Immunoblot (IB) data of co-immunoprecipitation (IP) experiments indicate that treating HeLa cells with arsenic enhances the physical interaction between β-catenin and E-cadherin at the membrane, accompanied by an increase in cyclin D1 expression. The following assumptions were made: A. Arsenic activates a non-canonical β-catenin pathway (independent of Wnt). B. Arsenic leads to cellular proliferation under these conditions. C. Arsenic leads to proteasomal degradation of β-catenin. D. Arsenic induces immediate apoptosis in these HeLa cells. Which one of the following options represents the combination of all correct assumptions?

Arrange the following events in the correct chronological order during receptor-mediated endocytosis of LDL and its subsequent intracellular fate: A. LDL binds to the LDL receptor in a clathrin-coated pit at the plasma membrane B. Dynamin oligomerises at the neck of the coated pit and hydrolyses GTP to pinch off the vesicle C. Clathrin triskelions are recruited via AP-2 adaptor binding to the NPXY internalisation signal of the LDL receptor D. Acidification of the early endosome (pH ~6) causes dissociation of LDL from its receptor E. LDL receptor is recycled to the plasma membrane via Rab11-positive recycling endosomes F. Cholesterol esters are hydrolysed by lysosomal acid lipase after late endosome–lysosome fusion

A researcher treats cultured mammalian cells with Brefeldin A (BFA) for 30 minutes and then labels newly synthesised proteins with 35S-methionine. She finds that: - Labelled proteins accumulate in the ER. - The cis-Golgi marker GM130 redistributes to the ER. - Lysosomal enzyme precursors (bearing mannose-6-phosphate) are secreted into the medium instead of reaching lysosomes. Which of the following mechanistic statements best explains all three observations?