FEBS Letters RSS feed: Current Issue. FEBS Letters is one of the world's leading journals in biochemistry and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, hypotheses and research letters that merit urgent publication. FEBS Letters offers: • Faster publication: ? Accepted articles are published online in 3 days ? The print version of the article is published in 3 to 5 weeks after acceptance • Full-text article disclosure in HTML and PDF formats • Articles in Press are included in PubMed • Easy online manuscript submission system • Transparent online peer review and manuscript tracking system • No page charges • Free color figures Subject Coverage: The subject area of FEBS Letters is broad. It covers biochemistry (including protein chemistry, enzymology, nucleic acid chemistry, metabolism, and immunochemistry), structural biology, biophysics, computational biology (genomics, proteomics, bioinformatics), molecular genetics, molecular biology and molecular cell biology (signal transduction, intracellular traffic, regulation of cellular proliferation, cell-cell interactions) and systems biology. Studies on microbes, plants and animals at the molecular level are within the scope of FEBS Letters. Submitting Authors: Manuscripts can be submitted to FEBS Letters at: http://ees.elsevier.com/febsletters/ http://www.febsletters.org/?rss=yesElsevier Inc.en © 2010 Published by Elsevier Inc. All rights reserved. FEBS Letters0014-579358455 March 2010 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.febsletters.org/article/PIIS0014579310001237/abstract?rss=yesEditorial Board10.1016/S0014-5793(10)00123-7FEBS Letters 584, 5 (2010)2010-03-05FEBS Letters2010-03-055845S0014-5793(10)X0004-7iihttp://www.febsletters.org/article/PIIS0014579310001055/abstract?rss=yesEach year we look forward and plan new strategies for the journal. We also take the time to look at the changes that we have made over the last years and evaluate their impact on FEBS Letters.10.1016/j.febslet.2010.02.011FEBS Letters 584, 5 (2010)2010-02-08FEBS Letters2010-02-085845S0014-5793(10)X0004-7843844http://www.febsletters.org/article/PIIS0014579310000694/abstract?rss=yesAbstract: In every synapse, a large number of proteins interact with other proteins in order to carry out signaling and transmission in the central nervous system. In this study, we used interaction proteomics to identify novel synaptic protein interactions in mouse cortical membranes under native conditions. Using immunoprecipitation, immunoblotting, and mass spectrometry, we identified a number of novel synaptic protein interactions involving soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), calcium-activated potassium channel (BKCa) alpha subunits, and dynamin-1. These novel interactions offer valuable insight into the protein–protein interaction network in intact synapses that could advance understanding of vesicle trafficking, release, and recycling.Structured summary: MINT-7543319: Snap-25 (uniprotkb:P60879) physically interacts (MI:0914) with Tubulin beta-5 chain (uniprotkb:P99024), V-type proton ATPase subunit d 1 (uniprotkb:P51863), Zinc finger homeobox protein 3 (uniprotkb:Q61329), Tubulin beta-2A chain (uniprotkb:Q7TMM9), Synaptophysin (uniprotkb:Q62277), Gapdh (uniprotkb:P16858), Basement membrane-specific heparan sulfate proteoglycan core protein (uniprotkb:Q05793), Tubulin alpha-4A chain (uniprotkb:P68368), Tubulin alpha-1A chain (uniprotkb:P68369), Microtubule-associated protein 6 (uniprotkb:Q7TSJ2), AP-2 complex subunit beta (uniprotkb:Q9DBG3), Phosphofurin acidic cluster sorting protein 1 (uniprotkb:Q8K212), AP-2 complex subunit alpha-1 (uniprotkb:P17426), Kinesin-1 heavy chain (uniprotkb:Q617r68), Kinesin heavy chain isoform 5C (uniprotkb:P28738), Sodium/potassium-transporting ATPase subunit alpha-1 (uniprotkb:Q8VDN2) and Nck-associated protein 1 (uniprotkb:P28660) by anti bait co-immunoprecipitation (MI:0006)MINT-7543636: Calcium-activated potassium channel subunit alpha-1 (uniprotkb:Q08460) physically interacts (MI:0914) with AMP deaminase 2 (uniprotkb:Q9DBT5), Gamma-tubulin complex component 4 (uniprotkb:Q9D4F8), Gamma-tubulin complex component 2 (uniprotkb:Q921G8), Sodium/potassium-transporting ATPase subunit alpha-1 (uniprotkb:Q8VDN2), Phosphoinositide 3-kinase regulatory subunit 4 (uniprotkb:Q8VD65), Beta-centractin (uniprotkb:Q8R5C5), KIAA1107 (uniprotkb:Q80TK0), Sodium/potassium-transporting ATPase subunit alpha-2 (uniprotkb:Q6PIE5), Sodium/potassium-transporting ATPase subunit alpha-3 (uniprotkb:Q6PIC6), Phosphatidylinositol 3-kinase catalytic subunit type 3 (uniprotkb:Q6PF93), KH domain-containing, RNA-binding, signal transduction-associated protein 1 (uniprotkb:Q60749), Tubulin gamma-1 chain (uniprotkb:P83887), Heat shock cognate 71kDa protein (uniprotkb:P63017), Alpha-centractin (uniprotkb:P61164), Gamma-tubulin complex component 3 (uniprotkb:P58854), Dynamin-1 (uniprotkb:P39053), Kinesin heavy chain isoform 5C (uniprotkb:P28738), Elongation factor 1-alpha 1 (uniprotkb:P10126), Kinesin light chain 2 (uniprotkb:O88448), Activated CDC42 kinase 1 (uniprotkb:O54967) and Syntaxin-binding protein 1 (uniprotkb:O08599) by anti bait co-immunoprecipitation (MI:0006)MINT-7544031: Calcium-activated potassium channel subunit alpha-1 (uniprotkb:Q08460) physically interacts (MI:0914) with Syntaxin-binding protein 1 (uniprotkb:O08599), Syntaxin-1A (uniprotkb:O35526) and Dynamin-1 (uniprotkb:P39053) by anti bait co-immunoprecipitation (MI:0006)MINT-7543287: Syntaxin-1A (uniprotkb:O35526) physically interacts (MI:0914) with Vamp2 (uniprotkb:P63044), Snap-25 (uniprotkb:P60879), munc-18 (uniprotkb:O08599) and BKCa alpha subunit (uniprotkb:Q08460) by anti bait co-immunoprecipitation (MI:0006)MINT-7543972: Vamp-2 (uniprotkb:P63044) physically interacts (MI:0914) with Dynamin-1 (uniprotkb:P39053), Snap-25 (uniprotkb:P60879), Syntaxin-1A (uniprotkb:O35526) and Synaptophysin (uniprotkb:Q62277) by anti bait co-immunoprecipitation (MI:0006)MINT-7543728: Dynamin-1 (uniprotkb:P39053) physically interacts (MI:0914) with Clathrin heavy chain 1 (uniprotkb:Q68FD5) and Calcium-activated potassium channel subunit alpha-1 (uniprotkb:Q08460) by anti bait co-immunoprecipitation (MI:0006)MINT-7543905: Snap-25 (uniprotkb:P60879) physically interacts (MI:0914) with Syntaxin-1A (uniprotkb:O35526) and Vamp-2 (uniprotkb:P63044) by anti bait co-immunoprecipitation (MI:0006)MINT-7543476: Vamp-2 (uniprotkb:P63044) physically interacts (MI:0914) with Syntaxin-7 (uniprotkb:O70439), Neuronal membrane glycoprotein M6-a (uniprotkb:P35802), Syntaxin-1B (uniprotkb:P61264), Beta-soluble NSF attachment protein (uniprotkb:P28663), Guanine nucleotide-binding protein G(I)/G(S)/G(T) subunit beta-3 (uniprotkb:Q61011), Guanine nucleotide-binding protein G(I)/G(S)/G(T) subunit beta-1 (uniprotkb:P62874), Guanine nucleotide-binding protein G(o) subunit alpha (uniprotkb:P18872), V-type proton ATPase subunit d 1 (uniprotkb:P51863), Zinc transporter 3 (uniprotkb:P97441), Sodium/potassium-transporting ATPase subunit alpha-2 (uniprotkb:Q6PIE5), Sodium/potassium-transporting ATPase subunit alpha-3 (uniprotkb:Q6PIC6), Sodium/potassium-transporting ATPase subunit alpha-1 (uniprotkb:Q8VDN2), Potassium-transporting ATPase alpha chain 1 (uniprotkb:Q64436), Synaptophysin (uniprotkb:Q62277), Syntaxin-1A (uniprotkb:O35526) and Dynamin-1 (uniprotkb:P39053) by anti bait co-immunoprecipitation (MI:0006)Dynamin-1 co-associates with native mouse brain BKCa channels: Proteomics analysis of synaptic protein complexesGiorgio Gorini, Olga Ponomareva, Kevin S. Shores, Maria D. Person, R. Adron Harris, R. Dayne Mayfield10.1016/j.febslet.2009.12.061FEBS Letters 584, 5 (2010)2010-01-27FEBS Letters2010-01-275845S0014-5793(10)X0004-7Research Letters with SDA845851http://www.febsletters.org/article/PIIS0014579310000815/abstract?rss=yesAbstract: Thrombomodulin (TM) is an important vascular protective molecule that has anticoagulant, anti-inflammatory and anti-apoptotic properties. TM is downregulated in many thrombotic and vascular diseases. However, the mechanisms responsible for TM suppression are not completely understood. In this study, we investigated the mechanism involved in fatty acid-induced suppression of TM expression in human aortic endothelial cells. We found that palmitic acid inhibited TM expression through the JNK and p38 pathways. ATF-2, a JNK and p38 target transcription factor, was involved in the suppression. ATF-2 can bind to the TM promoter, recruit HDAC4 and form a transcriptional repression complex in the promoter, which may lead to chromatin condensation and transcriptional arrest. This study provides novel insight into TM down-regulation by stress signaling pathways.Structured summary: MINT-7555703, MINT-7555712: HDAC4 (uniprotkb:P56524) physically interacts (MI:0915) with ATF-2 (uniprotkb:P15336) by anti bait coimmunoprecipitation (MI:0006)JNK-ATF-2 inhibits thrombomodulin (TM) expression by recruiting histone deacetylase4 (HDAC4) and forming a transcriptional repression complex in the TM promoterYuanyuan Rong, Mei Zhang, Lin Zhang, Xing Li Wang, Ying H. Shen10.1016/j.febslet.2010.01.048FEBS Letters 584, 5 (2010)2010-01-29FEBS Letters2010-01-295845S0014-5793(10)X0004-7Research Letters with SDA852858http://www.febsletters.org/article/PIIS0014579310000803/abstract?rss=yesAbstract: A significant proportion of the human genome codes for transcription factors. Balanced activity of transcriptional activators and repressors is essential for normal development and differentiation. Previously we reported that a classical C2H2 zinc finger DNA binding protein ZNF652 functionally interacts with CBFA2T3 to repress transcription of genes containing ZNF652 consensus DNA binding sequence within the promoters of these target genes. Here we show that ZNF651 is a ZNF652 paralogue that shares a common DNA binding sequence with ZNF652 and represses target gene expression through the formation of a CBFA2T3–ZNF651 corepressor complex. It is suggested that CBFA2T3–ZNF651 and CBFA2T3–ZNF652 repressor complexes perform functionally similar roles in a tissue-specific manner.Structured summary: MINT-7555667: CBFA2T3 (uniprotkb:O75081) physically interacts (MI:0915) with ZNF651 (uniprotkb:Q9UFB7) by anti tag co-immunoprecipitation (MI:0007)CBFA2T3–ZNF651, like CBFA2T3–ZNF652, functions as a transcriptional corepressor complexRaman Kumar, Kelly M. Cheney, Paul M. Neilsen, Renèe B. Schulz, David F. Callen10.1016/j.febslet.2010.01.047FEBS Letters 584, 5 (2010)2010-01-29FEBS Letters2010-01-295845S0014-5793(10)X0004-7Research Letters with SDA859864http://www.febsletters.org/article/PIIS0014579310000943/abstract?rss=yesAbstract: Epstein–Barr virus latent membrane protein 1 (LMP1) activates NF-κB signaling pathways through two C-terminal regions, CTAR1 and CTAR2. Previous studies have demonstrated that BS69, a multidomain cellular protein, regulates LMP1/CTAR2-mediated NF-κB activation by interfering with the complex formation between TRADD and LMP1/CTAR2. Here, we found that BS69 directly interacted with the LMP1/CTAR1 domain and regulated LMP1/CTAR1-mediated NF-κB activation and subsequent IL-6 production. Regarding the mechanisms involved, we found that BS69 directly interacted with TRAF3, a negative regulator of NF-κB activation. Furthermore, small-interfering RNA-mediated knockdown experiments revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-κB activation.Structured summary: MINT-7556591: lmp1 (uniprotkb:P03230) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)MINT-7556646: TRAF6 (uniprotkb:Q9Y4K3) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)MINT-7556658, MINT-7556670: TRAF3 (uniprotkb:Q13114) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)MINT-7556607: TRAF1 (uniprotkb:Q13077) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)MINT-7556634: TRAF5 (uniprotkb:O00463) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)MINT-7556622: TRAF2 (uniprotkb:Q12933) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI:0007)BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activationOsamu Ikeda, Yuto Miyasaka, Ryuji Yoshida, Akihiro Mizushima, Kenji Oritani, Yuichi Sekine, Makoto Kuroda, Teruhito Yasui, Masahiro Fujimuro, Ryuta Muromoto, Asuka Nanbo, Tadashi Matsuda10.1016/j.febslet.2010.01.060FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters with SDA865872http://www.febsletters.org/article/PIIS0014579310001018/abstract?rss=yesAbstract: The myeloid translocation gene (MTG) homologue Nervy associates with PlexinA on the plasma membrane, where it functions as an A-kinase anchoring protein (AKAP) to modulate plexin-mediated semaphorin signaling in Drosophila. Mammalian MTG16b is an AKAP found in immune cells where plexin-mediated semaphorin signaling regulates immune responses. This study provides the first evidence that MTG16b is a dual AKAP capable of binding plexins. These interactions are selective (PlexinA1 and A3 bind MTG, while PlexinB1 does not) and can be regulated by PKA-phosphorylation. Collectively, these data suggest a possible mechanism for the targeting and integration of adenosine 3′,5′-cyclic monophosphate (cAMP) and semaphorin signaling in immune cells.Structured summary: MINT-7556975: PlexinA3 (uniprotkb:P51805) physically interacts (MI:0915) with MTG 16b (uniprotkb:O75081) by anti tag coimmunoprecipitation (MI:0007)MINT-7557008: RI alpha (uniprotkb:Q9DBC7) physically interacts (MI:0915) with MTG 16b (uniprotkb:O75081) by anti bait coimmunoprecipitation (MI:0006)MINT-7556989: MTG 16b (uniprotkb:O75081) physically interacts (MI:0915) with PlexinA3 (uniprotkb:P51805) by pull down (MI:0096)Myeloid translocation gene 16b is a dual A-kinase anchoring protein that interacts selectively with plexins in a phospho-regulated mannerSarah E. Fiedler, Robynn V. Schillace, Crystal J. Daniels, Sarah F. Andrews, Daniel W. Carr10.1016/j.febslet.2010.02.007FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters with SDA873877http://www.febsletters.org/article/PIIS0014579310001031/abstract?rss=yesAbstract: LMAN1 is a glycoprotein receptor, mediating transfer from the ER to the ER–Golgi intermediate compartment. Together with the co-receptor MCFD2, it transports coagulation factors V and VIII. Mutations in LMAN1 and MCFD2 can cause combined deficiency of factors V and VIII (F5F8D). We present the crystal structure of the LMAN1/MCFD2 complex and relate it to patient mutations. Circular dichroism data show that the majority of the substitution mutations give rise to a disordered or severely destabilized MCFD2 protein. The few stable mutation variants are found in the binding surface of the complex leading to impaired LMAN1 binding and F5F8D.Structured summary: MINT-7557086: lman1 (uniprotkb:P49257) and mcfd2 (uniprotkb:Q8NI22) bind (MI:0407) by X-ray crystallography (MI:0114)Crystal structure of the LMAN1-CRD/MCFD2 transport receptor complex provides insight into combined deficiency of factor V and factor VIIIEdvard Wigren, Jean-Marie Bourhis, Inari Kursula, Jodie E. Guy, Ylva Lindqvist10.1016/j.febslet.2010.02.009FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters with SDA878882http://www.febsletters.org/article/PIIS0014579310000219/abstract?rss=yesAbstract: NADH:ubiquinone oxidoreductase (complex I) is the entry enzyme of mitochondrial oxidative phosphorylation. To obtain the structural information on inhibitor/quinone binding sites, we synthesized [3H]benzophenone-asimicin ([3H]BPA), a photoaffinity analogue of asimicin, which belongs to the acetogenin family known as the most potent complex I inhibitor. We found that [3H]BPA was photo-crosslinked to ND2, ND1 and ND5 subunits, by the three dimensional separation (blue-native/doubled SDS–PAGE) of [3H]BPA-treated bovine heart submitochondrial particles. The cross-linking was blocked by rotenone. This is the first finding that ND2 was photo-crosslinked with a potent complex I inhibitor, suggesting its involvement in the inhibitor/quinone-binding.The ND2 subunit is labeled by a photoaffinity analogue of asimicin, a potent complex I inhibitorEiko Nakamaru-Ogiso, Hongna Han, Akemi Matsuno-Yagi, Ehud Keinan, Subhash C. Sinha, Takao Yagi, Tomoko Ohnishi10.1016/j.febslet.2010.01.004FEBS Letters 584, 5 (2010)2010-01-13FEBS Letters2010-01-135845S0014-5793(10)X0004-7Research Letters883888http://www.febsletters.org/article/PIIS0014579310000335/abstract?rss=yesAbstract: Using Arabidopsis plants transformed with a redox-sensing green fluorescent protein targeted to the cytosol (c-roGFP1), we have demonstrated, in real time, measurements of reversible changes of redox status in the cytosol of plants subjected to a gradual water-stress, followed by re-watering. Plants sensed water stress, and changed the redox potential of their cytosol to a more oxidized value after a gradually-imposed water stress. Small variations in the cytosol redox potential and ascorbate (AA) values suggest that this parameter was tightly regulated. The re-watering was paralleled by a return of water stress, redox potential and ascorbate to initial values, showing the reversibility of water stress and its consequences.Use of a redox-sensing GFP (c-roGFP1) for real-time monitoring of cytosol redox status in Arabidopsis thaliana water-stressed plantsT. Jubany-Mari, L. Alegre-Batlle, K. Jiang, L.J. Feldman10.1016/j.febslet.2010.01.014FEBS Letters 584, 5 (2010)2010-01-14FEBS Letters2010-01-145845S0014-5793(10)X0004-7Research Letters889897http://www.febsletters.org/article/PIIS0014579310000359/abstract?rss=yesAbstract: Biochemical circadian oscillation of KaiC phosphorylation, by mixing three Kai proteins and ATP, has been proven to be the central oscillator of the cyanobacterial circadian clock. In vivo, the intracellular levels of KaiB and KaiC oscillate in a circadian fashion. By scrutinizing KaiC phosphorylation rhythm in a wide range of Kai protein concentrations, KaiA and KaiB were found to be “parameter-tuning” and “state-switching” regulators of KaiC phosphorylation rhythm, respectively. Our results also suggest a possible entrainment mechanism of the cellular circadian clock with the circadian variation of intracellular levels of Kai proteins.In vitro regulation of circadian phosphorylation rhythm of cyanobacterial clock protein KaiC by KaiA and KaiBMasato Nakajima, Hiroshi Ito, Takao Kondo10.1016/j.febslet.2010.01.016FEBS Letters 584, 5 (2010)2010-01-14FEBS Letters2010-01-145845S0014-5793(10)X0004-7Research Letters898902http://www.febsletters.org/article/PIIS001457931000044X/abstract?rss=yesAbstract: The comparative gene identification-58 (CGI-58) gene, mutations of which are linked to Chanarin-Dorfman syndrome, encodes a protein of the α/β hydrolase domain subfamily. We report here a new alternative splicing isoform of the murine CGI-58 gene, termed mCGI-58S. Sequence comparison indicates the lack of second and third exons in this cDNA variant. While the full-length protein displayed perilipin-dependent localization to lipid droplets, mCGI-58S showed a predominant cytoplasmic staining when expressed in cells. mCGI-58S was incapable of activating adipose triglyceride lipase but retained the capacity to acylate lysophosphatidic acid. Overexpression of mCGI-58S failed to promote lipid droplet turnover and loss of intracellular triacylglycerols. These results suggest that this splicing event may be involved in the regulation of lipid homeostasis.Identification of a novel splicing isoform of murine CGI-58Xingyuan Yang, Xin Lu, Jun Liu10.1016/j.febslet.2009.12.058FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters903910http://www.febsletters.org/article/PIIS0014579310000451/abstract?rss=yesAbstract: Recent studies have revealed that bacteria target stem cells for long-term survival in a Drosophila model. However, in mammalian models, little is known about bacterial infection and intestinal stem cells. Our study aims at understanding bacterial regulation of the intestinal stem cell in a Salmonella colitis mouse model. We found that Salmonella activates the Wnt/β-catenin signaling pathway that is known to regulate stem cells. We identified Salmonella protein AvrA that modulates Wnt signaling including upregulating Wnt expression, modifying β-catenin, increasing total β-catenin expression, and activating Wnt/β-catenin transcriptional activity in the intestinal epithelial cells. The numbers of stem cells and proliferative cells increased in the intestine infected with Salmonella expressing AvrA. Our study provides insights into bacterial infection and stem cell maintenance.Salmonella regulation of intestinal stem cells through the Wnt/β-catenin pathwayXingyin Liu, Rong Lu, Shaoping Wu, Jun Sun10.1016/j.febslet.2010.01.024FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters911916http://www.febsletters.org/article/PIIS0014579310000463/abstract?rss=yesAbstract: Hydrogen peroxide production by the NADPH oxidase Duox1 occurs during activation of respiratory epithelial cells stimulated by purified bacterial ligands, such as lipopolysaccharide. Here, we characterize Duox activation using intact bacterial cells of several airway pathogens. We found that only Pseudomonas aeruginosa, not Burkholderia cepacia or Staphylococcus aureus, triggers H2O2 production in bronchial epithelial cells in a calcium-dependent but predominantly ATP-independent manner. Moreover, by comparing mutant Pseudomonas strains, we identify several virulence factors that participate in Duox activation, including the type-three secretion system. These data provide insight on Duox activation by mechanisms unique to P. aeruginosa.Characterization of hydrogen peroxide production by Duox in bronchial epithelial cells exposed to Pseudomonas aeruginosaBalázs Rada, Thomas L. Leto10.1016/j.febslet.2010.01.025FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters917922http://www.febsletters.org/article/PIIS0014579310000517/abstract?rss=yesAbstract: We found that both wild type and Nrf3 (NF-E2-related factor 3) deficient mice are sensitive to BHT single administration exhibiting respiratory distress and considerably lose body weight following treatment. At time of sacrifice, the BHT-treated Nrf3−/− mice had lost significantly more body weight than their WT counterparts. In the lung, transcript levels of the transcription factors Nrf1, Nrf2 and Nrf3 were differentially regulated by BHT treatment. In addition, genes implicated in adipogenesis were repressed following BHT exposure in the white adipose tissue. Together, our data provide the first evidence that BHT exposure not only affects lung function but also leads to impaired adipogenesis in adipocytes.Nrf3-deficient mice are not protected against acute lung and adipose tissue damages induced by butylated hydroxytolueneGrégory Chevillard, Zaynab Nouhi, Derjuga Anna, Marilène Paquet, Volker Blank10.1016/j.febslet.2010.01.028FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters923928http://www.febsletters.org/article/PIIS0014579310000529/abstract?rss=yesAbstract: ClpB is a member of the AAA+ superfamily that forms a ring-shaped homohexamer. Each protomer contains two nucleotide binding domains arranged in two rings that hydrolyze ATP. We extend here previous studies on ClpB nucleotide utilization requirements by using an experimental approach that maximizes random incorporation of different subunits into the protein hexamer. Incorporation of one subunit unable to bind or hydrolyze ATP knocks down the chaperone activity, while the wt hexamer can accommodate two mutant subunits that hydrolyze ATP in only one protein ring. Four subunits seem to build the functional cooperative unit, provided that one of the protein rings contains active nucleotide binding sites.Nucleotide utilization requirements that render ClpB active as a chaperoneUrko del Castillo, José Ángel Fernández-Higuero, Sergio Pérez-Acebrón, Fernando Moro, Arturo Muga10.1016/j.febslet.2010.01.029FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters929934http://www.febsletters.org/article/PIIS0014579310000530/abstract?rss=yesAbstract: We have studied the formation of histone Hv1–DNA complexes using an acoustic biosensor and AFM imaging. Our results show that DNA and histone molecules aggregate into amorphous accumulations which form a compact rigid layer on the sensor’s surface. By measuring changes in the acoustic wave amplitude, it was possible to titrate surface bound DNA with Hv1 and discriminate between DNA molecules of different size and shape. From the kinetic analysis of real time data, Keq was found equal to 3×105M−1.Characterization of DNA–Hv1 histone interactions; discrimination of DNA size and shapeGeorge Papadakis, Achilleas Tsortos, Konstantinos Mitsakakis, Electra Gizeli10.1016/j.febslet.2010.01.030FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters935940http://www.febsletters.org/article/PIIS0014579310000542/abstract?rss=yesAbstract: Breitling et al. introduced a statistical technique, the rank product method, for detecting differentially regulated genes in replicated microarray experiments. The technique has achieved widespread acceptance and is now used more broadly, in such diverse fields as RNAi analysis, proteomics, and machine learning. In this note, we relate the rank product method to linear rank statistics and provide an alternative derivation of distribution theory attending the rank product method.Comments on the rank product method for analyzing replicated experimentsJames A. Koziol10.1016/j.febslet.2010.01.031FEBS Letters 584, 5 (2010)2010-01-20FEBS Letters2010-01-205845S0014-5793(10)X0004-7Research Letters941944http://www.febsletters.org/article/PIIS0014579310000566/abstract?rss=yesAbstract: The RNA silencing suppressor 2b protein of Cucumber mosaic virus (CMV) is difficult to produce in Escherichia coli. We compared two CMV 2b proteins that differ in their toxicity against E. coli and found that the acidic amino acid residues in the C-terminal significantly affected the toxicity and expression level of the protein in E. coli. In addition, in a DNA-binding assay, 2b had the ability to bind to DNA, and this ability was affected by the charge on the C-terminal residues of 2b. We concluded that the C-terminal residues were important for 2b’s DNA-binding ability, which may partly explain the toxicity of the protein.The C-terminal residues of the 2b protein of Cucumber mosaic virus are important for efficient expression in Escherichia coli and DNA-bindingKae Sueda, Hanako Shimura, Ayano Meguro, Takeshi Uchida, Jun-ichi Inaba, Chikara Masuta10.1016/j.febslet.2010.01.033FEBS Letters 584, 5 (2010)2010-01-21FEBS Letters2010-01-215845S0014-5793(10)X0004-7Research Letters945950http://www.febsletters.org/article/PIIS0014579310000402/abstract?rss=yesAbstract: The GroEL/GroES protein folding chamber is formed and dissociated by ATP binding and hydrolysis. ATP hydrolysis in the GroES-bound (cis) ring gates entry of ATP into the opposite unoccupied trans ring, which allosterically ejects cis ligands. While earlier studies suggested that hydrolysis of cis ATP is the rate-limiting step of the cycle (t½∼10s), a recent study suggested that ADP release from the cis ring may be rate-limiting (t½∼15–20s). Here we have measured ADP release using a coupled enzyme assay and observed a t½ for release of ⩽4–5s, indicating that this is not the rate-limiting step of the reaction cycle.ATP-triggered ADP release from the asymmetric chaperonin GroEL/GroES/ADP7 is not the rate-limiting step of the GroEL/GroES reaction cycleNavneet K. Tyagi, Wayne A. Fenton, Arthur L. Horwich10.1016/j.febslet.2010.01.021FEBS Letters 584, 5 (2010)2010-01-18FEBS Letters2010-01-185845S0014-5793(10)X0004-7Research Letters951953http://www.febsletters.org/article/PIIS0014579310000578/abstract?rss=yesAbstract: Mitochondrial apoptotic pathway is precisely controlled by BCL-2 family. Complex interactions of BCL-2 family proteins constitute a bistable switch of which detailed experimental and theoretical delineation remains elusive. In this paper, combined approaches were used to explore the bistability of Bax activation switch. We found that Bax activation is indeed in an ‘all-or-none’ manner. The ‘variable-delay, snap-action’ nature for Bax activation is further explored theoretically. We suggest that bistability is largely attributed to topological structure and shows considerable robustness. Therefore, our study characterizes dynamics and sensitivities in intrinsic apoptotic pathway.Evaluating bistability of Bax activation switchTingzhe Sun, Xuzhu Lin, Yinna Wei, Yichen Xu, Pingping Shen10.1016/j.febslet.2010.01.034FEBS Letters 584, 5 (2010)2010-01-21FEBS Letters2010-01-215845S0014-5793(10)X0004-7Research Letters954960http://www.febsletters.org/article/PIIS0014579310000591/abstract?rss=yesAbstract: Here we report that miR-26b is involved in COX-2 overexpression in desferrioxamine (DFOM)-treated carcinoma of nasopharyngeal epithelial (CNE) cells. The level of miR-26b in DFOM-treated CNE cells is inversely proportional to the expression level of the COX-2 protein. Overexpression of miR-26b in DFOM-treated CNE cells inhibits cell proliferation. A luciferase reporter gene experiment suggests that the 3′ untranslated region of COX-2 carries a binding site for miR-26b. Overexpression of miR-26b marginally reduces the levels of COX-2 protein in DFOM-treated CNE cells. Moreover, knockdown of COX-2 expression had a similar effect to overexpression of miR-26b. Taken together, these results suggest that miR-26b regulates COX-2 expression in DFOM-treated cells.MiRNA-26b regulates the expression of cyclooxygenase-2 in desferrioxamine-treated CNE cellsYanhong Ji, Yonghong He, Le Liu, Xingyuan Zhong10.1016/j.febslet.2010.01.036FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters961967http://www.febsletters.org/article/PIIS0014579310000633/abstract?rss=yesAbstract: C1qTNF-related proteins (CTRPs) are involved in diverse processes including metabolism, inflammation host defense, apoptosis, cell differentiation, autoimmunity, hibernation, and organogenesis. However, the physiological role of CTRP6 remains poorly understood. Here we demonstrate that the globular domain of CTRP6 mediates the phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) in skeletal muscle cells. In parallel with the activation of AMPK, CTRP6 induces the phosphorylation of acetyl coenzyme A carboxylase (ACC) and fatty acid oxidation in myocytes. Thus, CTRP6 plays a role in fatty acid metabolism via the AMPK-ACC pathway.C1qTNF-related protein-6 mediates fatty acid oxidation via the activation of the AMP-activated protein kinaseWan Lee, Mi-Jin Kim, Eun-Ju Park, Young-Jin Choi, Seung-Yoon Park10.1016/j.febslet.2010.01.040FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters968972http://www.febsletters.org/article/PIIS0014579310000645/abstract?rss=yesAbstract: The peridinin–chlorophyll a-protein (PCP) from dinoflagellates is a soluble light harvesting antenna which gathers incoming photons mainly by the carotenoid peridinin. In PCPs reconstituted with different chlorophylls, the peridinin to chlorophyll energy transfer rates are well predicted by a Förster-like theory, but only if the pigment arrangements are identical in all PCPs. We have determined the X-ray structures of PCPs reconstituted with Chlorophyll-b (Chl-b), Chlorophyll-d (Chl-d) and Bacteriochlorophyll-a (BChl-a) to resolutions ⩽2Å. In all three cases the pigment arrangements are essentially the same as in native PCP. Hydrogen bonding is not responsible for preferential incorporation of “non-native” chlorophylls over Chl-a.X-ray structures of the peridinin–chlorophyll-protein reconstituted with different chlorophyllsTim Schulte, Roger G. Hiller, Eckhard Hofmann10.1016/j.febslet.2010.01.041FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters973978http://www.febsletters.org/article/PIIS0014579310000657/abstract?rss=yesAbstract: We determined the kinetics of the reaction of human neuronal enolase and yeast enolase 1 with the slowly-reacting chromophoric substrate d-tartronate semialdehyde phosphate (TSP), each in tris (tris (hydroxymethyl) aminomethane) and another buffer at several Mg2+ concentrations, 50 or 100μM, 1mM and 30mM. All data were biphasic, and could be satisfactorily fit, assuming either two successive first-order reactions or two independent first-order reactions. Higher Mg2+ concentrations reduce the relative magnitude of the slower reaction. The results are interpreted in terms of a catalytically significant interaction between the two subunits of these enzymes.Stopped-flow studies of the reaction of d-tartronate semialdehyde-2-phosphate with human neuronal enolase and yeast enolase 1John M. Brewer, Jared S. McKinnon, Robert S. Phillips10.1016/j.febslet.2010.01.042FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters979983http://www.febsletters.org/article/PIIS0014579310000682/abstract?rss=yesAbstract: Keratin 8 and 18 are simple epithelial intermediate filament (IF) proteins, whose expression is differentiation- and tissue-specific, and is maintained during tumorigenesis. Vimentin IF is often co-expressed with keratins in cancer cells. Recently, IF have been proposed to be involved in signaling pathways regulating cell growth, death and motility. The PI3K/Akt pathway plays a pivotal role in these processes. Thus, we investigated the role of Akt (1 and 2) in regulating IF expression in different epithelial cancer cell lines. Over-expression of Akt1 increases K8/18 proteins. Akt2 up-regulates K18 and vimentin expression by an increased mRNA stability. To our knowledge, these results represent the first indication that Akt isoforms regulate IF expression and support the hypothesis that IFs are involved in PI3K/Akt pathway.Akt isoforms regulate intermediate filament protein levels in epithelial carcinoma cellsAnne-Marie Fortier, Céline Van Themsche, Éric Asselin, Monique Cadrin10.1016/j.febslet.2010.01.045FEBS Letters 584, 5 (2010)2010-01-27FEBS Letters2010-01-275845S0014-5793(10)X0004-7Research Letters984988http://www.febsletters.org/article/PIIS0014579310000669/abstract?rss=yesAbstract: The small regulator SipA, interacts with the ATP-binding domain of non-bleaching sensor histidine kinase (NblS), the most conserved histidine kinase in cyanobacteria. NblS regulates photosynthesis and acclimation to a variety of environmental conditions. We show here that SipA is a highly stable protein in a wide pH range, with a thermal denaturation midpoint of 345K. Circular dichroism and 1D 1H NMR spectroscopies, as well as modelling, suggest that SipA is a β-II class protein, with short strands followed by turns and long random-coil polypeptide patches, matching the SH3 fold. The experimentally determined m-value and the heat capacity change upon thermal unfolding (ΔCp) closely agreed with the corresponding theoretical values predicted from the structural model, further supporting its accuracy.The regulatory factor SipA is a highly stable β-II class protein with a SH3 foldMaría Luisa López-Redondo, Asunción Contreras, Alberto Marina, José L. Neira10.1016/j.febslet.2010.01.043FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters989994http://www.febsletters.org/article/PIIS0014579310000670/abstract?rss=yesAbstract: TNF-α-induced insulin resistance is associated with generation of reactive oxygen species (ROS). This study aims at defining the link between ROS production and hepatic insulin resistance. Treatment with TNF-α increased ROS generation through activating NADPH oxidase 3 (NOX3) in HepG2 hepatocytes. Down-regulation of NOX3 using siRNA prevented TNF-α-induced decrease of cellular glycogen. In the cells treated with TNF-α, there were NOX3-dependent activation of JNK, inhibition of IRS1 and phosphorylation of AKT/PKB and GSK. In conclusion, the effects of TNF-α on hepatic insulin resistance appear to be, at least in part, mediated by NOX3-derived ROS through a JNK pathway.NOX3-derived reactive oxygen species promote TNF-α-induced reductions in hepatocyte glycogen levels via a JNK pathwayLanfang Li, Qinghua He, Xiuqing Huang, Yong Man, Yingsheng Zhou, Shu Wang, Jianye Wang, Jian Li10.1016/j.febslet.2010.01.044FEBS Letters 584, 5 (2010)2010-01-25FEBS Letters2010-01-255845S0014-5793(10)X0004-7Research Letters9951000http://www.febsletters.org/article/PIIS0014579310000700/abstract?rss=yesAbstract: Hepatic inflammation is the key factor in non-alcoholic steatohepatitis (NASH) and promotes progression to liver damage. We recently identified dietary cholesterol as the cause of hepatic inflammation in hyperlipidemic mice. We now show that hepatic transcriptome responses are strongly dependent on cholesterol metabolism during diet-induced NASH and its inhibition by fenofibrate. Furthermore, we show that, despite doubling hepatic steatosis, pharmacological LXR activation reverses hepatic inflammation, in parallel with reversing hepatic cholesterol levels. Together, the results indicate a prominent role of cholesterol during the development, inhibition and reversal of hepatic inflammation in NASH and reveal potential new therapeutic strategies against NASH.Intrahepatic cholesterol influences progression, inhibition and reversal of non-alcoholic steatohepatitis in hyperlipidemic miceKristiaan Wouters, Marc van Bilsen, Patrick J. van Gorp, Veerle Bieghs, Dieter Lütjohann, Anja Kerksiek, Bart Staels, Marten H. Hofker, Ronit Shiri-Sverdlov10.1016/j.febslet.2010.01.046FEBS Letters 584, 5 (2010)2010-01-27FEBS Letters2010-01-275845S0014-5793(10)X0004-7Research Letters10011005http://www.febsletters.org/article/PIIS0014579310000827/abstract?rss=yesAbstract: The tumor suppressor Kruppel-like factor 6 (KLF6) is frequently inactivated in hepatocellular carcinoma (HCC). To unearth downstream transcriptional targets of KLF6, cDNA microarray analysis of whole liver was compared between KLF6+/+ and KLF6+/− mice. Pituitary tumor transforming gene 1 (PTTG1), an oncogene, was the most up-regulated transcript in KLF6+/− liver. In human HCCs, KLF6 mRNA was significantly decreased, associated with increased PTTG1. In HepG2, KLF6 transcriptionally repressed PTTG1 by direct promoter interaction. Whereas KLF6 downregulation by siRNA increased HepG2 proliferation, siRNA to PTTG1 was anti-proliferative. PTTG1 downregulation represents a novel tumor suppressor pathway of KLF6.Tumor suppressor activity of KLF6 mediated by downregulation of the PTTG1 oncogeneUrsula E. Lee, Zahra Ghiassi-Nejad, Andrew J. Paris, Steven Yea, Goutham Narla, Martin Walsh, Scott L. Friedman10.1016/j.febslet.2010.01.049FEBS Letters 584, 5 (2010)2010-01-29FEBS Letters2010-01-295845S0014-5793(10)X0004-7Research Letters10061010http://www.febsletters.org/article/PIIS0014579310000840/abstract?rss=yesAbstract: The crystal structure of the free form of IF1 from Mycobacterium tuberculosis has been determined at 1.47Å resolution. The structure adopts the expected OB fold and matches the high structural conservation among IF1 orthologues. In order to further explore the function of Mtb-IF1, we built a model of its interaction with the 30S ribosomal subunit based on the crystal structure of the complex from Thermus thermophilus. The model suggests that several functionally important side chain residues undergo large movements while the rest of the protein in complex shows only very limited conformational change as compared to its form in solution.Structure of translation initiation factor 1 from Mycobacterium tuberculosis and inferred binding to the 30S ribosomal subunitGeorgios N. Hatzopoulos, Jochen Mueller-Dieckmann10.1016/j.febslet.2010.01.051FEBS Letters 584, 5 (2010)2010-02-02FEBS Letters2010-02-025845S0014-5793(10)X0004-7Research Letters10111015http://www.febsletters.org/article/PIIS0014579310000888/abstract?rss=yesAbstract: We have recently demonstrated that reactive oxygen species (ROS) play an important role in RAW264.7 cell apoptosis induced by cationic liposomes composed of stearylamine (SA-liposomes). In this study, we investigated whether protein kinase Cδ PKCδ) is involved in apoptosis induced by cationic liposomes. Tyrosine phosphorylation, nuclear localization, and cleavage of PKCδ were observed following the treatment of cells with SA-liposomes, suggesting that SA-liposomes activate PKCδ. Rottlerin, a specific inhibitor of PKCδ, inhibited ROS generation and also suppressed apoptosis. Cell surface proteoglycans may contribute to PKCδ activation by SA-liposomes. These findings suggest that PKCδ is strongly associated with apoptosis induced by SA-liposomes.Involvement of protein kinase Cδ in induction of apoptosis by cationic liposomes in macrophage-like RAW264.7 cellsMasaya Arisaka, Tomoko Nakamura, Akiko Yamada, Yoichi Negishi, Yukihiko Aramaki10.1016/j.febslet.2010.01.055FEBS Letters 584, 5 (2010)2010-02-01FEBS Letters2010-02-015845S0014-5793(10)X0004-7Research Letters10161020http://www.febsletters.org/article/PIIS0014579310000852/abstract?rss=yesAbstract: The effect of the plastoquionone (PQ) pool oxidation state on minimum chlorophyll fluorescence was studied in the green alga Chlamydomonas reinhardtii. In wild type and a mutant strain that lacks both photosystems but retains light harvesting complexes, oxygen depletion induced a rise in minimum chlorophyll fluorescence. An increase in minimum fluorescence yield is also observed when the PQ pool becomes reduced in the presence of oxygen and after application of an ionophore that collapses the transmembrane proton gradient. Together these results indicate that minimum chlorophyll fluorescence is modulated by the PQ oxidation state.The redox state of the plastoquinone pool directly modulates minimum chlorophyll fluorescence yield in Chlamydomonas reinhardtiiMartin F. Hohmann-Marriott, Kenji Takizawa, Julian J. Eaton-Rye, Laurens Mets, Jun Minagawa10.1016/j.febslet.2010.01.052FEBS Letters 584, 5 (2010)2010-02-01FEBS Letters2010-02-015845S0014-5793(10)X0004-7Research Letters10211026http://www.febsletters.org/article/PIIS0014579310000876/abstract?rss=yesAbstract: The crystal structure of reduced tryparedoxin peroxidase shows Cys47 close to Gln82 and Trp137 and helix formation of residues 87 to 97 whereas the NMR structure of the reduced C76S mutant adopts a different conformation similar to the oxidized protein. Circular dichroism (CD), fluorescence and NMR spectroscopy reveal that the fully active C76S mutant differs from the wildtype (WT) enzyme mainly in its reduced form both in secondary structure content and Trp137 environment. This implies that Cys76 plays a critical role for the reduced enzyme assuming different conformational states and that the catalytic triad may only be necessary as short-lived intermediate during catalysis.The conserved Cys76 plays a crucial role for the conformation of reduced glutathione peroxidase-type tryparedoxin peroxidaseClaudia Muhle-Goll, Florian Füller, Anne S. Ulrich, R. Luise Krauth-Siegel10.1016/j.febslet.2010.01.054FEBS Letters 584, 5 (2010)2010-02-01FEBS Letters2010-02-015845S0014-5793(10)X0004-7Research Letters10271032http://www.febsletters.org/article/PIIS001457931000092X/abstract?rss=yesAbstract: The activation of cysteine-aspartic proteases or caspases and the dynamic arrangement of cytoskeletal components are crucial during apoptosis. Here we describe the fate of Fas downstream of the FasL-induced internalization step, including formation of caspase-dependent SDS-stable Fas complexes, which is mediated by cytoskeleton integrity. We show, in particular, that following FasL treatment, the Fas lower aggregate complex can be co-immunoprecipitated with tubulin and an active form of caspase-8 and that this interaction contributes to the propagation of FasL-induced cell death. The importance of cytoskeletal components during FasL-induced apoptosis is highlighted by our detection of a pool of microtubule-associated Fas complexes.A novel role of microtubular cytoskeleton in the dynamics of caspase-dependent Fas/CD95 death receptor complexes during apoptosisEszter Doma, Krittalak Chakrabandhu, Anne-Odile Hueber10.1016/j.febslet.2010.01.059FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters10331040http://www.febsletters.org/article/PIIS0014579310000980/abstract?rss=yesAbstract: Here we show a unique example of male infertility conferred by a gene knockout of the sperm-specific, pH-dependent SLO3 potassium channel. In striking contrast to wild-type sperm which undergo membrane hyperpolarization during capacitation, we found that SLO3 mutant sperm undergo membrane depolarization. Several defects in SLO3 mutant sperm are evident under capacitating conditions, including impaired motility, a bent “hairpin” shape, and failure to undergo the acrosome reaction (AR). The failure of AR is rescued by valinomycin which hyperpolarizes mutant sperm. Thus SLO3 is the principal potassium channel responsible for capacitation-induced hyperpolarization, and membrane hyperpolarization is crucial to the AR.The SLO3 sperm-specific potassium channel plays a vital role in male fertilityCelia M. Santi, Pablo Martínez-López, José Luis de la Vega-Beltrán, Alice Butler, Arturo Alisio, Alberto Darszon, Lawrence Salkoff10.1016/j.febslet.2010.02.005FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters10411046http://www.febsletters.org/article/PIIS0014579310000979/abstract?rss=yesAbstract: Using conservation of synteny I show how the four thymosins expressed by teleost fish are related to the three of tetrapods, which is not evident from their protein sequences. This clarification was aided by identification of a novel thymosin of reptilians that replaces the β10 thymosin of mammals. Recent reconstruction of the ancestral vertebrate genome suggests that divergence of β-thymosins began with duplication preceding the two rounds of whole genome duplication.Vertebrate β-thymosins: Conserved synteny reveals the relationship between those of bony fish and of land vertebratesJohn Edwards10.1016/j.febslet.2010.02.004FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters10471053http://www.febsletters.org/article/PIIS0014579310000992/abstract?rss=yesAbstract: aP2-Cre mice have amply been used to generate conditional adipose selective inactivation of important signaling molecules. We show that the efficiency of Cre mediated recombination in adipocytes and adipose selectivity is not always guaranteed. In particular, Cre activity was found in ganglia of the peripheral nervous system (PNS), in adrenal medulla and in neurons throughout the central nervous system (CNS). Because these tissues have an important impact on adipose tissue, care should be taken when using aP2-Cre mice to define the role of the targeted genes in adipose tissue function.Ectopic recombination in the central and peripheral nervous system by aP2/FABP4-Cre mice: Implications for metabolism researchKatrin Martens, Astrid Bottelbergs, Myriam Baes10.1016/j.febslet.2010.01.061FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters10541058http://www.febsletters.org/article/PIIS0014579310001043/abstract?rss=yesAbstract: The molecular mechanics property is the foundation of many characters of proteins. Based on intramolecular hydrophobic force network, the representative family character underlying a protein’s mechanics property is described by a simple two-letter scheme. The tendency of a sequence to become a member of a protein family is scored according to this mathematical representation. Remote homologs of the WW-domain family could be easily designed using such a mechanistic signature of protein homology. Experimental validation showed that nearly all artificial homologs have the representative folding and bioactivity of their assigned family. Since the molecular mechanics property is the only consideration in this study, the results indicate its possible role in the generation of new members of a protein family during evolution.Generating artificial homologous proteins according to the representative family character in molecular mechanics properties – an attempt in validating an underlying rule of protein evolutionXin Liu, Ya-Pu Zhao10.1016/j.febslet.2010.02.010FEBS Letters 584, 5 (2010)2010-02-05FEBS Letters2010-02-055845S0014-5793(10)X0004-7Research Letters10591065http://www.febsletters.org/article/PIIS0014579310001067/abstract?rss=yesAbstract: Inositol requiring enzyme-1α (IRE1α) is an ER-located transmembrane RNase whose activation leads to the production of the transcription factor X-box binding protein 1 (XBP1). Recently, we showed that the IRE1α–XBP1 pathway plays an essential role in the placenta. However, details of its function remain unclear. To address this point, we searched for IRE1α- or XBP1-regulated genes in the placenta, and identified the CEA family as a novel target of the IRE1α–XBP1 pathway. Moreover, PSG genes, which also belong to the CEA family, were up-regulated by XBP1. We have therefore identified a new aspect of the physiological function of the IRE1α–XBP1 pathway in the placenta.Positive contribution of the IRE1α–XBP1 pathway to placental expression of CEA family genesDaisuke Oikawa, Ryoko Akai, Takao Iwawaki10.1016/j.febslet.2010.02.012FEBS Letters 584, 5 (2010)2010-02-08FEBS Letters2010-02-085845S0014-5793(10)X0004-7Research Letters10661070http://www.febsletters.org/article/PIIS0014579310001080/abstract?rss=yesAn unfortunate error occurred in the first sentence of the second paragraphin the Introduction. The sentence “The phosphagen kinase family includes the well-studied creatine kinase (CK) found only in vertebrates and arginine kinase (AK), which is most widely distributed in invertebrates, being present in deuterostomes, protostomes, basal metazoans, and some protozoans [3]”should read “The phosphagen kinase family includes the well-studied creatine kinase (CK), the sole PK in vertebrates and arginine kinase (AK), which is most widely distributed in invertebrates, being present in deuterostomes, protostomes, basal metazoans, and some protozoans [3].”Corrigendum to“Molecular cloning and characterization and kinetic properties of a novel two-domain taurocyamine kinase from the lung fluke Paragonimus westermani” [FEBS Lett. 583 (2009) 2218–2224]Blanca R. Jarilla, Shinji Tokuhiro, Mitsuru Nagataki, Sung-Jong Hong, Kouji Uda, Tomohiko Suzuki, Takeshi Agatsuma10.1016/j.febslet.2010.02.014FEBS Letters 584, 5 (2010)2010-02-10FEBS Letters2010-02-105845S0014-5793(10)X0004-7Corrigendum10711071