Cytoprotective proteins Coding genes that neutralize reactive molecules to eliminate, dam Accused macromolecules to reduce the inflammation and cellular recovery Ren redox Hom Homeostasis. 8.9 Nrf2 is described on activated in response to stress caused by mechanisms such as above. Nrf2 on or off when the load subsidized by a separate mechanism. Fyn tyrosine kinase phosphorylates Lapatinib Tykerb Nrf2Y568, nuclear export and degradation of Nrf2. 10.9 Switching, ON and OFF, protects cells and Nrf2 f Promotes the survival of the cell. INrf2-0 M Usen shown persistent accumulation of Nrf2 in the nucleus, the postnatal death by Unterern Currency from hyperkeratosis in the feeder Hre and stomach out. 11 Undo Ngig Ph Genotype INrf2 deficiency by breeding to Nrf2-null M Nozzles suggested that strictly regulated negative feedback k Nnte crucial for the survival of the cell.
8 Systemic analysis showed INrf2 genomic PHA-680632 locus in the human lung cancer cell lines that deletion mutations, missense and insertion in functionally important Dom NEN INrf2 has a reduction in the affinity t High for INrf2 expression Nrf2 and cytoprotective genes. 12.13 activation of Nrf2 in rat cells obtained Ht the risk of side effects, including normal the survival of protected Defendants cells, tumor formation and resistance. 9 Therefore, it appears that cells t cellular Ren mechanisms that regulate the abundance of Nrf2 included. 14 In other words, to induce the transcription of Nrf2 INrf2 Selbstzerst Tion. The structural and functional analysis identified a chalice INrf2 Dom ne, which interacts with several proteins.
Although Nrf2 is a substrate for the liquid is known INrf2 Che INrf2 DGR has been reported to other proteins, including normal NRF1 bind a clone of the fetal and IKKB Prothymosin Alz 1. 15 18 It should be noted that the binding of a protein with lead region INrf2 DGR not always to the degradation of the protein. We have recently shown that a necessary with the prothymosin DGR Dom ne INrf2 and this interaction on nuclear localization of INrf2 interacts. 1 Therefore INrf2 and its interaction partners have many r In various cell signaling and survival. B-cell CLL / lymphoma 2 family of proteins regulates cell death and survival. 19.20 Bcl 2 proteins Are key regulators of caspase activation and play an r Key in the cell death by monitoring the integrity of the membranes of the endoplasmic reticulum and mitochondria.
21.22 The Bcl-2 family of proteins is divided into three subfamilies. The subfamily includes Bcl 2 Bcl 2, Bcl xL, Bcl and w, all of which are in the anti-Cell Death and sequence homology intervention, particularly in the four regions, areas bra 1 4. The Bax subfamily consists of Bax and Bak, contain BH1, BH2, BH3 and Homologiedom NEN, But not BH4 Dom ne and are proapoptotic. The subfamily Bik Bik, who understands and offer contains Lt only the BH3 Dom ne and lack BH1, BH2, BH3 and Dom NEN. Bik are proapoptotic members. An important feature of Bcl 2 proteins Is that they form the F Ability, homodimers and heterodimers. The life or death of a cell can be determined by the Bcl-2 family of proteins in two ways, either by heterodimerization between anti-apoptotic and pro-apoptotic members or independent-Dependent functions of these proteins. Both