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您的检索式：作者名="DU LinFang"
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| 1 | The presence of phosphorylation form of D1 protein in its cross-linked aggregates in high light treated spinach leaves in vivo显示文摘In the present study, using specific antibody against D1 protein, we detected four ag- gregates of D1 protein in thylakoid membranes from spinach leaves illuminated at high light (800―2500 μmol photons·m?2·s?1) for 3 h. Their accumulations were dependent on the light intensity to which the leaves had been subjected. Further immunoblot analysis indicated that 70 kD aggregate was a prod- uct of D1 protein cross-linked with CP43, 65 and 60 kD aggregate were two cross-linked products be- tween D1 and D2 proteins, and 41 kD aggregate was one cross-linked D1 with α-subunit of cytochrome b559 (Cyt b559). This result provided the evidence for the existence of the aggregation of the D1 protein in vivo. The maximal level of D1/Cyt b559 aggregate occurred at 1000 μmol photons·m?2·s?1 but drastically decreased with further increasing light intensity. Im- munoblot analysis with phosphothreonine (Thr (P)) antibody indicated that D1/CP43 and D1/Cyt b559 aggregates contained the phosphorylated protein(s). In vitro dephosphorylation experiment also showed that D1/Cyt b559 and D1/CP43 aggregates lost the immunoreactivity with Thr (P) antibody after the phosphatase treatment of the membranes from high-light-illuminated leaves. Our results demon- strated that strong illumination of spinach leaves in- duced cross-linked products of D1 protein with its nearby polypeptides of PS Ⅱ , some of which con- tained the phosphorylated D1 protein. | WEI Huimin GUO Junwei ZHANG Shuang HUANG Bo LIU Yinqiu DU Linfang | 2006 | Chinese Science Bulletin2006，51，1： | 12 |
| 2 | Effects of temperature on the expression of STN7 andphosphorylation of LHCII proteins in Arabidopsis thaliana显示文摘In Arabidopsis thaliana, STN7 kinase is required for phosphorylation of LHCII and for state transitions. In this paper, a hydrophilic polypeptide, derived from the amino acid sequence of STN7, was conjugated to a carrier protein, bovine serum albumin (BSA), to obtain the polyclonal antibody. Immunogenicity and specificity of the polyclonal antibody were evaluated by agar gel immunodiffusion (AGID) test and Western blot analysis. The results show that besides the phosphorylation of LHCII proteins, also the expression of STN7 was regulated by temperature conditions. In addition, the change tendency of LHCII proteins phosphorylation was not only coherent with expression of STN7 with respect to increasing temperature, but also closely related to state transitions. These results would provide useful information for studying regulatory mechanism of LHCII proteins phosphorylation and expression of STN7. | HU Yuan GAO Xiu JIANG JiaHong RAN Yan DU LinFang | 2008 | Chinese Science Bulletin2008，53，17： | 4 |
| 3 | The E3 ubiquitin ligase NEDD4-1 protects against acetaminophen-induced liver injury by targeting VDAC1 for degradation显示文摘Acetaminophen(APAP)overdose is a major cause of liver injury.Neural precursor cell expressed developmentally downregulated 4—1(NEDD4-1)is an E3 ubiquitin ligase that has been implicated in the pathogenesis of numerous liver diseases;however,its role in APAP-induced liver injury(AILI)is unclear.Thus,this study aimed to investigate the role of NEDD4-1 in the pathogenesis of AILI.We found that NEDD4-1 was dramatically downregulated in response to APAP treatment in mouse livers and isolated mouse hepatocytes.Hepatocyte-specific NEDD4-1 knockout exacerbated APAP-induced mitochondrial damage and the resultant hepatocyte necrosis and liver injury,while hepatocyte-specific NEDD4-1 overexpression mitigated these pathological events both in vivo and in vitro.Additionally,hepatocyte NEDD4-1 deficiency led to marked accumulation of voltage-dependent anion channel 1(VDAC1)and increased VDAC1 oligomerization.Furthermore,VDAC1 knockdown alleviated AILI and weakened the exacerbation of AILI caused by hepatocyte NEDD4-1 deficiency.Mechanistically,NEDD4-1 was found to interact with the PPTY motif of VDAC1 through its WW domain and regulate K48-linked ubiquitination and degradation of VDAC1.Our present study indicates that NEDD4-1 is a suppressor of AILI and functions by regulating the degradation of VDAC1. | Yiwei Zhu Lin Lei Xinghui Wang Linfang Chen Wei Li Jinxia Li Chenchen Zhao Xiliang Du Yuxiang Song Wenwen Gao Guowen Liu Xinwei Li | 2023 | Acta Pharmaceutica Sinica B2023，13，4： | 1 |
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