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首页> 外文期刊>Journal of Cellular Physiology >Starvation-induced lysosomal degradation of aldolase B requires glutamine 111 in a signal sequence for chaperone-mediated transport.
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Starvation-induced lysosomal degradation of aldolase B requires glutamine 111 in a signal sequence for chaperone-mediated transport.

机译：Starvation-induced溶酶体降解醛缩酶B需要谷氨酰胺111年的一个信号即使伴娘运输序列。

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Aldolase B is an abundant cytosolic protein found in all eukaryotic cells. Like many glycolytic enzymes, this protein was sequestered into lysosomes for degradation during nutrient starvation. We report here that the degradation of recombinant aldolase B was enhanced two-fold when rat and human hepatoma cells were starved for amino acid and serum. In addition, starvation-induced degradation of aldolase B was inhibited by chloroquine, an inhibitor of lysosomal proteinases and by 3-methyladenine, an inhibitor of autophagy. Aldolase B has three lysosomal targeting motifs (Q(12)KKEL, Q(58)FREL, and IKLDQ(111)) that have been proposed to interact with hsc73 thereby initiating its transport into lysosomes. In this study, we have mutated the essential glutamine residues in each of these hsc73-binding motifs in order to evaluate their roles in the lysosomal degradation of aldolase B during starvation. We have found that when glutamines 12 or 58 are mutated to asparagines enhanced degradation of aldolase B proceeded normally. However, when glutamine 111 was mutated to an asparagine or a threonine, starvation-induced degradation was completely suppressed. These mutations did not appear to alter the tertiary structure of aldolase B since enzymatic activity was not affected. Our results suggest that starvation-induced lysosomal degradation of aldolase B requires both autophagy and glutamine 111. We discuss the possible roles for autophagy and hsc73-mediated transport in the lysosomal sequestration of aldolase B. Copyright 2001 Wiley-Liss, Inc.
机译：醛缩酶B是一个丰富的胞质蛋白质在所有真核细胞。酶,这种蛋白质是隔离在养分溶酶体的降解饥饿。重组醛缩酶B的双重提高当老鼠和人类肝癌细胞被饿死了氨基酸和血清。starvation-induced醛缩酶B的降解抑制剂的抑制,氯喹溶酶体蛋白酶3-methyladenine,自噬抑制剂。lysosomal定位,Q (12) (KKEL、Q(58岁)FREL和IKLDQ(111))被提出与hsc73从而启动它运输到溶酶体。突变的基本谷氨酰胺残基这些hsc73-binding图案来评估他们的角色在溶酶体降解醛缩酶B的饥饿。当谷氨酰胺12或58突变天冬增强醛缩酶B的降解正常进行。天冬酰胺或苏氨酸突变,starvation-induced退化完全抑制。改变醛缩酶B的三级结构酶活性没有影响。表明starvation-induced溶酶体醛缩酶B的降解需要自噬111年,谷氨酰胺。自噬和hsc73-mediated运输的醛缩酶b .著作权的固溶酶体2001 Wiley-Liss, Inc。

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