Sentence examples for predominantly defective from inspiring English sources

Exact(1)

Interestingly, data in HCV-infected chimpanzees indicate a predominantly defective hepatic response to IFN, which is probably mediated through the activation of SOCS3 and may explain the lack of response to IFN-based treatment in many HCV patients.

Similar(59)

Applied to ADO II this suggests that G213R related ADO II is predominantly caused by defective trafficking, while the impaired transporter activity of the mutant ClC-7 plays only a marginal role.

Lagging chromosomes in RBS were found to be primarily C-group and smaller chromosomes (Van Den Berg and Francke, 1993), indicating that the segregation might be defective predominantly in submetacentric and acrocentric chromosomes.

RASopathies, a family of disorders characterized by cardiac defects, defective growth, facial dysmorphism, variable cognitive deficits and predisposition to certain malignancies, are caused by constitutional dysregulation of RAS signalling predominantly through the RAF/MEK/ERK (MAPK) cascade.

This consideration, together with evidence that NHEJ efficiency declines with aging (Vyjayanti & Rao, 2006; Vaidya et al, 2014), may explain the predominantly neurological manifestations of defective DNA repair disorders, including those associated with abolition of XCCR4.

In agreement, Lim et al [ 11] and Molyneux et al [ 31] have demonstrated that the cell of origin of BRCA1 defective breast carcinomas, a predominantly triple negative type of breast cancer, is also in the Ep-CAMhigh/CD49f + luminal progenitor cells.

Pale Soft Exudative [ PSE"] meat is the term used to describe a defective type of meat, seen predominantly in pork, but also in poultry.

A selective marker was pif2 encoded per os infection factor which predominantly deleted, along with the adjacent pif1, in defective viruses.

In addition, exogenous hCNT1 predominantly accumulated in intracytoplasmic vesicles in CCC suggesting defective cellular trafficking of hCNT1 as a contributing factor to transport deficiency.

This insert in the catalytic domain of TrkC results in defective MAPK activation which may result predominantly from an inhibition of high-affinity Shc binding [ 29].

This is indicated by the persistence of nearly wild-type levels of CG and CHG methylation in mutants defective in RNA-directed DNA methylation, which lose predominantly CHH methylation.

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