The geographical distribution of these variants is however unknown.
With the exception of TLR1, the association evidence of other TLR variants are, however, not conclusive.
These risk variants are, however, of small effect and together only partially explain BD's heritability [ 3, 4].
The regulatory mechanisms underlying alternative splicing, as well as the biological significance and function of individual gene splice variants are, however, still very poorly understood (4).
These results suggested increased activity of at least two efflux pumps as a result of doxorubicin- and paclitaxel-selection. Doxorubicin net accumulation in the variants was however variable in comparison to the parental cell line (MDA-MB-435S-F/Taxol-10p – 81.45±5.3%, MDA-MB-435S-F/Taxol-10p4p – 110.78±14.1%, MDA-MB-435S-F/Adr-10p – 128.41±5.3%, MDA-MB-435S-F/Adr-10p10p – 97.06±6.1%).
The D414H variant was, however, unable to form a hydroxylated product detectable by either the HPLC-based enzyme assay or mass spectrometry.
After correction for multiple testing this variant was, however, not associated with type 2 diabetes in the present meta-analysis including 55,521 individuals (OR = 1.05, 1.01 1.1, P = 0.012).
The occurrence of this shorter variant was, however, prevented by monoHER.
The elevation of risk for each individual variant is, however, low, and incomplete penetrance is evident for all prothrombotic variants.
