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Based on the defined biology of mammalian Cas proteins (reviewed in [50]), the defects seen with Dcas and Fak56 mutant flies may reflect defects in cellular morphology (e.g., attachment and polarization) that inhibit appropriate migration during development.

We suggest that the reduced lysosomal compartment may reflect defects in protein recycling, which may in turn be responsible for altered localisation of the efflux transporters ATP7A and ATP7B in the A2780cis resistant cell line.

Aberrant alternative splicing of many genes (CD3ζ, CD44, CREM) is observed in SLE T cells and may reflect a global deregulation of this process, which may be of genetic origin or may reflect defects in the cellular microenvironment.

Because strains in this class form significant numbers of spores, their loss of staining may reflect defects in generation of the iodine reactive alpha-glucan component of the spore wall (Garcia et al. 2006).

Expression of LIN-45 V627E) LIN-45 V627ED) wandpreviousLIN-45 EDfied LIN-45 EDonally cause the vulva to burst at the L4-to-adult molt, wasch may reflect defects in either the Vpreviouslycatidentified resultong vulval cells [ 31].

Similar(55)

The aberrant branching that increases with the age of the mutants may also reflect defects in microtubule stability and transport that slowly become more severe as axons grow to their full adult size.

Here, we particularly focused on the molecular species whose level was significantly altered in the frontal but not in the occipital cortex because such an abnormal pattern may reflect anatomical defects that may be attributed to schizophrenia [ 22, 23]; this molecule was identified as PC (diacyl-16:0/20:4).

Pathogenetic mechanisms that cause tissue damage in diabetes may reflect molecular defects that lead to increased cellular production of superoxide anion (O2●-) in affected tissues [ 13, 14]: examples are excessive O2●- production through mitochondrial dysfunction [ 15] coupled with diminished O2●- clearance through impaired SOD activity (reviewed in [ 16]).

This phenotype may reflect a defect in the mechanics of kinetochore-MT binding or involvement of accelerated progress through mitosis [15].

In particular, telomerase-deficient mice display hypersensitivity to ionizing radiation and delays in DSB repair that may reflect a defect in HR [37].

This observation is in agreement with other studies [10], [22], [40] and may reflect a defect in transcription due to decreased Elongator activity, as previously proposed [10].

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