肠外营养相关性肝病（PNALD）是严重威胁新生儿健康的重大疾病，但其发病机制不甚明了，尚无理想防治方法。uc007gqg.1是我们基于lncRNA芯片筛选获得、差异高表达于PNALD患儿血清及模式动物肝脏组织、多物种间高度保守、功能未知的一条lncRNA。前期发现，uc007gqg.1过表达诱导肝细胞功能损伤；生物信息学分析及预实验提示GRP94是其潜在靶基因；文献及预实验均表明GRP94促进肝细胞功能损伤。据此，我们推测uc007gqg.1可能通过GRP94诱导肝细胞功能损伤。本研究拟采用过表达和敲低策略，在细胞和动物水平系统论证uc007gqg.1在肝细胞中的功能；通过挽救实验及CHRIP、RNA pull-down 等技术深入探讨uc007gqg.1调控GRP94表达的分子机制。本研究将揭示uc007gqg.1在肝细胞生理过程中的功能与机制，有望为肝功能损伤的防治提供潜在的新靶标。

Parenteral nutrition-associated liver disease (PNALD) is a major disease which seriously threatens neonatal health, however its pathogenesis remains unclear，but there is no ideal control method. Uc007gqg.1, a long non-coding RNA which highly conserved in multi-species and unknown, is differentially and highly expressed in PNALD patients serum and the liver tissue of model animals, detected by high-throughput lncRNA chip screening technology. In previouse study, we found that the overexpression of uc007gqg.1 induced liver cell dysfunction. Bioinformatics analysis and pre-experiment indicated that GRP94 was a potential target gene. Both the literature and the previous experiments showed that GRP94 could promote the damage of hepatocytes. Based on this, we hypothesized that uc007gqg.1 might induce hepatocyte injury through GRP94. In this study, overexpression and knockdown strategies were proposed to further demonstrate the function of uc007gqg.1 in hepatocytes and in cell and animal level .By means of rescue strategy, CHRIP and RNA pull-down, to investigate the mechanism of uc007gqg.1 in regulating the function of hepatocytes through GRP94 expression. This study will reveal the function and molecular mechanism of uc007gqg.1 in hepatocyte physiological process, which is expected to provide a potential new target for prevention and treatment of liver injury.