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Transcriptional dysregulation occurs early in the molecular pathology of HD and has been recapitulated across multiple HD model systems (reviewed in [10]).
Instead, ideas about immune system synergisms and trade-offs are often based on general immunological knowledge from humans, domesticated animals and other model systems (reviewed in [1], [3], [7], [11]) or rooted in life-history hypotheses (e.g. [9]).
The data from model systems, reviewed above, suggest that MMPs are involved in most phases of carcinogenesis from initiation to metastasis.
The fluid pressures we observed in autochthonous PDAs are significantly larger than those reported in a variety of in vitro, xenograft and allograft tumour model systems (reviewed in Heldin et al, 2004).
Maternal age-related defects in the oocyte meiotic maturation process represent the largest single source of birth defects and infertility in developed countries, which motivates studies in both mammalian and invertebrate model systems (reviewed by Hassold and Hunt 2009).
The fact that HPV16E6E7 have convincingly been demonstrated to induce genetic instability in in vitro model systems (reviewed by Korzenievski [ 49]), would argue for the presence of a genetic instable environment in HPV16-positive CIN3.
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Caenorhabditis elegans is a well-established model system (reviewed by Hodgkin [ 1]) that is increasingly being used for genetic and molecular investigations into conserved biological processes, including those involved in human disease [ 2- 5].
Both biospheric importance and intracellular abundance of Rubisco stimulated plenitude of molecular studies using Rubisco as a model system (reviewed in [ 12]), but despite significant progress our understanding of Rubisco functioning and evolution is still far from complete [ 13].
For arthropods, on the other hand, a substantial amount of research toward the understanding of mtDNA replication is available, using D. melanogaster as a model system (reviewed in Oliveira et al. 2010).
Principal mechanisms have been revealed in great detail in the last two decades using yeast as a model system (reviewed in [ 5]); however, a wealth of information has also been accumulated regarding mammalian cell-cycle progression, in which the cyclin E/CDK (cyclin-dependent kinase) 2 signalling controls S-phase entry (reviewed in [ 4, 6]).
Some promising applications of this chemistry to model systems is reviewed, including the fast and convenient covalent labelling of G-protein-coupled receptors (GPCRs) in intact cells, with an emphasis on the perspectives of mapping signalling events triggered by these complexes.
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