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Choline uptake and metabolism modulate macrophage IL-1beta and IL-18 production
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Ciliary defects resulting from cytoplasmic dynein inhibition are rescued by Mak and Ick activation Given that deficiency of Mak and Ick impaired retrograde IFT, we hypothesized that Mak and Ick activation could also restore the ciliary abnormalities caused by retrograde IFT defects related to other gene mutations
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