Timmers K I, Clark A E, Omatsu-Kanbe M, Whiteheart S W, Bennett M K, Holman G D, Cushman S W
Experimental Diabetes, Metabolism and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Biochem J. 1996 Dec 1;320 ( Pt 2)(Pt 2):429-36. doi: 10.1042/bj3200429.
The vesicle-associated membrane proteins [VAMPs; vesicle SNAP receptors (v-SNAREs)] present on GLUT4-enriched vesicles prepared from rat adipose cells [Cain, Trimble and Lienhard (1992) J. Biol. Chem. 267, 11681-11684] have been identified as synaptobrevin 2 (VAMP 2) and cellubrevin (VAMP 3) by using isoform-specific antisera. Additional antisera identify syntaxins 2 and 4 as the predominant target membrane SNAP receptors (t-SNAREs) in the plasma membranes (PM), with syntaxin 3 at one-twentieth the level. Syntaxins 2 and 4 are enriched 5-10-fold in PM compared with low-density microsomes (LDM). Insulin treatment results in an 11-fold increase in immunodetectable GLUT4 in PM and smaller (approx. 2-fold) increases in VAMP 2 and VAMP 3, whereas the subcellular distributions of the syntaxins are not altered by insulin treatment. To determine which of the SNAP receptors (SNAREs) in PM might participate in SNARE complexes with proteins from GLUT4 vesicles, complexes were immunoprecipitated with anti-myc antibody from solubilized membranes after the addition of myc-epitope-tagged N-ethylmaleimide-sensitive fusion protein (NSF) and recombinant alpha-soluble NSF attachment protein (alpha-SNAP). These complexes contain VAMPs 2 and 3 and syntaxin 4, but not syntaxins 2 or 3. Complex formation requires ATP and is disrupted by ATP hydrolysis. When all membrane fractions are prepared from basal cells, few or no VAMPs and no syntaxin 4 are immunoprecipitated in SNARE complexes obtained from LDM alone (or from immunoisolated GLUT4 vesicles). The content of syntaxin 4 depends on the presence of PM, and participation of VAMPs 2 and 3 is enhanced 4-6-fold by the addition of solubilized GLUT4 vesicles to PM. The latter increase is greater than can be explained by the 2-fold higher levels of VAMPs added to the reaction mixture. When all membrane fractions are prepared from insulin-stimulated cells, SNARE complexes formed from PM alone contain similar levels of syntaxin 4 but 5-6-fold higher levels of VAMPs 2 and 3 compared with PM alone from basal cells. Addition of GLUT4 vesicle proteins to PM from insulin-treated cells results in a further 2-fold increase in VAMP 2 recovered in SNARE complexes. Therefore the VAMPs in PM of insulin-treated but not basal cells, and in GLUT4-vesicles from cells in either condition, are in a form that readily forms a SNARE complex with PM t-SNAREs and NSF. Insulin seems to activate PM and/or GLUT4 vesicles so as to increase the efficiency of SNARE complex formation.
利用同工型特异性抗血清,已将从大鼠脂肪细胞制备的富含葡萄糖转运蛋白4(GLUT4)的囊泡上存在的囊泡相关膜蛋白[VAMPs;囊泡SNAP受体(v-SNAREs)]鉴定为突触小泡蛋白2(VAMP 2)和细胞ubrevin(VAMP 3)。其他抗血清将 syntaxin 2和4鉴定为质膜(PM)中主要的靶膜SNAP受体(t-SNAREs),而syntaxin 3的水平仅为前者的二十分之一。与低密度微粒体(LDM)相比,syntaxin 2和4在PM中富集5至10倍。胰岛素处理导致PM中可免疫检测的GLUT4增加11倍,VAMP 2和VAMP 3增加较小(约2倍),而胰岛素处理不改变syntaxin的亚细胞分布。为了确定PM中的哪些SNAP受体(SNAREs)可能与GLUT4囊泡中的蛋白质形成SNARE复合物,在添加了带有myc表位标签的N-乙基马来酰亚胺敏感融合蛋白(NSF)和重组α-可溶性NSF附着蛋白(α-SNAP)后,用抗myc抗体从溶解的膜中免疫沉淀复合物。这些复合物包含VAMPs 2和3以及syntaxin 4,但不包含syntaxin 2或3。复合物的形成需要ATP,并被ATP水解破坏。当所有膜组分均从基础细胞制备时,仅从LDM(或从免疫分离的GLUT4囊泡)获得的SNARE复合物中几乎没有或没有VAMPs,也没有syntaxin 4被免疫沉淀。syntaxin 4的含量取决于PM的存在,并且通过向PM中添加溶解的GLUT4囊泡,VAMPs 2和3的参与增加了4至6倍。后一种增加幅度大于反应混合物中添加的VAMPs水平高出2倍所能解释的程度。当所有膜组分均从胰岛素刺激的细胞制备时,仅由PM形成的SNARE复合物与基础细胞单独的PM相比,含有相似水平的syntaxin,但VAMPs 2和3的水平高出5至6倍。将GLUT4囊泡蛋白添加到胰岛素处理细胞的PM中,会使SNARE复合物中回收的VAMP 2进一步增加2倍。因此,胰岛素处理但非基础细胞的PM中的VAMPs,以及任何一种情况下细胞的GLUT4囊泡中的VAMPs,都处于一种易于与PM t-SNAREs和NSF形成SNARE复合物的形式。胰岛素似乎激活了PM和/或GLUT4囊泡,从而提高了SNARE复合物形成的效率。