Acta Biochimica et Biophysica Sinica Journal Impact Factor & Information

Publisher: Oxford University Press (OUP)

Journal description

Acta Biochimica et Biophysica Sinica (ABBS) is a scientific journal publishing monthly research papers, short communications and minireviews in biochemistry, molecular biology and biophysics. Research papers and short communications report on original work, with minireviews providing a concise introduction to the subject matter to inform the readers of the latest developments in a certain area.

Current impact factor: 2.09

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.089
2012 Impact Factor 1.807
2011 Impact Factor 1.376
2010 Impact Factor 1.547
2009 Impact Factor 1.482
2008 Impact Factor 1.086
2007 Impact Factor 1.017
2006 Impact Factor 0.931
2005 Impact Factor 0.505
2004 Impact Factor 0.36

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.90
Cited half-life 4.30
Immediacy index 0.40
Eigenfactor 0.01
Article influence 0.48
Website Acta Biochimica et Biophysica Sinica website
ISSN 1745-7270
OCLC 209162005
Material type Series, Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Oxford University Press (OUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Pre-print can only be posted prior to acceptance
    • Pre-print must be accompanied by set statement (see link)
    • Pre-print must not be replaced with post-print, instead a link to published version with amended set statement should be made
    • Pre-print on author's personal website, employer website, free public server or pre-prints in subject area
    • Post-print in Institutional repositories or Central repositories
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • The publisher will deposit in PubMed Central on behalf of NIH authors
    • Publisher last contacted on 19/02/2015
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Autophagy is a highly regulated and multistep biological process whereby cells under metabolic, proteotoxic, or other stresses remove dysfunctional organelles and/or misfolded/polyubiquitinated proteins by shuttling them via specialized structures called autophagosomes to the lysosome for degradation. Although autophagy is generally considered to be a non-selective process, accumulating evidence suggests that it can also selectively degrade specific target cargoes. These selective targets include proteins, mitochondria, and even invading bacteria. The discovery and characterization of autophagic adapters, such as p62/Sequestosome 1 (SQSTM1) and Neighbor of BRCA1 gene 1 (NBR1), have provided mechanistic insights into selective autophagy. These receptors are all able to act as cargo receptors for the degradation of ubiquitinated substrates. This review mainly summarizes the most up-to-date findings regarding the key receptor proteins that play important roles in regulating selective autophagy. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv055
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    ABSTRACT: Feruloyl esterase A from Aspergillus niger (AnFaeA) contains three intramolecular disulfide bonds and one free cysteine at position 235. Saturated mutagenesis at Cys235 was carried out to produce five active mutants, all of which displayed unusual thermal inactivation patterns with the most residual activity achieved at 75°C, much higher than the parental AnFaeA. But their optimal reaction temperatures were lower than the parental AnFaeA. Extensive investigation into their free thiol and disulfide bond, circular dichroism spectra and fluorescence spectra revealed that the unfolding of the parental enzyme was irreversible on all the tested conditions, while that of the Cys235 mutants was reversible, and their ability to refold was highly dependent on the denaturing temperature. Mutants denatured at 75°C were able to efficiently reverse the unfolding to regain native structure during the cooling process. This study provided valid evidence that free cysteine substitutions can reduce irreversible thermal inactivation of proteins. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv057
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    ABSTRACT: To explore the effect of microRNA-26b (miR-26b) in non-small cell lung cancer (NSCLC) cells, we investigated the mRNA levels of miR-26b in 4 NSCLC cell lines and 10 clinical samples from human patients with NSCLC by quantitative reverse transcriptase polymerase chain reaction. It was found that miR-26b was significantly down-regulated in both NSCLC cells and human carcinoma tissues. Synthetic oligonucleotides were used to up-regulate or down-regulate miR-26b in NSCLC cell lines H1299 and A549 cells. Results showed that both down-regulating and up-regulating miR-26b had no effect on cancer cell proliferation in H1299 or A549 cells, whereas miR-26b over-expression increased cancer cell migration and reduced cisplatin chemosensitivity. Phosphatase and tensin homolog (PTEN) was confirmed to be directly bound by miR-26b by dual-luciferase reporter assay, and was down-regulated in miR-26b over-expressing NSCLC cells. Finally, when PTEN was up-regulated in NSCLC cells, it reversed the effects of miR-2b over-expression on NSCLC migration and cisplatin chemosensitivity. In conclusion, our data showed a functional mechanism of miR-26b in regulating NSCLC. It indicates that miR-26b may regulate NSCLC migration and chemosensitivity through the regulation of PTEN. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv046
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    ABSTRACT: The cellular and molecular mechanisms responsible for human idiopathic ascending aortic aneurysm (IAAA) remain unknown. Matrix metalloproteinase-2 (MMP-2) is a key enzyme for the degradation of extracellular matrix in aneurysmal walls. The aim of this study was to elucidate the role of the angiotensin II (Ang II) pathway in MMP-2 induction in IAAA aortic walls. Quantitative polymerase chain reaction and western blot analysis were used to compare the MMP-2 mRNA and protein levels in ascending aortic specimens with those in IAAA patients (n = 10) and heart transplant donors (n = 5) without any aortopathy. It was found that MMP-2 expression was significantly increased, which was associated with elastic lamellae disruption in IAAA walls. Additionally, the expression levels of angiotensinogen (AGT) and Ang II in the ascending aortic tissues from individuals with and without IAAAs were detected by western blot analysis and radioimmunoassay, respectively. The results demonstrated that the expressions of AGT and Ang II protein were significantly increased in the ascending aortic tissues of IAAA patients. Furthermore, whether Ang II induces MMP-2 expression was investigated using human IAAA walls ex vivo culture. It was found that exogenous Ang II increased the MMP-2 expression in a dose-dependent manner, which was completely inhibited by the Ang II type 1 receptor (AT1R) inhibitor candesartan and was mediated by c-Jun N-terminal kinase (JNK) activation. Taken together, these results indicate that Ang II can induce an increase of MMP-2 expression via AT1R and JNK in ex vivo cultured IAAA aortic walls, and suggest that angiotensin receptor blocker (ARB) drugs and JNK inhibitors have the potential in the prevention or treatment of IAAAs. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv047
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    ABSTRACT: Estrogens are strongly implicated in gender differences in immune responses by influencing the development and activation of immune cells. Recent studies have shown that myeloid-derived suppressor cells (MDSCs), derived from CD11b(+)Gr-1(+) myeloid cells under pathological conditions, play vital roles in modulating immune responses. However, it is still unknown the effects of estrogens on MDSCs. In the present study, we investigated the effects and mechanisms of estrogens on regulating the accumulation of MDSCs. It was found that, compared with male patients with systemic lupus erythematosus (SLE), female patients with SLE showed a higher frequency of MDSCs in peripheral blood mononuclear cells and a higher level of tumor necrosis factor α (TNF-α) in serum. Notably, estradiol level in the serum of female patients with SLE was positively correlated with the frequency of MDSCs. Moreover, 17β-estradiol could promote TNF-α-induced accumulation of MDSCs in vivo by increasing the fundamental frequency of CD11b(+)Gr-1(+) cells. Furthermore, 17β-estradiol promoted the secretion of TNF-α in vivo, which contributed to the increase of the frequency of CD11b(+)Gr-1(+) cells. In addition, it was also found that female mice showed a higher frequency of CD11b(+)Gr-1(+) cells and a higher TNF-α level in blood than the age-matched male mice. These data indicate that 17β-estradiol contributes to the accumulation of MDSCs in blood by promoting TNF-α secretion, which increases the fundamental frequency of CD11b(+)Gr-1(+) cells. Our findings provide a new insight into the mechanism of gender difference in the prevalence of inflammation and autoimmune diseases. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv053
  • Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv051
  • Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv048
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    ABSTRACT: Apoptosis is a crucial mode of cell death induced by ischemia and reperfusion, and ischemic postconditioning (PostC) has been reported to inhibit cell apoptosis. Inducible nitric oxide synthase (iNOS) has been confirmed to play an important role in triggering and mediating the late cardio-protection against ischemia/hypoxia. In this study, we found that hypoxic PostC remarkably up-regulated the expression of iNOS and decreased cardiomyocyte apoptosis. Pre-treatment with 1400w (a highly selective inhibitor of iNOS) or iNOS siRNA weakened the anti-apoptotic effect of hypoxic PostC. These findings suggested that iNOS may be one of the key molecular mechanisms responsible for the inhibition of apoptosis by hypoxic PostC. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 06/2015; DOI:10.1093/abbs/gmv043
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    ABSTRACT: Methyl 3,5-di-caffeoylquinate (3,5-diCQM) has been used for the treatment of various diseases in oriental medicine, but its effect on melanogenesis has not been reported yet. In this study, the molecular mechanism of 3,5-diCQM-induced melanogenesis was investigated. It was found that 3,5-diCQM induced synthesis of melanin pigments in murine B16F10 melanoma cells in a concentration-dependent manner. Treatment of cells with 3,5-diCQM for 48 h increased extracellular and intracellular melanin production and tyrosinase activity. The expressions of tyrosinase, tyrosinase-related protein 1 (TRP1), and TRP2 were up-regulated in a dose-dependent manner 48 h after 3,5-diCQM treatment. Western blot analysis showed that 3,5-diCQM increased the phosphorylation of p38 mitogen-activated protein kinase and cAMP responsive element binding as well as the expression of microphthalmia-associated transcription factor. In addition, 3,5-diCQM-stimulated cAMP production, and 3,5-diCQM-induced tyrosinase activity and melanin synthesis were attenuated by H89, a protein kinase A inhibitor. These results suggested that 3,5-diCQM-mediated activation of the p38 pathway may represent a novel approach for an effective therapy for vitiligo and hair graying. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; DOI:10.1093/abbs/gmv040
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    ABSTRACT: The ubiquitin ligase Parkin and autophagic adapter protein p62 are known to function in a common pathway controlling mitochondrial autophagy (mitophagy). However, the evidence supporting that p62 is directly recruited by ubiquitinated proteins remains undetermined. Here, we demonstrate that mitochondrial fission factor (Mff) associates with Parkin and carbonyl cyanide m-chlorophenyl hydrazone treatment significantly increases the affinity of Parkin with Mff. After recruitment to depolarized mitochondria, Parkin mediates poly-ubiquitination of Mff at lysine 251. Replacement of lysine 251 by arginine (K251R) totally abrogates Parkin-stimulated ubiquitination of Mff. Subsequently, the ubiquitinated Mff promotes its association with p62. Mff knockout interferes with p62 translocation to damaged mitochondria. Only re-transfection of Mff WT, but not K251R mutant, rescues this phenotype. Furthermore, loss of Mff results in failure of Parkin translocation and final clearance of damaged mitochondria. Thus, our data reveal functional links among Mff, p62, and the selective autophagy of mitochondria, which are implicated in the pathogenesis of neurodegeneration diseases. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; DOI:10.1093/abbs/gmv044
  • Acta Biochimica et Biophysica Sinica 05/2015; DOI:10.1093/abbs/gmv042
  • Acta Biochimica et Biophysica Sinica 05/2015; DOI:10.1093/abbs/gmv038
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    ABSTRACT: Specific tags with defined amino acid residues are widely used to purify or probe target proteins. Interestingly, the tagging system occasionally results in an increase of the recombinant protein expression in vivo. Here, we systematically examined this phenomenon using a poly-histidine (His)-tag fused to N- or C-terminal region of green, red, and blue fluorescent proteins by quantification and uneven distribution in cytoplasm of Escherichia coli. This effect was further supported by the distinct over-expression of several unrelated proteins, such as esterase, neopullulanase, and chloramphenicol acetyltransferase, tagging with the same tag. These results suggest that a poly-His-tag placed at N-terminal region can induce over-expression of recombinant protein via subcellular uneven distribution in vivo. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; DOI:10.1093/abbs/gmv036
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    ABSTRACT: Heat shock protein 90 (Hsp90) is a fascinating target for cancer therapy due to its significant role in the crossroad of multiple signaling pathways associated with cell proliferation and regulation. Hsp90 inhibitors have the potential to be developed into anti-cancer drugs. Here, we identified nicotinic-mycoepoxydiene (NMD), a structurally novel compound as Hsp90 inhibitor to perform the anti-tumor activity. The compound selectively bound to the Hsp90 N-terminal domain, and degraded the Hsp90 client protein Akt. The degradation of Akt detained Bad in non-phosphorylation form. NMD-associated apoptosis was characterized by the formation of fragmented nuclei, poly(ADP-ribose) polymerase cleavage, cytochrome c release, caspase-3 activation, and the increased proportion of sub-G1 phase cells. Interestingly, the apoptosis was accompanied with autophagy, by exhibiting the increased expression of LC-3 and the decrease of lysosome pH value. Our findings provide a novel cellular mechanism by which Hsp90 inhibitor adjusts cell apoptosis and autophagy in vitro, suggesting that NMD not only has a potential to be developed into a novel anti-tumor pharmaceutical, but also exhibits a new mechanism in regulating cancer cell apoptosis and autophagy via Hsp90 inhibition. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; 47(6). DOI:10.1093/abbs/gmv034
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    ABSTRACT: Non-small-cell lung cancer (NSCLC) is one of the most common lung cancers, and microRNAs (miRNAs) have been reported to play essential roles in NSCLC. Recent studies have indicated that miR-330-3p expression is up-regulated in NSCLC samples and in tissues of NSCLC brain metastasis. In this study, up-regulation of miR-330-3p expression was confirmed in NSCLC and 20 NSCLC patient samples. Furthermore, miR-330-3p was over-expressed in NSCLC cell lines A549 and H23, and the promotive function of miR-330-3p was investigated in regulating NSCLC cell proliferation and cell cycle distribution. To identify potential target genes of miR-330-3p in NSCLC, the miRNA target prediction databases were used. Luciferase activity assay and real-time RT-PCR analysis confirmed that miR-330-3p is negatively correlated with the expression of early growth response 2 (EGR2). Moreover, it was also found that EGR2 mRNA contains two potential binding sites for miR-330-3p. Knock-down of EGR2 with siRNA was demonstrated to have a similar effect as the over-expression of miR-330-3p in NSCLC cell lines. Taken together, our results show that EGR2 is a target of miR-330-3p. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; 47(6). DOI:10.1093/abbs/gmv032
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    ABSTRACT: Previous evidence has indicated that the microRNA-125b (miR-125b) family plays important roles in the regulation of cancer cell growth, development, differentiation, and apoptosis. However, whether they contribute to the process of adipocyte differentiation remains unclear. In the present study, we revealed that the expression level of miR-125b-5p, a member of miR-125b family, was dramatically up-regulated during differentiation of 3T3-L1 preadipocyte into mature adipocyte. Supplement of miR-125b-5p into 3T3-L1 cells promoted adipogenic differentiation as evidenced by increased lipid droplets and mRNA levels of adipocyte-specific molecular markers, including peroxisome proliferators-activated receptor γ, CCAAT/enhancer-binding protein α, fatty acid-binding protein 4, and lipoprotein lipase, and by triglyceride accumulation. CCK-8 assay showed that miR-125b-5p supplementation significantly inhibited cell proliferation. Flow cytometry analysis showed that miR-125b-5p impaired G1/S phase transition as well as the mRNA and protein expression of G1/S-related genes, such as Cyclin D2, Cyclin D3, and CDK4. Nevertheless, it had no effect on apoptosis. Additionally, by target gene prediction, we demonstrated that smad4 may be a potential target of miR-125b-5p in mouse 3T3-L1 preadipocytes, accounting for some of miR-125b-5p's functions. Taken together, these data indicated that miR-125b-5p may serve as an important positive regulator in adipocyte differentiation, at least partially through down-regulating smad4. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 05/2015; 47(5):355-61. DOI:10.1093/abbs/gmv024
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    ABSTRACT: Osteoarthritis (OA) is an age-related joint disease that is characterized by the degeneration of articular chondrocytes. Nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP-1) is associated with inflammation response. We investigated the role of PARP-1 in interleukin-1β (IL-1β)-stimulated human articular chondrocytes and its underlying mechanism. Cell viability and apoptosis were evaluated by using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay and flow cytometry, respectively. Tumor necrosis factor-α (TNF-α) level was measured by enzyme-linked immunosorbent assay. The mRNA and protein expression levels of PARP-1, IL-receptor (IL-1R), inducible nitric oxide synthase (iNOS), matrix metalloproteinases (MMPs), and tissue inhibitor of metalloproteinases-1 (TIMP-1) were determined by real-time reverse transcriptase-polymerase chain reaction and western blot analysis, respectively. The expression and phosphorylation of NF-кB p65 were measured by western blot analysis. Results showed that stimulation of chondrocytes with IL-1β caused a significant up-regulation of PARP-1 and IL-1R, resulting in NF-кB p65 nuclear translocation and phosphorylation associated with an increase of TNF-α secretion and iNOS expression. PARP-1 was inhibited by siRNA transfection. Results showed that PARP-1 inhibition suppressed IL-1β-induced reduction of cell viability and up-regulation of cell apoptosis, with a reduced IL-1R expression. PARP-1 inhibition also effectively reversed IL-1β-induced inflammatory response through inhibiting the IL-1R/NF-кB pathway. These data suggested that PARP-1 inhibition prevents IL-1β-induced inflammation response at least partly by inhibiting the IL-1R/NF-кB signaling pathway in human articular chondrocytes. Moreover, PARP-1 inhibition reduced MMPs expression and increased TIMP-1 expression, suggesting that PARP-1 inhibition could suppress cartilage destruction by modulating the balance between MMPs and TIMP-1. Inhibition of PARP-1 might be useful in the treatment of OA. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 04/2015; 47(6). DOI:10.1093/abbs/gmv033
  • Acta Biochimica et Biophysica Sinica 04/2015; 47(6). DOI:10.1093/abbs/gmv029
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    ABSTRACT: Transgenic mouse model with fluorescently labeled sperm has extensive application value. It is an auxiliary tool for investigating the mechanism of fertilization, especially for visualizing the oviduct-migrating ability of sperm in vivo. Here, we produced transgenic mouse lines whose sperm were tagged with enhanced green fluorescent protein (EGFP) according to the previously described method. Polymerase chain reaction analysis of tail-tip genomic DNA identified 13 founders, of which 5 male founders produced offspring to form transgenic lines. We showed that EGFP was testis-specifically expressed, sharing similar expression pattern with endogenous acrosin. It has luminal side restricted distribution in seminiferous tubules and acrosomal aggregation in mature sperm. In addition, interstrain hybridization obtained Prss37(-/-)EGFP(tg/+) males produced sperm with impaired oviduct-migrating ability as visualized under fluorescence microscope, compared with Prss37(+/+)EGFP(tg/+) counterparts. These results indicate that a transgenic mouse model with fluorescently labeled sperm has been successfully established and it is a useful tool for evaluating the oviduct-migrating ability of sperm. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
    Acta Biochimica et Biophysica Sinica 04/2015; 47(6). DOI:10.1093/abbs/gmv031