细胞的内膜系统课件.ppt

在肝细胞内的光面内质网膜上的糖原颗粒，能被磷酸化酶降解，形成1－磷酸葡萄糖，再在细胞质基质中转化为6－磷酸葡萄糖。然后再由光面内质网膜上的6－磷酸葡萄糖磷酸酶将6－磷酸葡萄糖的磷酸根脱掉，把葡萄糖转移到内质网腔中，最后再释放到血液中，随血液运输到各种细胞处，当细胞的生命活动需要能量时，葡萄糖再降解，同时形成能量提供给细胞。 * 细胞色素P-450参与有毒物质以及类固醇和脂肪酸的羟基化，羟基化涉及四个基本反应：被氧化的物质同细胞色素P-450结合→细胞色素P-450中的铁原子被NADPH还原→氧同细胞色素P-450结合→底物结合一个氧原子被氧化，另一个氧原子用于形成水。被氧化的底物由于带上羟基，增强水溶性，容易被分泌排出 * /nature/journal/v443/n7113/box/nature05293_BX2.html ER stress is coupled to specific independent death pathways, as well as demonstrating involvement with the intrinsic and extrinsic apoptotic pathways. Studies from various laboratories have disclosed the roles of several ER-stress-induced cell-death modulators and effectors through the use of biochemical, pharmacological and genetic tools. These ER-stress-induced cell-death modulators include various members of the Bcl-2 family (Bcl-2, Bcl-XL, BAX, BAK, BI-1 and BIK), BAP31 and p53-dependent gene products such as NOXA and PUMA. BAP31, an ER-membrane protein, binds Bcl-2 (or Bcl-XL) and a caspase-8-containing pro-apoptotic complex77. When BAP31 is cleaved, a pro-apoptotic p20 fragment is derived, which, among other effects, induces mitochondrial fission, enhancing cytochrome c release78. Conversely, BAR, which is expressed primarily in neurons of the central nervous system, also bridges Bcl-2 and caspase-8 but functions as an anti-apoptotic protein79. CHOP (also known as GADD153), a transcription factor induced during ER stress and activated by p38 mitogen-activated protein kinase, may also function as an ER-stress-induced cell-death modulator. It has been proposed to promote ER-stress-induced cell death by downregulating Bcl-2 expression. Recent data have also implicated the calcium-binding protein apoptosis-linked gene-2 (ALG-2), and valosin-containing protein (VCP) as mediators of ER-stress-induced PCD. p23 interacts with PUMA and inhibits apoptosis, an effect that is reversed after cleavage. An ALG-2-interacting protein known as ALIX (or AIP-1) links motor-neuron-cell death during development as w