pestis recruits host Rab1b protein to the phagosome, resulting in inhibition of phagosome acidification and disruption of the remaining phagolysosomal metabolic pathway (26,27,39-41).
pestis in macrophages occurs within YCVs, and the formation of YCVs requires metabolic pathway inhibition by recruitment of Rab1b GTPases.
Yersinia pestis requires host Rab1b for survival in macrophages.
Sequence-specific primers and fluorescence-labeled probes complementary to EI24, YWHAE, TFRC, CORO1C, S100A16, NLK, RAB1B, DEDD, CUL5, and PRDX3 and the endogenous reference GAPDH were used.
Six mRNAs were selected that exhibited an enrichment in the Ago complexes from PCa cells and were therefore potentially downregulated in cell lines and tumors: Etoposide induced 2.4 mRNA (EI24, alias p53-induced gene 8 protein), S100 calcium binding protein A16 (S100A16), Nemo-like kinase (NLK), RAS oncogene family member 1B (RAB1B), death effector domain-containing protein (DEDD), and cullin 5 (CUL5).
NLK and DEDD are suggested to induce apoptosis [31, 32] and loss of RAB1B was shown to enhance the aggressiveness of breast carcinoma .
Gao et al., "Loss of RAB1B promotes triple-negative breast cancer metastasis by activating TGF[beta]/SMAD signaling," Oncotarget, vol.
The fusion of autophagosome-lysosome fusion is mediated by key autophagic proteins such as RAB1B
, RAB22A, RAB14, RAB27A, LAMP2, and LAMP3.