of tG proteins Other downstream. After activation of transcription by ATF4, CHOP directly activates GADD34, f the protein Promoted by dephosphorylation phospho ER Customer Ser 51 of the subunit eIF 2a in stressed cells. Au Addition was proposed that CHOP Pro regulated apoptotic Bcl-2 and D Dampens the anti-apoptotic members, leading to Sch The. Due to the mitochondrial membrane and the release of cytochrome c into JTP-74057 GSK1120212 the cytosol Cytochrome c release in turn activates cytosolic apoptosis protease activating Factor 1, which activates caspase-9 and caspase-3 downstream Rts cascade dependent Dependent. K a number of ER stress conditions Can the release of calcium from the ER to the cytosol effect, k Can erh Hte cytosolic calcium also cause activation Calpa Alone, which induces cleavage of procaspase 12th After activation, the catalytic subunits of caspase 12 are released into the cytosol, where they independent caspase-9 Ngig cascade cytochrome c activate. It has also been proposed that can IRE1a activated receptor recruit expressing tumors necrosis factor associated factor 2, the four activated independently as procaspase mitochondrial apoptotic reaction Dependent. Both routes to the activation of the caspase cascade by caspase-9 and caspase-3, which then causes lead induced cell death. Second The unfolded protein response and its impact on tumor development A wide range of cancer types based on ER protein folding machinery correctly folded proteins Key pathway.
ER stress and the UPR are strongly induced in various tumors. There is evidence, has shown that the UPR is an important mechanism needed for cancer cells to maintain B Sartigkeit and resistance to treatment. Identify the components of the UPR are activated or suppressed in malignant and therapeutic potential against cancer by exploring the UPR are very active areas of research. UPR pathways are activated in a variety of tumor types and has been shown that essential for tumor cells to survive the hostile tumor microenvironment. There is evidence of expression w During XBP1s, ATF6 activation, the phosphorylation of eIF 2a, induction of ATF4 and chop in a variety of cancer cells. The ER chaperone BiP GRP78, protein GRP170 glucoseregulated 94 and were also upregulated. These studies were in prime Ren tumor cells or human cell lines and animal models of breast tumor, hepatocellular Rem carcinoma, gastric carcinoma, and adenocarcinoma Performed esophagus. UPR and stress response in general have also brought in oncogenesis participation induced inflammation. UPR is required for tumorigenesis. Animal studies have shown that tumor growth XBP1 was required in vivo. XBP1 and XBP1 knockdown cells formed tumors in usen no M, Although their rate of growth and secretion of Vaskul Ren endothelial growth factor in response to hypoxia in the in vitro treatment did not decrease. ER stress may also be anti-apoptotic responses. The activation of glycogen synthase kinase 3b leads to phosphorylation of p53, which increased its breakdown products Ht, protects cancer cells from p53-dependent Ngiger apoptosis. Zus Tzlich NF B w During ER stress is activated to induce anti-apoptotic responses. Heat shock proteins Have been reported to help cancer cells