Biochemical and Biophysical Research Communications Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Biochemical and Biophysical Research Communications is the premier international journal devoted to the very rapid dissemination (six weeks) of timely and significant experimental results in the diverse fields of biological research. Frequent publication (36 issues per year) ensures a steady stream of information. The development of the "Breakthroughs and Views" section brings the minireview format to the journal. In addition, the editors have expanded the journalís scope. Research Areas now include: Biochemistry Cell Biology; Developmental Biology; Immunology; Neurobiology; Biophysics; Molecular Biology; Plant Biology.

Current impact factor: 2.30

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.297
2013 Impact Factor 2.281
2012 Impact Factor 2.406
2011 Impact Factor 2.484
2010 Impact Factor 2.595
2009 Impact Factor 2.548
2008 Impact Factor 2.648
2007 Impact Factor 2.749
2006 Impact Factor 2.855
2005 Impact Factor 3
2004 Impact Factor 2.904
2003 Impact Factor 2.836
2002 Impact Factor 2.935
2001 Impact Factor 2.946
2000 Impact Factor 3.055
1999 Impact Factor 3.161
1998 Impact Factor 2.78
1997 Impact Factor 2.671
1996 Impact Factor 2.872
1995 Impact Factor 3.179
1994 Impact Factor 3.4
1993 Impact Factor 3.312
1992 Impact Factor 3.583

Impact factor over time

Impact factor

Additional details

5-year impact 2.38
Cited half-life 9.50
Immediacy index 0.48
Eigenfactor 0.10
Article influence 0.69
Website Biochemical and Biophysical Research Communications website
Other titles Biochemical and biophysical research communications (Online), Biochemical and biophysical research communications
ISSN 1090-2104
OCLC 35247010
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • David J Lindberg · Elin K Esbjörner ·
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    ABSTRACT: Identification of the chemical and biological properties of amyloid fibrils is important for understanding their roles in human diseases and to clarify the physico-chemical mechanisms that govern their formation. In pursuit of these goals, small molecule fluorescent dyes have received increasing attention as probes of amyloid conformations. In this study, we report on the ability of YOYO-1, a homodimeric derivative of oxazole yellow, to detect fibrils formed by the Alzheimer's disease related Aβ(1-42) peptide. We find that YOYO-1 binds to Aβ(1-42) fibrils with the long axes of its oxazole yellow moieties parallel to the fibril axis, resulting in a 200x emission enhancement; a result that shows that YOYO-1 is a sensitive amyloid probe. Further, YOYO-1 exhibits characteristic absorption shifts upon binding to the Aβ(1-42) fibrils that we attribute to a self-stacking to non-stacking transition in its homodimer configuration; herein we show how this phenomenon can be exploited to estimate the degree of dye binding. Furthermore, we show that YOYO-1 can be used to monitor the kinetics in amyloid formation reactions. Taken together, our result that YOYO-1 is a sensitive amyloid probe that can operate with both absorption and fluorescence read-outs suggests that this commercially available dye could become a useful complement to thioflavin-T for in vitro amyloid-sensing applications.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.051
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    ABSTRACT: Autoimmune regulator (AIRE) activates the transcription of many genes in an unusual promiscuous and stochastic manner. The mechanism by which AIRE binds to the chromatin and DNA is not fully understood, and the regulatory elements that AIRE target genes possess are not delineated. In the current study, we demonstrate that AIRE activates the expression of transiently transfected luciferase reporters that lack defined promoter regions, as well as intron and poly(A) signal sequences. Our protein-DNA interaction experiments with mutated AIRE reveal that the intact homogeneously staining region/caspase recruitment domain (HSR/CARD) and amino acids R113 and K114 are key elements involved in AIRE binding to DNA.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.056
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    ABSTRACT: miR-4458, a new tumor-suppressor, was reported to down-regulated in human hepatocellular carcinoma. The expression status, roles and inhibitory mechanisms of miR-4458 in other tumors still need to be clarified. The aim of this study is to investigate the effects of miR-4458 and to elucidate the potential mechanism in colon cancer cells. Using bioinformatic databases, we predicted that hexokinase2 (HK2), a rate-limiting enzyme in the glycolytic pathway, was a target of miR-4458, so the effects of miR-4458 on glycolysis and lactate production was assessed in colon cancer cells. We found that miR-4458 was down-regulated and HK2 was up-regulated in colon cancer cells. Overexpression of miR-4458 inhibited proliferation, glycolysis, and lactate production under both normoxic and hypoxic conditions. Luciferase activity assays showed that HK2 was a direct target of miR-4458. Moreover, knockdown of HK2 by specific RNAi also suppressed proliferation, glycolysis, and lactate production under both normoxic and hypoxic conditions. In conclusion, our findings suggested that miR-4458 inhibited the progression of colon cancer cells by inhibition of glycolysis and lactate production via directly targeting HK2 mRNA.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.066
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    ABSTRACT: Histone H3S10 phosphorylation has been known as a cell cycle-specific marker and has a role in transcriptional activation. Various kinases phosphorylate H3S10 in different species, however, the role of the mitotic serine/threonine protein kinase Aurora A (AURKA) is largely unknown. Here we present evidence that AURKA phosphorylates H3S10 and activates target gene transcription. We show that down-regulation of AURKA level during leukemia cell differentiation results in decreased H3S10 phosphorylation level. We further show that AURKA is recruited to target gene promoters and activates transcription via H3S10 phosphorylation. Furthermore, this recruitment can be disrupted by the AURKA inhibitor Alisertib and results in H3K9-me2 recruitment by G9a.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.063
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    ABSTRACT: Oleanolic acid (OA) is an active ingredient in natural plants. It has been reported to possess a variety of pharmacological activities, but very little is known about its effects of anti-aging. We investigate here whether OA has an impact on longevity in vivo, and more specifically, we have examined effects of OA on the lifespan and stress tolerance in Caenorhabditis elegans (C.elegans). Our results showed that OA could extend the lifespan, increase its stress resistance and reduce the intracellular reactive oxygen species (ROS) in wild-type worms. Moreover, we have found that OA-induced longevity may not be associated with the calorie restriction (CR) mechanism. Our mechanistic studies using daf-16 loss-of-function mutant strains (GR1307) indicated that the extension of lifespan by OA requires daf-16. In addition, OA treatment could also modulate the nuclear localization, and the quantitative real-time PCR results revealed that up-regulation of daf-16 target genes such as sod-3, hsp-16.2 and ctl-1 could prolong lifespan and increase stress response in C.elegans. This study overall uncovers the longevity effect of OA and its underpinning mechanisms.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.042
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    ABSTRACT: Metabolic syndrome characterized by hyperglycemia contributes to nonalcoholic steatohepatitis-associated liver fibrosis. This study was to investigate the effects of Acid-sensing ion Channel 1a (ASIC1a) on the process of liver fibrosis under hyperglycemia. Results showed that high glucose significantly worsen the pathology of liver fibrosis in vivo. In vitro, high glucose stimulated proliferation, activation and extracellular matrix (ECM) production in HSCs, and enhance the effect of PDGF-BB on the activation and proliferation of HSCs. These effects could be attenuated by ASIC1a specific inhibitor Psalmotoxin-1(PcTx1) or specific ShRNA for ASIC1a through Notch1/Hes-1 pathways. These data indicate that ASIC1a plays an important role in diabetes complication liver fibrosis.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.029
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    ABSTRACT: The voltage-gated proton channel Hv1 is a potent acid extruder that participates in the extrusion of the intracellular acid. Here, we showed for the first time, Hv1 is highly expressed in mouse and human pancreatic islet β-cells, as well as β-cell lines. Imaging studies demonstrated that Hv1 resides in insulin-containing granules in β-cells. Knockdown of Hv1 with RNA interference significantly reduces glucose- and K(+)-induced insulin secretion in isolated islets and INS-1 (832/13) β-cells and has an impairment on glucose- and K(+)-induced intracellular Ca(2+) homeostasis. Our data demonstrated that the expression of Hv1 in pancreatic islet β-cells regulates insulin secretion through regulating Ca(2+) homeostasis.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.027
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    ABSTRACT: Th17 cells, which have been implicated in autoimmune diseases including rheumatoid arthritis (RA), require the JAK-STAT3 pathway for their differentiation and functions. Recently, JAK inhibitors have been developed as a therapeutic drug for RA. However, the current JAK inhibitors are not optimized to STAT3 compared with other STATs. In this study, we found a new lead compound of a low-molecular-weight JAK-STAT inhibitor, 2-[(3-Carbamoyl-2-thienyl)amino]-2-oxoethyl(2,6-dichlorophenyl)acetate, which inhibits STAT3 as efficiently as other STATs. This compound, named JI069, was selected by STAT3 reporter assay in combination with an in silico docking model. JI069 inhibited gp130 signaling by inducing dissociation between gp130 and JAK1. In HEK293T cells and primary T cells, JI069 suppressed STAT3 activation as efficiently as other STATs, including STAT1, STAT5, and STAT6. JI069 effectively suppressed Th1, Th2, and Th17 differentiation while strongly promoted iTreg differentiation. JI069 suppressed symptoms of the collagen-induced arthritis (CIA) model in mice, and inhibited the cytokine production from T cells as well as the STAT3 phosphorylation of synovial cells. These data suggest that JI069 is a new type of JAK inhibitor which has potential for the treatment of immunological disorders.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.030
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    ABSTRACT: Tetraspanin 8 (TSPAN8) is a tumor-associated antigen implicated in tumor progression and metastasis. However, the validation of TSPAN8 as a potential therapeutic target in metastatic colorectal cancer (mCRC) has not yet been studied. In this study, through several in vitro methodologies, we identified a large extracellular loop of TSPAN8 (TSPAN8-LEL) as a key domain for regulating mCRC invasion. Using phage display technology, we developed a novel anti-TSPAN8-LEL human antibody with subnanomolar affinity that specifically recognizes amino acids 140-205 of TSPAN8-LEL in a conformation-dependent manner. Finally, we demonstrated that the antibody specifically reduces invasion in the HCT116 and LoVo mCRC cell lines more potently than in the HCT-8 and SW480 non-mCRC cell lines. Our data suggest that TSPAN8-LEL may play an important role in mCRC cell invasion, and that the antibody we have developed could be a useful tool for inhibiting the invasion of TSPAN8-expressing mCRCs.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.031
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    ABSTRACT: Insulin resistance plays an important role in the development of hypertension, which is seriously detrimental to human health. Recently, Sirtuin-1 (SIRT1) has been found to participate in regulation of insulin resistance. Therefore, further studies focused on the SIRT1 regulators might provide a potential approach for combating insulin resistance and hypertension. Interestingly, in this study, we found that SIRT1 was the target gene of the miR-543 by the Dual-Luciferase Reporter Assay. Moreover, the miR-543 expression notably increased in the insulin-resistant HepG2 cells induced by TNF-α. Further analysis showed that the overexpression of the miR-543 lowered the SIRT1 mRNA and protein levels, resulting in the insulin resistance in the HepG2 cells; the inhibition of miR-543, however, enhanced the mRNA and protein expression of the SIRT1, and alleviated the insulin resistance. Furthermore, the SIRT1 overexpression abrogated the effect of miR-543 on insulin resistance. In addition, the overexpression of the miR-543 by the lentivirus-mediated gene transfer markedly impaired the insulin signaling assessed by the Western blot analysis of the glycogen synthesis and the phosphorylation of Akt and GSK3β. In summary, our study suggested that the downregulation of the miR-543 could alleviate the insulin resistance via the modulation of the SIRT1 expression, which might be a potential new strategy for treating insulin resistance and a promising therapeutic method for hypertension.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.032
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    ABSTRACT: Invasion and migration of glioblastoma multiforme (GBM) is a multistep process and an important phenotype that causes this disease to invade surrounding tissues in the brain. The purpose of this study was to determine the role of miR-590-3p in regulation of epithelial mesenchymal transition (EMT) and metastasis of GBM cells. Expression levels of miR-590-3p in 15 GBM specimens with adjacent tissues and five GBM cell lines were assessed by quantitative RT-PCR. We found that miR-590-3p was down-regulated in detected GBM tissue samples and all of the GBM cell lines. In addition, Ectopic expression of miR-590-3p suppressed and miR-590-3p-in promoted EMT, migration, and invasion in U87MG and A172 cells. Bioinformatics coupled with luciferase and Western blot assays also revealed that miR-590-3p inhibited expression of ZEB1 and ZEB2, which are master regulators of tumor metastasis. Our study first indicates that miR-590-3p functions as a suppressor of GBM EMT and metastasis by targeting ZEB1 and ZEB2, and it may be a therapeutic target for metastatic GBM.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.025
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    ABSTRACT: HNF1α (Hepatocyte Nuclear Factor 1α) is one of the master regulators in pancreatic beta-cell development and function, and the mutations in Hnf1α are the most common monogenic causes of diabetes mellitus. As a member of the POU transcription factor family, HNF1α exerts its gene regulatory function through various molecular interactions; however, there is a paucity of knowledge in their functional complex formation. In this study, we identified the Groucho protein AES (Amino-terminal Enhancer of Split) as a HNF1α-specific physical binding partner and functional repressor of HNF1α-mediated transcription, which has a direct link to glucose-stimulated insulin secretion in beta-cells that is impaired in the HNF1α mutation-driven diabetes.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.007
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    ABSTRACT: MicroRNAs play an important role in regulating the inflammatory response, and are critically involved in the development of inflammatory disorders, including those affecting the lungs. While the microRNA miR-221 is involved in embryonic lung branching morphogenesis and epithelial cell development, its importance in lung inflammation has not been previously explored. In our current study, expression of miR-221 was selectively decreased by exposure to lipopolysaccharides (LPS) both in vitro and in vivo. Enforced expression of miR-221 significantly increased the production of proinflammatory cytokines TNF-α and IL-6, and enhanced the activation of NF-κB and MAPKs upon LPS stimulation. Accordingly, intratracheal stimulation of miR-221 was shown to aggravate endotoxin-induced acute lung injuries and inflammation in mice. Mechanistic studies showed that miR-221 directly targets A20, a master regulator of NF-κB and MAPK signaling, and thus represses inflammatory signaling. Restoration of A20 in macrophages abolished the stimulatory effect of miR-221 on production of proinflammatory cytokines. Together, these results indicate the presence of a novel miRNA-mediated feed-back mechanism that controls inflammation, and suggest involvement of aberrant miR-221 expression in the development of inflammatory lung disorders.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.009
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    ABSTRACT: Microgravity induces observed bone loss in spaceflight or simulated experiments, while the mechanism underlying it is still obscure. Here, we utilized a clinostat to model simulated microgravity (SMG) and found that SMG obviously inhibited osteogenic differentiation of rat bone marrow mesenchymal stem cells (BMSCs). We detected that SMG dramatically inhibited the expression of the transcriptional coactivator with PDZ-binding motif (TAZ), which acts as a vital regulator of osteogenesis. Interestingly, we found that lysophosphatidic acid (LPA) could activate TAZ and retain osteogenic differentiation of BMSCs under SMG. Our data further demonstrated that depletion of TAZ by siRNA blocked the LPA-induced increase in osteogenic differentiation of BMSCs under SMG. Moreover, Y27632 (the Rock inhibitor) abrogated the activation of TAZ and the increased osteogenic differentiation induced by LPA. Taken together, we propose that microgravity inhibits osteogenic differentiation of BMSCs due to decreased TAZ expression and that LPA can efficiently reverse the reduced osteogenic differentiation via the Rock-TAZ pathway.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.006
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    ABSTRACT: Autophagy is a bulk degradation system that functions in response to cellular stresses such as metabolic stress, endoplasmic reticulum stress, oxidative stress, and developmental processes. During autophagy, cytoplasmic components are captured in double-membrane vesicles called autophagosomes. The autophagosome fuses with the lysosome, producing a vacuole known as an autolysosome. The cellular components are degraded by lysosomal proteases and recycled. Autophagy is important for maintaining cellular homeostasis, and the process is evolutionarily conserved. Kibra is an upstream regulator of the hippo signaling pathway, which controls organ size by affecting cell growth, proliferation, and apoptosis. Kibra is mainly localized in the apical membrane domain of epithelial cells and acts as a scaffold protein. We found that Kibra is required for autophagy to function properly. The absence of Kibra caused defects in the formation of autophagic vesicles and autophagic degradation. We also found that the well-known cell polarity protein aPKC interacts with Kibra, and its activity affects autophagy upstream of Kibra. Constitutively active aPKC decreased autophagic vesicle formation and autophagic degradation. We confirmed the interaction between aPKC and Kibra in S2 cells and Drosophila larva. Taken together, our data suggest that Kibra and aPKC are essential for regulating starvation-induced autophagy.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.011
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    ABSTRACT: Calcium (Ca(2+)) serves as a critical messenger in a number of adaptation and developmental processes. In plants, CBL family represents a unique group of calcium sensors that decodes calcium signals. Several CBL members have been functionally characterized in the model plant Arabidopsis thaliana, but the role of CBL7 remains unknown. Here, we report that CBL7 is involved in the regulation of low-nitrate response in Arabidopsis. Expression of CBL7 was predominant in the root of young seedlings and substantially induced by nitrate starvation. Cbl7 mutant was more inhibited in root growth upon nitrate starvation compared to the wild-type. Interestingly, the growth arrest of cbl7 under low-nitrate conditions relied on acidic pH. Further analyses revealed that expression of two high-affinity nitrate transporter genes, NRT2.4 and NRT2.5, was down-regulated in cbl7 under nitrogen-starvation condition. Accordingly, the cbl7 mutant plants retained lower nitrate content than wild-type plants under low-nitrate condition. Taken together, our results uncover a novel role of CBL7 in the response to nitrate deficiency in Arabidopsis.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.10.164
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    ABSTRACT: MicroRNAs acting as oncogenes or tumor suppressor genes play crucial roles in human cancers. Sphingosine kinase 1 (SPHK1) and its metabolite sphingosine 1-phosphate (S1P) contribute to tumor angiogenesis. We have reported that the down-regulation of miR-506 targeting YAP mRNA results in the hepatocarcinogenesis. In the present study, we report a novel function of miR-506, which suppresses tumor angiogenesis through targeting SPHK1 mRNA in liver cancer. Bioinformatics analysis showed that miR-506 might target 3'-untranslated region (3'UTR) of SPHK1 mRNA. Then, we validated that by luciferase reporter gene assays. MiR-506 was able to reduce the expression of SPHK1 at the levels of mRNA and protein using reverse transcription-polymerase chain reaction and Western blot analysis in hepatoma HepG2 cells. Functionally, human umbilical vein endothelial cell (HUVEC) tube formation assays demonstrated that the forced miR-506 expression remarkably inhibited the production of S1P in the supernatant of hepatoma cells. The supernatant resulted in the inhibition of tumor angiogenesis. Interestingly, the supernatant with overexpression of SPHK1 could rescue the inhibition of angiogenesis of liver cancer mediated by miR-506. Anti-miR-506 increased the production of S1P in the supernatant of hepatoma cells, but the supernatant with silencing of SPHK1 abolished anti-miR-506-induced acceleration of tumor angiogenesis. Clinically, we observed that the levels of miR-506 were negatively related to those of SPHK1 mRNA in liver cancer tissues. Thus, we conclude that miR-506 depresses the angiogenesis of liver cancer through targeting 3'UTR of SPHK1 mRNA. Our finding provides new insights into the mechanism of tumor angiogenesis.
    Biochemical and Biophysical Research Communications 11/2015; DOI:10.1016/j.bbrc.2015.11.008