnaK for allosteric coupling of NBD and SBD, the interaction of chaperone with the critical HSP40 cochaperone, or overall bacterial viability.
Scientists at the Institute of Cancer Research in London, who have been screening men from families with a history of prostate cancer, have established that 14 mutations in known cancer genes can predict life-threatening disease.
Previous reports have established that p53 mutation data can be used as a predictive marker for cancer development in Barrett's patients (Schneider et al, 1996), and that the presence of p53 mutations can predict poor 5-year survival rates of Barrett's tumour patients postoperatively (Schneider et al, 2000).
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