ER stress 相关基因

1、常用的ER stress marker 有ATF6、XBP1、PERK、IRE1alpha、eIF2alpha、ATF4(ER stress 通路中的基因)、GRP78/Bip、PDI、GRP94（内质网的分子伴侣）CHOP(C/EBP 的同源蛋白，是内质网应激源性的)其中eIF2alpha，GRP78、PDI、GRP94、在睾丸蛋白谱中都没有明显改变1、CASP8: caspase8 凋亡相关蛋白 2.141666ER stress caspase 8 细胞凋亡 2、HMOX1：血红素氧化酶 1.515822 Heme oxygenase-1 comes back to endoplasmi

2、c reticulum（BBRC404 (2011) 15）3、HSPB1:热休克蛋白27 1.715609ER stress induces the phosphorylation of small heat shock protein,Hsp27.(J cell Biochem,2005 Aug)4、CPE：carboxypeptidase E 羧肽酶 2.394951Thus, carboxypeptidase E degradation contributes to palmitate-induced beta-cell ER stress and apoptosis. CPE is

3、a major link between hyperlipidemia and beta-cell death pathways in diabetes.（Carboxypeptidase E mediates palmitate-induced beta-cell ER stress and apoptosisPNAS-2008-Jeffrey-8452-7）5、CSK：c-Src kinase 1.546242Our studies provide a molecular link that connects the c-Src tyrosine kinase transduction p

4、athway to ER stress-induced transcriptional activation of Grp78mediated by TFII-I. （Transcriptional regulation of the Grp78 promoter by endoplasmic reticulum stress: role of TFII-I and its tyrosine phosphorylationJ Biol Chem. 2005 Apr 29;280(17):16821-8. Epub 2005 Jan 21.)6、MCL1: 骨髓白血病细胞蛋白1 1.900026

5、 Bcl-2家族的抗凋亡蛋白7、CPT1A：肉毒碱棕榈酰基转移酶1A 1.568594 The mitochondrial oxidation of long-chain fatty acids is initiated by the sequential action of carnitine palmitoyltransferase I (which is located in the outer .ER stress 通路In non-stressed cells (not shown), the ER chaperone BiP binds to the luminal domains

6、 of the ER-stress sensors IRE1, PERK and ATF6, maintaining these proteins in an inactive state. During ER stress (shown), BiP （就是GRP78）preferentially binds to unfolded or misfolded proteins, thus driving the equilibrium of BiP binding away from IRE1, PERK and ATF6. These three proteins are the initi

7、ators of the three main signalling cascades of the UPR. The release of BiP results in the activation of PERK, through PERK homodimerization and trans-autophosphorylation. Activated PERK then phosphorylates the translation-initiation factor eIF2, reducing the overall frequency of messenger RNA transl

8、ation initiation. However, selected mRNAs, such as ATF4 mRNA, are preferentially translated in the presence of phosphorylated eIF2. ATF4 activates the transcription of UPR target genes encoding factors involved in amino-acid biosynthesis, the antioxidative-stress response and apoptosis. The release

9、of BiP also allows IRE1 to dimerize, activating its protein-kinase activity (through autophosphorylation) and its endoribonuclease activity. IRE1 then removes a 26-base intron from XBP1 mRNA. The spliced XBP1 mRNA encodes a potent transcription factor that translocates to the nucleus, activating the expression of UPR target genes. The release of BiP from ATF6 allows ATF6 to translocate to the Golgi apparatus, where it is cleaved by the proteases S1P and S2P, yielding an active cytosolic ATF6 fragment (ATF6 p50). This frag