Sentence examples for mutations reviewed in from inspiring English sources

β-catenin is a key player in the Wnt pathway, transmitting Wnt signals to the nucleus and critically contributing to tumorigenesis through activation of oncogenes (e.g. cyclin D1 and c-myc) or through its own sporadic mutations (reviewed in [18].

Inactivation occurs early in development, thus much of our knowledge regarding the initial events has been derived from studies utilizing mouse embryos or differentiating mouse ES cells containing Xist transgenes or mutations (reviewed in [1]).

For example, it has been suggested that of the lack of PTEN can be detrimental to tumour growth in the absence of other mutations (reviewed in [29]), and complete loss of this tumour suppressor can promote a senescence response that opposes tumour progression [30].

This likely reflects a Darwinian adaptive process at the cellular level, leading to accumulation of second-site point mutations (reviewed in [8]), gene amplification, increased activation of distinct receptor tyrosine kinases [9], [10] or transcriptional induction of alternative growth factor receptor pathways as detailed herein.

Each of these pairs of mutations are often accompanied by other accessory mutations (reviewed in Blanco et al.[ 90]).

Mutant screens for decreased auxin sensitivity have identified several Aux/IAA proteins with stabilizing mutations (reviewed in [ 18]).

However, recent years have shown that key developmental decisions, such as the selection, polarization, or localization of the oocyte (the future egg cell) are made during the very early steps of oogenesis, before the arrest caused by the ovoD mutation (reviewed in Huynh and St Johnston 2004).

Prosser J, van Heyningen V. PAX6 mutations reviewed.

For example, both the Dutch AβPP mutation (p.E693Q; reviewed in [ 6]) and the Italian mutation (p.E693K; [ 7, 8]) within the Aβ sequence cause amyloid angiopathy with intracerebral hemorrhages, whereas parenchymal AD pathology and dementia are subsidiary.

For example, part of the process by which precursor lesions progress to SCCs may represent a mtDNA mutation bottleneck (reviewed in Chinnery et al, 2000) where deleterious mutations are selected against.

If interactions between resistance mutations are additive, then the fitness of a strain carrying multiple resistance mutations is equal to the product of the fitness of strains carrying each mutation individually (reviewed in de Visser et al. 2011).