Induction of ER stress in macrophages of tuberculosis granulomas.

Perante esta hipótese e tendo em conta as evidências reportadas por Kinnman (2005), parece fundamental aprofundar este caminho de investigação, procurando os significados, as

subject to Ire1-mediated unconventional splicing In the conventional UPR signaling pathway, Ire1 activates its downstream transcription factor Hac1/Xbp1 upon ER-stress by removing

aeruginosa, containing secreted virulence factors, induces ER stress in primary bronchial epithelial cells as evidenced by splicing of XBP1 mRNA and induction of CHOP, GRP78 and

All this evidence suggests that PP2Ce is essential for adaptive ER stress response at the onset of lactation and its deficiency can trigger pathological stress signaling in

Using a murine Burkitt´s lymphoma model over-expressing human c-MYC [β0], we show here that immunization of mice with human c-MYC protein and c-MYC derived

It was shown in HCV expressing cells from HCV-Tg mice, and liver tissue from HCV infected patients, that induction of ER stress resulted in up-regulation of protein phosphatase

Methodology/Principal Findings: a -TEA induces endoplasmic reticulum (ER) stress as indicated by increased expression of CCAAT/enhancer binding protein homologous protein (CHOP) as

Infected plants also showed induction of transcripts representing putative defense- and stress-related genes that code for protein disulfide isomerase, peroxidase, super-