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The second distinctive phenotype of Arfrp1vil−/− mice was a dramatic decrease in ApoA-I release from the enterocytes. ApoA-I can be secreted from the intestine as a component of HDL or chylomicrons. Thereby, ApoA-I generated in the ER is transported to the Golgi separately from pre-chylomicron vesicles and is added within the Golgi to the chylomicron before the mature particle is secreted into the lymph () [,].

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