Fuchu He

Fudan University, Shanghai, Shanghai Shi, China

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Publications (274)1480.56 Total impact

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    ABSTRACT: Inhaled xenobiotics such as tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone are mainly metabolized by phase I oxidase cytochrome P450, family 2, subfamily A, polypeptide 13 (CYP2A13), phase II conjugate UDP glucuronosyltransferase 2 family, polypeptide B17 (UGT2B17), and phase III transporter ATP-binding cassette, subfamily B (MDR/TAP), member 1 (ABCB1), with genetic polymorphisms implicated in lung cancer. Their genetic interaction and pulmonary expression regulation are largely unknown. We analyzed joint association for CYP2A13 and ABCB1 polymorphisms in 2 independent lung cancer case populations (669 and 566 patients) and 1 common control population (749 subjects), and characterized the trans-acting function of the lung development-related transcription factor forkhead box A2 (FOXA2). We undertook FOXA2 overexpression and down-regulation in lung epithelial cell lines, analyzed functional impact on the transactivation of CYP2A13, UGT2B17, and ABCB1, and measured correlation for their expressions in lung tissues. We found a substantial reduction in cancer risk (OR 0.39; 95% CI 0.25-0.61; Pinteraction = 0.029) associated with combined genotypes for CYP2A13 R257C and a functionary regulatory variant in the cis element of ABCB1 synergistically targeted by GATA binding protein 6 and FOXA2. Genetic manipulation of FOXA2 consistently influenced its binding to and transactivation of the promoters of CYP2A13, UGT2B17, and ABCB1, whose mRNA and protein expressions were all consistently correlated with those of FOXA2 in both tumorous and normal lung tissues. We therefore establish FOXA2 as a core transcriptional modulator for pulmonary xenobiotic metabolic pathways and uncover an etiologically relevant interaction between CYP2A13 and ABCB1, furthering our understanding of expression and function of the xenobiotic metabolism system.-Xiang, C, Wang, J., Kou, X., Chen, X., Qin, Z., Jiang, Y., Sun, C., Xu, J., Tan, W., Jin, L., Lin, D., He, F., and Wang, H. Pulmonary expression of CYP2A13 and ABCB1 is regulated by FOXA2 and their genetic interaction is associated with lung cancer. © FASEB.
    The FASEB Journal 02/2015; · 5.48 Impact Factor
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    ABSTRACT: Currently, major concerns about the safety and efficacy of RNA interference (RNAi)-based bone anabolic strategies still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRNAs. Here we screened the aptamer CH6 by cell-SELEX, specifically targeting both rat and human osteoblasts, and then we developed CH6 aptamer-functionalized lipid nanoparticles (LNPs) encapsulating osteogenic pleckstrin homology domain-containing family O member 1 (Plekho1) siRNA (CH6-LNPs-siRNA). Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents. These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level.
    Nature medicine. 02/2015;
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    ABSTRACT: Previously isolated pathways screened from individual genes were investigated at either the transcriptional or translational level; however, the consistency between the pathways screened at the gene expression levels was obscure in metastatic human hepatocellular carcinoma (HCC). To elucidate this question, we performed a transcriptomic (16353 genes) and proteomic (7861 proteins) analysis simultaneously on six metastatic HCC cell lines against two non-metastatic HCC cell lines, with all HBV traceable and close genetic-backgrounds for a comparative study. The quantitative and integrated results showed that significant genes were screened differentially with 351 transcripts from the transcriptome and 304 proteins from the proteome, with limited overlapping genes (7%). However, we discovered that these discrete 351 transcripts and 304 proteins screened share extrusive significant-pathways/networks with a 77% overlap, including active TGF-β, RAS, NFκB, and Wnt, and inactive HNF4A, which are responsible for HCC metastasis. We conclude that the discrete, but significant genes predicted by either ome play intrinsically important roles in the linkage of responsible pathways shared by both omes in HCC metastasis. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    PROTEOMICS 02/2015; · 3.97 Impact Factor
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    ABSTRACT: Motivation: Anatomical Therapeutic Chemical (ATC) classification system, widely applied in almost all drug utilization studies, is currently the most widely recognized classification system for drugs. Currently new drug entries are added into the system only on users’ requests, which leads to seriously incomplete drug coverage of the system, and bioinformatics prediction is helpful during this process. Results: Here we propose a novel prediction model of drug-ATC code associations, using logistic regression to integrate multiple heterogeneous data sources including chemical structures, target proteins, gene expression, side-effects and chemical-chemical associations. The model obtains good performance for the prediction not only on ATC codes of unclassified drugs but also on new ATC codes of classified drugs assessed by cross-validation and independent test sets, and its efficacy exceeds previous methods. Further to facilitate the use, the model is developed into a user-friendly web service SPACE (Similarity-based Predictor of ATC CodE), which for each submitted compound, will give candidate ATC codes (ranked according to the decreasing probability_score predicted by the model) together with corresponding supporting evidence. This work not only contributes to knowing drugs’ therapeutic, pharmacological and chemical properties, but also provides clues for drug repositioning and side-effect discovery. In addition, the construction of the prediction model also provides a general framework for similarity-based data integration which is suitable for other drug-related studies such as target, side-effect prediction etc.. Availability: The web service SPACE is available at http://www.bprc.ac.cn/space.
    Bioinformatics 01/2015; · 4.62 Impact Factor
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    ABSTRACT: As a central event in liver fibrogenesis, hepatic stellate cell (HSC) transdifferentiation involves loss of regulation by adipogenic transcription factors such as peroxisome proliferator-activated receptor γ; (PPARγ), which is epigenetically silenced during HSC activation. We hypothesized that JMJD1A, an H3K9 demethylase involved in adipogenic metabolism, could regulate PPARγ. In human HSC cell line, rat primary HSCs, and carbontetrachloride-induced mouse liver fibrogenesis model, we down-regulated the expression of JMJD1A using small interfering or short hairpin RNAs, and overexpressed its wild-type and mutant. We analyzed the effects of JMJD1A manipulation on the histone di-methyl-H3K9 (H3k9me2) status of PPARγ gene and the expression of PPARγ and fibrosis markers using chromatin immunoprecipitation, real-time quantitative RT-PCR and Western blot, and also investigated the in vitro and in vivo consequences on liver fibrosis and necrosis by Masson or hematoxylin-eosin staining, respectively. JMJD1A knockdown in HSCs correlated with reinforced H3K9me2 in the PPARγ gene promoter, and its down-regulation in both mRNA and protein led to increased expression of fibrosis markers, which could be consistently rescued by JMJD1A overexpression. Jmjd1a knockdown in situ resulted in significantly increased expression of α-smooth muscle actin (P = 0.005) and Col1a (P = 0.036), strengthened production of collagens (P = 0.028), and remarkably enhanced necrosis (P = 0.007) 4 weeks after treatment. This study suggests JMJD1A as a novel epigenetic regulator that modulates HSC activation and liver fibrosis through targeting PPARγ gene expression.- Jiang, Y., Wang, S., Zhao, Y., Lin, C., Zhong, F., Jin, L., He, F., and Wang, H. Histone H3K9 demethylase JMJD1A modulates hepatic stellate cells activation and liver fibrosis by epigenetically regulating peroxisome proliferator-activated receptor γ. © FASEB.
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 01/2015;
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    ABSTRACT: Integration of pathway and protein-protein interaction (PPI) data can provide more information that could lead to new biological insights. PPIs are usually represented by a simple binary model, whereas pathways are represented by more complicated models. We developed a series of rules for transforming protein interactions from pathway to binary model, and the protein interactions from seven pathway databases, including PID, BioCarta, Reactome, NetPath, INOH, SPIKE and KEGG, were transformed based on these rules. These pathway-derived binary protein interactions were integrated with PPIs from other five PPI databases including HPRD, IntAct, BioGRID, MINT and DIP, to develop integrated dataset (named PathPPI). More detailed interaction type and modification information on protein interactions can be preserved in PathPPI than other existing datasets. Comparison analysis results indicate that most of the interaction overlaps values (OAB) among these pathway databases were less than 5%, and these databases must be used conjunctively. The PathPPI data was provided at http://proteomeview.hupo.org.cn/PathPPI/PathPPI.html .
    Science China. Life sciences. 01/2015;
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    ABSTRACT: Although glial cell line-derived neurotrophic factor (GDNF)/Ret signaling is essential for enteric nervous system (ENS) development, the positive regulators regulating GDNF/Ret signaling and controlling ENS development are poorly understood. Here, we show that NEDD4-related E3 ubiquitin ligase-2 (NEDL2), plays an essential and positive physiological role in regulating ENS development and GDNF/Ret signaling. All of the NEDL2-deficient mice die within 2weeks after birth, showing low body weight. These mice showed a progressive bowel motility defect resulting from intestinal aganglionosis. We show that NEDL2 positively regulates enteric neural precursor proliferation through the GDNF/Akt signaling pathway. Together, these findings unveil the physiological function of NEDL2 in vivo. Copyright © 2014. Published by Elsevier Inc.
    Cellular Signalling 12/2014; · 4.47 Impact Factor
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    ABSTRACT: Infection by human coronaviruses is usually characterized by rampant viral replication and severe immunopathology in host cells. Recently, the coronavirus papain-like proteases (PLPs) have been identified as suppressors of the innate immune response. However, the molecular mechanism of this inhibition remains unclear. Here, we provide evidence that PLP2, a catalytic domain of the nonstructural protein 3 of human coronavirus NL63 (HCoV-NL63), deubiquitinates and stabilizes the cellular oncoprotein MDM2 and induces the proteasomal degradation of p53. Meanwhile, we identify interferon regulatory factor 7 (IRF7) as a bona fide target gene of p53 to mediate the p53-directed production of type I interferon and the innate immune response. By promoting p53 degradation, PLP2 inhibits the p53-mediated antiviral response and apoptosis to ensure viral growth in infected cells. Thus, our study reveals that coronavirus engages PLPs to escape from the innate antiviral response of the host by inhibiting p53-IRF7-IFNβ signaling. Copyright © 2014, The American Society for Biochemistry and Molecular Biology.
    The Journal of biological chemistry. 12/2014;
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    ABSTRACT: HBV X protein plays crucial roles during viral infection and hepatocellular carcinoma (HCC) development through interaction with various host factors. Here, we mapped the interactome of HBx using a yeast two-hybrid screen. Nine human proteins were identified as novel interacting partners of HBx, one of which is phospholipid scramblase 1 (PLSCR1). PLSCR1 is an interferon-inducible protein that mediates antiviral activity against DNA and RNA viruses. However, the molecular mechanisms of PLSCR1 activity against HBV remain unclear. Here, we reported that PLSCR1 promotes HBx degradation by a proteasome- and ubiquitin-dependent mechanism. Furthermore, we found that PLSCR1 inhibits HBx-mediated cell proliferation. After HBV infection, the protein level of PLSCR1 in plasma is elevated, and chronic hepatitis B patients with low plasma levels of PLSCR1 have a high risk of developing HCC. These results suggest that the nuclear trafficking of PLSCR1 mediates the antiviral activity and anti-carcinogenesis against HBV by regulating HBx stability.
    Journal of Proteome Research 11/2014; · 5.06 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) are considered as the developmental origin of multiple lineage cells including osteocytes, adipocytes, and muscle cells. Previous studies demonstrated that the PH domain-containing protein CKIP-1 plays an important role in the development of osteoblasts and cardiomyocytes. However, whether CKIP-1 is involved in the generation of adipocytes as well as the MSC differentiation remains unknown. Here we show that CKIP-1 is a novel regulator of MSCs differentiating into adipocytes. MSCs derived from CKIP-1-deficient mice display enhanced adipogenesis upon the induction. Further analysis showed that CKIP-1 interacts with the histone deacetylase HDAC1 in the nucleus and inhibits the transcription of CCAAT/enhancer-binding protein α (C/EBPα), which is a crucial adipogenic transcription factor. Ectopic expression of CKIP-1 in a MSC-like cell line C3H/10T1/2 reduced the generation of adipocytes due to suppression of adipogenic factors, including C/EBPα. Moreover, CKIP-1-deficient mice showed an increase in body weight and white adipose tissue gains when fed on a high-fat diet. Collectively, these results suggest that CKIP-1 is a novel inhibitor of MSC-originated adipogenesis by enhancing HDAC1-associated repression of C/EBPα.
    Journal of molecular cell biology. 09/2014;
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    ABSTRACT: We developed an adenovirus-based CRISPR/Cas9 system for gene editing in vivo. In the liver, we demonstrated that the system could reach the level of tissue-specific gene knockout, resulting in phenotypic changes. Given the wide spectrum of cell types susceptible to adenoviral infection, and the fact that adenoviral genome rarely integrates into its host cell genome, we believe the adenovirus-based CRISPR/Cas9 system will find applications in a variety of experimental settings.
    FEBS Letters 09/2014; · 3.34 Impact Factor
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    ABSTRACT: Proteomics focuses on the systematic identification and quantification of entire proteomes and interpretation of proteins' biological functions. During the last decade, proteomics in China has grown much faster than other research fields in the life sciences. At the beginning of the second decade of the 21(st) century, the rapid development of high-resolution and high-speed mass spectrometry makes proteomics a powerful tool to study the mechanisms underlying physiological/pathological processes in organisms. This article provides a brief overview of proteomics technology development and representative scientific progress of the Human Liver Proteome Project (HLPP) in China over the past three years.
    Science China. Life sciences 08/2014; · 1.51 Impact Factor
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    ABSTRACT: Activated hepatic stellate cell (HSC) is the main myofibroblast cell in the liver fibrosis(LF). An important characteristic of the recovery of LF is not only the apoptosis of activated HSCs but also reversal of myofibroblast-like phenotype to a quiescent-like phenotype. Understanding the changes of secreted proteins in the reversion of activated HSCs may provide the broader view of cellular regulatory networks and discover candidate markers or targets for therapeutic strategies of LF. In this study, stable isotope labeling with amino acids (SILAC) combining with LTQ-FT mass spectrometer were performed on in vitro activated HSCs and reverted HSCs to obtain a proteomic view of secretory proteins. In total, 330 proteins showed significant differences in reverted HSCs. Among these, 109 up-regulated proteins were mainly involved in amino acid metabolism pathway and glucose metabolism pathway using GeneGO/MetaCore software, while 221 down-regulated proteins are closely associated with HSCs activation, such as cytoskeleton remodeling, chemokines and cell adhesion. Additionally, a set of novel proteins associated with HSCs activation and reversion were validated by Western blotting in the cell secretion and in the sera of LF, including Vitronectin, laminin beta 1(LAMB1) and Ubiquitin conjugation factor E4B(UBE4B). Our study provided the valuable insight into the mechanisms in the reversion of activated HSCs and identified some potential biomarkers of LF in clinical studies.This article is protected by copyright. All rights reserved
    Proteomics 07/2014; · 3.97 Impact Factor
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    ABSTRACT: G protein-coupled receptor kinase-interactor 2 (GIT2) regulates thymocyte positive selection, neutrophil-direction sensing, and cell motility during immune responses by regulating the activity of the small GTPases ADP ribosylation factors (Arfs) and Ras-related C3 botulinum toxin substrate 1 (Rac1). Here, we show that Git2-deficient mice were more susceptible to dextran sodium sulfate (DSS)-induced colitis, Escherichia coli, or endotoxin-shock challenge, and a dramatic increase in proinflammatory cytokines was observed in Git2 knockout mice and macrophages. GIT2 is a previously unidentified negative regulator of Toll-like receptor (TLR)-induced NF-κB signaling. The ubiquitination of TNF receptor associated factor 6 (TRAF6) is critical for the activation of NF-κB. GIT2 terminates TLR-induced NF-κB and MAPK signaling by recruiting the deubiquitinating enzyme Cylindromatosis to inhibit the ubiquitination of TRAF6. Finally, we show that the susceptibility of Git2-deficient mice to DSS-induced colitis depends on TLR signaling. Thus, we show that GIT2 is an essential terminator of TLR signaling and that loss of GIT2 leads to uncontrolled inflammation and severe organ damage.
    Proceedings of the National Academy of Sciences 05/2014; · 9.81 Impact Factor
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    ABSTRACT: Compared to the well-defined anti-apoptotic role of myeloid cell leukemia sequence 1 (MCL1), its antiproliferative function in tumorigenesis is less studied. We had recently reported that regulatory variants of MCL1 contribute to enhanced promoter activity but reduced risk of lung cancer. We hypothesized that MCL1 expression may manifest antiproliferative phenotype and its functional variations may have etiological relevance for breast cancer. We manipulated MCL1 expression in MCF-7 cells and MDA231 with overexpression and knockdown, analyzed the effects on cell viability and cell cycling phase, and characterized the correlation with expression profiles of key regulators of cell cycle. We further genotyped the -190 insertion polymorphism and the neighboring single nucleotide polymorphisms (SNPs) in 745 breast cancer patients and 537 controls and analyzed their association with cancer risk. We confirmed that heightened expression of MCL1 resulted in decreased proliferation ability of breast cancer cells. We further observed that MCL1 overexpression in breast cancer cells resulted in cell cycle progression arresting in S phase and concomitant enhanced expression of p27, which could be rescued by p27 knockdown with co-transfection of small interfering RNA (siRNA). Furthermore, we found a significant reduction in breast cancer risk [odds ratio (OR) = 0.74; 95 % confidence interval (CI) = 0.59-0.93] associated with -190 insertion genotype; the expression-enhancing regulatory haplotype (OR 0.79; 95 % CI 0.66-0.95) and diplotype (OR 0.71; 95 % CI 0.57-0.89) were consistently associated with decreased cancer susceptibility. The study demonstrates that the expression-enhancing regulatory variants of MCL1 are protective modifiers of breast cancer risk, and reduced cell proliferation and arrested cell cycle progression partly mediated by p27 might be the underlying mechanism.
    Tumor Biology 05/2014; 35(8). · 2.84 Impact Factor
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    ABSTRACT: The ubiquitin ligase Smad ubiquitination regulatory factor-1 (Smurf1) negatively regulates bone morphogenetic protein (BMP) pathway by ubiquitinating certain signal components for degradation. Thus, it can be an eligible pharmacological target for increasing BMP signal responsiveness. We established a strategy to discover small molecule compounds that block the WW1 domain of Smurf1 from interacting with Smad1/5 by structure based virtual screening, molecular experimental examination and cytological efficacy evaluation. Our selected hits could reserve the protein level of Smad1/5 from degradation by interrupting Smurf1-Smad1/5 interaction and inhibiting Smurf1 mediated ubiquitination of Smad1/5. Further, these compounds increased BMP-2 signal responsiveness and the expression of certain downstream genes, enhanced the osteoblastic activity of myoblasts and osteoblasts. Our work indicates targeting Smurf1 for inhibition could be an accessible strategy to discover BMP-sensitizers that might be applied in future clinical treatments of bone disorders such as osteopenia.
    Scientific Reports 05/2014; 4:4965. · 5.08 Impact Factor
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    ABSTRACT: Neddylation, the covalent attachment of ubiquitin-like protein Nedd8, of the Cullin-RING E3 ligase family regulates their ubiquitylation activity. However, regulation of HECT ligases by neddylation has not been reported to date. Here we show that the C2-WW-HECT ligase Smurf1 is activated by neddylation. Smurf1 physically interacts with Nedd8 and Ubc12, forms a Nedd8-thioester intermediate, and then catalyses its own neddylation on multiple lysine residues. Intriguingly, this autoneddylation needs an active site at C426 in the HECT N-lobe. Neddylation of Smurf1 potently enhances ubiquitin E2 recruitment and augments the ubiquitin ligase activity of Smurf1. The regulatory role of neddylation is conserved in human Smurf1 and yeast Rsp5. Furthermore, in human colorectal cancers, the elevated expression of Smurf1, Nedd8, NAE1 and Ubc12 correlates with cancer progression and poor prognosis. These findings provide evidence that neddylation is important in HECT ubiquitin ligase activation and shed new light on the tumour-promoting role of Smurf1.
    Nature Communications 05/2014; 5:3733. · 10.74 Impact Factor
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    ABSTRACT: Macrophages play pivotal roles in development, homeostasis, tissue repair and immunity. Macrophage proliferation is promoted by macrophage colony-stimulating factor (M-CSF)-induced Akt signaling; yet, how this process is terminated remains unclear. Here, we identify casein kinase 2-interacting protein-1 (CKIP-1) as a novel inhibitor of macrophage proliferation. In resting macrophages, CKIP-1 was phosphorylated at Serine 342 by constitutively active GSK3β, the downstream target of Akt. This phosphorylation triggers the polyubiquitination and proteasomal degradation of CKIP-1. Upon M-CSF stimulation, Akt is activated by CSF-1R-PI3K and then inactivates GSK3β, leading to the stabilization of CKIP-1 and β-catenin proteins. β-catenin promotes the expression of proliferation genes including cyclin D and c-Myc. CKIP-1 interacts with TRAF6, a ubiquitin ligase required for K63-linked ubiquitination and plasma membrane recruitment of Akt, and terminates TRAF6-mediated Akt activation. By this means, CKIP-1 inhibits macrophage proliferation specifically at the late stage after M-CSF stimulation. Furthermore, CKIP-1 deficiency results in increased proliferation and decreased apoptosis of macrophages in vitro and CKIP-1(-/-) mice spontaneously develop a macrophage-dominated splenomegaly and myeloproliferation. Together, these data demonstrate that CKIP-1 plays a critical role in the regulation of macrophage homeostasis by inhibiting TRAF6-mediated Akt activation.Cell Research advance online publication 29 April 2014; doi:10.1038/cr.2014.53.
    Cell Research 04/2014; · 11.98 Impact Factor
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    ABSTRACT: Co-inhibitory molecules of T cell immune responses have received considerable attention for their successful clinical effects during immunotherapy for the treatment of multiple cancers. LSECtin, a cell-surface member of the C-type lectin DC-SIGN family, has been shown to inhibit T cell responses and viral clearance in the liver. However, its role in antitumor immunity and tumor growth remains unclear. Herein, we detected LSECtin expression in approximately 50% of melanoma samples in a human tumor tissue array. In a B16 melanoma model, we revealed that LSECtin, when expressed on B16 cells, promoted tumor growth and LSECtin blockade resulted in significantly slower tumor growth in both WT and LSECtin KO mice; this LSECtin-mediated tumor-promoting effect was abrogated in Rag1-/- mice or in response to CD4+ or CD8+ T cell depletion. We further determined that LSECtin inhibited the proliferation of tumor-specific effector T cells by downregulating cell cycle-regulating kinases such as CDK2, CDK4, and CDK6. Consistently, LSECtin expressed on B16 tumor cells inhibited tumor-specific T cell responses in vivo and in vitro. Importantly, we indicated that LSECtin interacted with LAG-3, and LAG-3 blockade restored the reduced IFN-γ secretion mediated by melanoma-derived LSECtin. Together, LSECtin expressed on melanoma cells appears to be a novel possible mechanism of immune escape of melanoma cells and provides a foundation for potential combinatorial immunotherapy strategies.
    Cancer Research 04/2014; · 9.28 Impact Factor
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    ABSTRACT: Study of site-specific N-glycosylation in complex sample remains a huge analytical challenge, because protein glycosylation is structurally diverse in post translational modifications resulting in an intricacy of N-glycopeptides. Here we have developed a novel approach for high-throughput N-glycopeptide profiling, based on a network-centric algorithm for deciphering glycan fragmentation in mass-spectrometry. We performed an extensive validation and a high-throughput N-glycosylation study on serum and identified thousands of N-glycopeptide spectra with high confidence. The results revealed a similar level of glycan microheterogeneity to that of conventional glycomics approach on individual proteins, and provided the unique in-depth site-specific information that could only be studied through glycopeptide profiling.
    Journal of Proteome Research 04/2014; · 5.06 Impact Factor

Publication Stats

5k Citations
1,480.56 Total Impact Points


  • 2006–2015
    • Fudan University
      • • Department of Chemistry
      • • Institutes of Biomedical Sciences
      Shanghai, Shanghai Shi, China
    • Beijing Proteome Research Center
      Peping, Beijing, China
    • Peking University
      • College of Chemistry and Molecular Engineering
      Beijing, Beijing Shi, China
  • 2013
    • Huazhong University of Science and Technology
      • Department of Infectious Diseases
      Wuhan, Hubei, China
  • 2001–2013
    • China Institute for Radiation Protection
      Peping, Beijing, China
  • 2012
    • Chinese PLA General Hospital (301 Hospital)
      Peping, Beijing, China
    • Peking Union Medical College Hospital
      Peping, Beijing, China
    • Anhui Medical University
      Luchow, Anhui Sheng, China
  • 2006–2012
    • Tsinghua University
      • • Department of Biomedical Engineering
      • • School of Life Sciences
      Peping, Beijing, China
  • 2010
    • Shenyang Agricultural University
      Feng-t’ien, Liaoning, China
  • 2008
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2006–2008
    • National University of Defense Technology
      • College of Mechatronic Engineering and Automation
      Ch’ang-sha-shih, Hunan, China
  • 2001–2007
    • Beijing Genomics Institute
      Bao'an, Guangdong, China
  • 2005
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 1999–2005
    • Chinese National Human Genome Center
      Peping, Beijing, China
  • 2001–2004
    • Government of the People's Republic of China
      Peping, Beijing, China
  • 2002
    • 307 Hospital of the Chinese People's Liberation Army
      Peping, Beijing, China