Fuchu He

Beijing Proteome Research Center, Peping, Beijing, China

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Publications (264)1461.68 Total impact

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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;
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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;
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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; · 4.43 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 of the United States of America. 05/2014;
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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.
    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 05/2014;
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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; · 10.53 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
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    ABSTRACT: Comprehensively identifying gene expression in both transcriptomic and proteomic levels of one tissue is a prerequisite for a deeper understanding of its biological functions. Alternative splicing and RNA-editing, two main forms of transcriptional processing, play important roles in transcriptome and proteome diversity and result in multiple isoforms for one gene, which are hard to identify by mass spectrometry (MS)-based proteomics approach due to the relative lack of isoform information in standard protein databases. In our study, we employed MS and RNA-Seq in parallel into mouse liver tissue and captured a considerable catalogue of both transcripts and proteins that respectively covered 60% and 34% of protein-coding genes in Ensembl. We then developed a bioinformatics workflow for building a customized protein database that for the first time included new splicing-derived peptides and RNA-editing-caused peptide variants, allowing us to more completely identify protein isoforms. Using this experimentally determined database, we totally identified 150 peptides not present in standard biological databases at false discovery rate (FDR) of <1%, corresponding to 72 novel splicing isoforms, 43 new genetic regions and 15 RNA-editing sites. Of these, 11 randomly selected novel events passed experimental verification by PCR and Sanger sequencing. New discoveries of gene products with high confidence in two omics levels demonstrated the robustness and effectiveness of our approach and its potential application into improve genome annotation.
    Journal of Proteome Research 04/2014; · 5.06 Impact Factor
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    ABSTRACT: Faithful DNA replication is essential for the maintenance of genome integrity. Incomplete genome replication leads to DNA breaks and chromosomal rearrangements, which are causal factors in cancer and other human diseases. Despite their importance, the molecular mechanisms that control human genome stability are incompletely understood. Here, we report a pathway that is required for human genome replication and stability. This pathway has three components: an E3 ubiquitin ligase, a transcriptional repressor, and a replication protein. The E3 ubiquitin ligase RBBP6 ubiquitinates and destabilizes the transcriptional repressor ZBTB38. This repressor negatively regulates transcription and levels of the MCM10 replication factor on chromatin. Cells lacking RBBP6 experience reduced replication fork progression and increased damage at common fragile sites due to ZBTB38 accumulation and MCM10 downregulation. Our results uncover a pathway that ensures genome-wide DNA replication and chromosomal stability.
    Cell Reports 04/2014; · 7.21 Impact Factor
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    ABSTRACT: p73, a structural and functional homologue of p53, plays an important role in modulating cell-cycle control and apoptosis. We examined whether the p73 G4C14-to-A4T14 polymorphism was related to the risk of nasopharyngeal carcinoma (NPC) among Chinese populations. The G4C14-to-A4T14 polymorphism was genotyped in 593 NPC cases and 480 controls, and in 102 NPC trios. Logistic regression analysis and transmission/disequilibrium tests (TDT) were performed to evaluate whether there was an association between the polymorphism and NPC, respectively. Functional analyses were conducted to verify the biological relevance of the polymorphism. We observed that compared with the GC/GC genotype, the genotypes containing AT allele (GC/AT + AT/AT genotypes) were associated with significantly increased susceptibility to NPC [odd ratio (OR), 1.51; 95% confidence interval (CI), 1.16-1.95; P = 0.002]. Furthermore, compared with the GC/GC genotype, the GC/AT + AT/AT genotypes were significantly associated with the advanced lymph node metastasis (OR, 1.47; 95% CI, 1.02-2.11; P = 0.041). A significantly greater than expected transmission of the AT allele from heterozygous parents to offspring was also observed (P = 0.049) using the TDT. By using the TdT-mediated dUPT-biotin nick end labeling (TUNEL) assay, we observed lower apoptosis in NPC tissues from the AT allele carriers compared with that from nocarriers. Furthermore, the relative TAp73 RNA levels of the AT allele were lower than those of the GC allele in heterozygous cells. Our findings suggest that the p73 G4C14-to-A4T14 polymorphism may play a role in mediating the susceptibility to NPC in Chinese populations.
    Carcinogenesis 03/2014; · 5.64 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 01/2014; 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 01/2014; 5:3733. · 10.74 Impact Factor
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    ABSTRACT: Phosphatase and tensin homolog (PTEN), v-akt murine thymoma viral oncogene homolog 1 (AKT1), mouse double minute 2 (MDM2) and p53 play important roles in the development of cancer. We examined whether the single nucleotide polymorphisms (SNPs) in the PTEN, AKT1, MDM2 and p53 genes were related to the risk and severity of nasopharyngeal carcinoma (NPC) in the Chinese population. Seven SNPs [p53 rs1042522, PTEN rs11202592, AKT1 SNP1-5 (rs3803300, rs1130214, rs3730358, rs1130233 and rs2494732)] were genotyped in 593 NPC cases and 480 controls by PCR direct sequencing or PCR-RFLP analysis. Multivariate logistic regression analysis was used to calculate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). None of the polymorphisms alone was associated with the risk or severity of NPC. However, haplotype analyses indicated that a two-SNP core haplotype (SNP4-5, AA) in AKT1 was associated with a significantly increased susceptibility to NPC risk (adjusted OR = 3.87, 95% CI = 1.96-7.65; P<0.001). Furthermore, there was a significantly increased risk of NPC associated with the combined risk genotypes (i.e., p53 rs1042522 Arg/Pro + Pro/Pro, MDM2 rs2279244 G/T + G/G, PTEN rs11202592 C/C, AKT1 rs1130233 A/A). Compared with the low-risk group (0-2 combined risk genotypes), the high-risk group (3-4 combined risk genotypes) was associated with a significantly increased susceptibility to NPC risk (adjusted OR = 1.67, 95% CI = 1.12-2.50; P = 0.012). Our results suggest that genetic variants in the PTEN, AKT1, MDM2 and p53 tumor suppressor-oncoprotein network may play roles in mediating the susceptibility to NPC in Chinese populations.
    PLoS ONE 01/2014; 9(3):e92135. · 3.53 Impact Factor
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    ABSTRACT: With the advance of experimental technologies, different stable isotope labeling methods have been widely applied to quantitative proteomics. Here, we present an efficient tool, named SILVER for processing the stable isotope labeling mass spectrometry data. SILVER implements novel methods for quality control of quantification at spectrum, peptide and protein levels respectively. Several new quantification confidence filters and indices are used to improve the accuracy of quantification results. The performance of SILVER was verified and compared with MaxQuant and Proteome Discoverer using a large-scale dataset and two standard datasets. The results suggest that SILVER shows high accuracy and robustness while consuming much less processing time. Additionally, SILVER provides user-friendly interfaces for parameter setting, result visualization, manual validation and some useful statistics analyses. SILVER and its source codes are freely available under the GNU General Public License v3.0 at http://bioinfo.hupo.org.cn/silver. zhuyunping@gmail.com.
    Bioinformatics 12/2013; · 5.47 Impact Factor
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    ABSTRACT: Background: Genetic variations in microRNAs may alter their processing, expression, and binding to target mRNAs, consequently affecting many cancer-related biological processes. Recently, a polymorphism rs11614913 in MIR196A2 was shown to affect the processing of the precursor microRNA into its mature forms and the repertoire of target mRNAs with which it interacts. We examined whether this polymorphism was relevant to the risk of occurrence or progression of nasopharyngeal carcinoma (NPC) in the Chinese population. Methods: We genotyped the MIR196A2 rs11614913 in a case-control study of 1084 patients with NPC and 1036 cancer-free controls using TaqMan assay. The genetic associations with the risk of occurrence and progression of NPC were analyzed by logistic regression. Results: We observed a significantly increased occurrence of NPC associated with the rs11614913 T allele (odds ratio [OR]=1.15, 95% confidence interval [CI]=1.02-1.32, p=0.026) compared with the C allele. The T allele was also significantly associated with the advanced local tumor invasion (T3+T4 vs. T1+T2; OR=1.27, 95% CI=1.04-1.54, p=0.015) and advanced lymph node metastasis (N2+N3 vs. N0+N1; OR=1.23, 95% CI=1.02-1.49, p=0.031) of NPC compared with the C allele. Furthermore, stratified analysis indicated that the increased susceptibility to advanced lymph node metastasis of NPC related to the T allele was more pronounced in patients with a positive family history (N2+N3 vs. N0+N1; p=0.016, test for homogeneity). Conclusions: Our study suggests that the functional polymorphism rs11614913 in the MIR196A2 gene may contribute to the risk of occurrence and progression of NPC in the Chinese population.
    Genetic Testing and Molecular Biomarkers 12/2013; · 1.44 Impact Factor
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    ABSTRACT: The Chromosome-centric Human Proteome Project (C-HPP) aims to map and annotate the entire human proteome by the "chromosome-by-chromosome" strategy. As the C-HPP proceeds, the increasing volume of proteomic datasets presents a challenge for customized and reproducible bioinformatics data analyses for mining biological knowledge. To address this challenge, we updated the previous static proteome browser CAPER into a higher version, CAPER 2.0 - an interactive, configurable and extensible workflow-based platform for C-HPP data analyses. In addition to the previous visualization functions of track-view and heatmap-view, CAPER 2.0 presents a powerful toolbox for C-HPP data analyses, and also integrates a configurable workflow system which supports the view, construction, edit, run and share of workflows. These features allow users to easily conduct their own C-HPP proteomic data analyses and visualization by CAPER 2.0. In this paper, we illustrated the usage of CAPER 2.0 with four specific workflows for finding missing proteins, mapping peptides to chromosomes for genome annotation, integrating peptides with transcription factor binding sites from ENCODE datasets, and functionally annotating proteins. The updated CAPER is available at http://www.bprc.ac.cn/CAPE.
    Journal of Proteome Research 11/2013; · 5.06 Impact Factor
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    ABSTRACT: To estimate the potential of the state-of-the-art proteomics technologies on full coverage of the encoding gene products, the Chinese Human Chromosome Proteome Consortium (CCPC) applied a multi-omics strategy to systematically analyze the transciptome, translatome and proteome of the same cultured hepatoma cells with varied metastatic potential qualitatively and quantitatively. The results provide a global view of gene expression profiles. The 9,064 identified high confident proteins covered 50.2% of all gene products in the translatome. Those proteins with function of adhesion, development, reproduction etc. are low abundance in transcriptome and translatome but absent in proteome. Taking the translatome as the background of protein expression, we found that the protein abundance plays a decisive role and hydrophobicity has a greater influence than molecular weight and isoelectric point on protein detectability. Thus, the enrichment strategy used for low-abundant transcription factors helped to identify missing proteins. In addition, those peptides with single amino acid polymorphisms negligibly contributed to new protein identification, although they might play significant role for the disease researches. The proteome raw and meta data of proteome were collected using the iProX submission system and ProteomeXchange (PXD000529, PXD000533 and PXD000535). All the detailed information in this study can be accessed from the Chinese Chromosome-Centric Human Proteome Database.
    Journal of Proteome Research 11/2013; · 5.06 Impact Factor

Publication Stats

4k Citations
1,461.68 Total Impact Points

Institutions

  • 2006–2014
    • 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
  • 2006–2013
    • National University of Defense Technology
      • College of Mechatronic Engineering and Automation
      Changsha, Hunan, China
  • 2001–2013
    • China Institute for Radiation Protection
      Peping, Beijing, China
  • 2012
    • Peking Union Medical College Hospital
      Peping, Beijing, China
    • Chinese PLA General Hospital (301 Hospital)
      Peping, Beijing, China
    • Anhui Medical University
      Luchow, Anhui Sheng, China
  • 2006–2012
    • Fudan University
      • • State Key Laboratory of Genetic Engineering
      • • Institutes of Biomedical Sciences
      • • Department of Chemistry
      • • Center for Evolutionary Biology
      Shanghai, Shanghai Shi, China
    • Tsinghua University
      • 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
  • 2002–2007
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • 307 Hospital of the Chinese People's Liberation Army
      Peping, Beijing, China
  • 2001–2007
    • Beijing Genomics Institute
      Bao'an, Guangdong, China
  • 2005
    • Northeast Institute of Geography and Agroecology
      • Institute of Biophysics
      Beijing, Beijing Shi, China
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 1999–2005
    • Chinese National Human Genome Center
      Peping, Beijing, China
  • 2004
    • Government of the People's Republic of China
      Peping, Beijing, China
    • Southwest Hospital
      Nan-ching-hsü, Jiangxi Sheng, China