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Nigerian Journal of Basic and Applied Sciences     Open Access   (Followers: 2)
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Nigerian Journal of Physiological Sciences     Open Access  
NJAS - Wageningen Journal of Life Sciences     Full-text available via subscription   (Followers: 1)
NMR in Biomedicine     Hybrid Journal   (Followers: 1)
Non-Genetic Inheritance     Open Access   (Followers: 1)
Nonlinear Biomedical Physics     Open Access  
Northern Territory Naturalist     Full-text available via subscription  

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Journal Cover Biochemistry and Cell Biology
   Journal TOC RSS feeds Export to Zotero [11 followers]  Follow    
   Full-text available via subscription Subscription journal
     ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
     Published by NRC Research Press Homepage  [18 journals]   [SJR: 1.488]   [H-I: 65]
  • Biochemistry and Cell Biology
    • Pages: iii - iii
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 5, Page iii-iii, October 2014.
      PubDate: Tue, 14 Oct 2014 11:37:26 GMT
      DOI: 10.1139/bcb-2014-0135
  • 35th Annual International Asilomar Chromatin & Chromosomes Conference
           / 35e conférence internationale annuelle d’Asilomar sur la
           chromatine et les chromosomes
    • Pages: v - v
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 5, Page v-v, October 2014.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 14 Oct 2014 11:37:04 GMT
      DOI: 10.1139/bcb-2014-0138
  • Biochemistry and Cell Biology
    • Pages: 1 - 30
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      PubDate: Fri, 19 Sep 2014 11:47:19 GMT
      DOI: 10.1139/bcb-2014-0111
  • Moringa oleifera leaf extract ameliorates alloxan-induced diabetes in rats
           by regeneration of β cells and reduction of pyruvate carboxylase
    • Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles. Moringa oleifera Lam. contains many active ingredients with nutritional and medicinal values. It is commonly used in folk medicine as an antidiabetic agent. The present study was designed to investigate how an aqueous extract from the leaves of M. oleifera reveals hypoglycemia in diabetic rats. M. oleifera leaf extract counteracted the alloxan-induced diabetic effects in rats as it normalized the elevated serum levels of glucose, triglycerides, cholesterol, and malondialdehyde, and normalized mRNA expression of the gluconeogenic enzyme pyruvate carboxylase in hepatic tissues. It also increased live body weight gain and normalized the reduced mRNA expression of fatty acid synthase in the liver of diabetic rats. Moreover, it restored the normal histological structure of the liver and pancreas damaged by alloxan in diabetic rats. This study revealed that the aqueous extract of M. oleifera leaves possesses potent hypoglycemic effects through the normalization of elevated hepatic pyruvate carboxylase enzyme and regeneration of damaged hepatocytes and pancreatic β cells via its antioxidant properties.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 04 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0081
  • Inhibitory effects of capsaicin on hepatic stellate cells and liver
    • Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles. Hepatic stellate cells (HSCs) play an important role in the process of liver fibrosis. In this study, we investigated the inhibitory effects of capsaicin on HSCs and liver fibrosis. Cultured HSCs were incubated with various concentrations of capsaicin. Cell proliferation was examined using a cell counting kit. Production of hydrogen peroxide was determined using a 2′,7′-dichlorofluorescin diacetate (DCFH-DA) assay. The mRNA and protein expression of target genes was analyzed by reverse transcription PCR and Western blot analysis, respectively. Cell apoptosis was evaluated by annexin V-FITC and propidium iodide (PI) costaining followed by flow cytometric analysis. A CCl4 rat liver fibrosis model was used to assess in vivo effects of capsaicin by histological examination and measurement of liver fibrosis markers, including hydroxyproline content, serum type III collagen, and hyaluronic acid (HA) levels. Our results show that capsaicin dose-dependently inhibited cell proliferation, suppressed cell activation, and decreased hydrogen peroxide production in cultured HSCs. Capsaicin reduced the mRNA levels of tissue inhibitors of metalloproteinase 1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in HSCs. Moreover, capsaicin-induced cell apoptosis was associated with increased expression of Bax, cytochrome c (cyt c), and caspase-3, but reduced levels of Bcl-2. The animal studies further revealed that capsaicin efficiently reduced the extent of liver fibrosis, inhibited HSC proliferation, and promoted cell apoptosis. Our findings suggest that capsaicin might inhibit fibrogenesis by inhibiting the activities of HSCs.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 04 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0036
  • Biochemistry and Cell Biology
    • Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      PubDate: Tue, 02 Sep 2014 11:15:53 GMT
      DOI: 10.1139/bcb-2014-0112
  • Astragalus membranaceus modulates Th1/2 immune balance and activates
           PPARγ in a murine asthma model
    • Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Astragalus membranaceus, a traditional Chinese herb, has been used to improve airway inflammation and asthma. The present study investigated whether A. membranaceus has immunotherapeutic effects on asthma, a chronic inflammatory mucosal disease that is associated with excess production of IgE, eosinophilia, T helper 2 (Th2) cytokines, and bronchial hyperresponsiveness. An ovalbumin (OVA)-induced, chronic inflammatory airway murine asthma model was used to examine the status of pulmonary inflammation after the administration of A. membranaceus. The IgE levels in serum and bronchoalveolar lavage fluid showed a tendency to decrease after the administration of A. membranaceus. The number of eosinophils decreased and infiltration of inflammatory cells and collagen deposition declined in lung sections after A. membranaceus administration. The RNA and protein levels of Th2 cytokines and the ratio of the GATA3/T-bet mRNA levels decreased after A. membranaceus treatment. Furthermore, the mRNA level of peroxisome proliferator-activated receptor γ (PPARγ), a nuclear hormone receptor, increased in the lung tissues of A. membranaceus–treated mice. Finally, an A. membranaceus water extract activated PPARγ activity in either human embryonic kidney 293 (HEK293) or A549 cells in a PPARγ-responsive element-containing luciferase reporter assay. These results indicate that A. membranaceus has an inhibitory effect on airway inflammation in a murine model of asthma through modulating the imbalanced relationship between Th1 and Th2 cytokines.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 02 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0008
  • The apelin receptor: physiology, pathology, cell signalling, and ligand
           modulation of a peptide-activated class A GPCR
    • Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles. The apelin receptor (AR or APJ) is a class A (rhodopsin-like) G-protein-coupled receptor with wide distribution throughout the human body. Activation of the AR by its cognate peptide ligand, apelin, induces diverse physiological effects including vasoconstriction and dilation, strengthening of heart muscle contractility, angiogenesis, and regulation of energy metabolism and fluid homeostasis. Recently, another endogenous peptidic activator of the AR, Toddler/ELABELA, was identified as having a crucial role in zebrafish (Danio rerio) embryonic development. The AR is also implicated in pathologies including cardiovascular disease, diabetes, obesity, and cancer, making it a promising therapeutic target. Despite its established importance, the precise roles of AR signalling remain poorly understood. Moreover, little is known about the mechanisms of peptide–AR activation. Additional complexity arises from modulation of the AR by 2 endogenous peptide ligands, both with multiple bioactive isoforms of variable length and distribution. The various apelin and Toddler/ELABELA isoforms may also produce distinct cellular effects. Further complexity arises through formation of functionally distinct heterodimers between the AR and other G-protein-coupled receptors. This minireview outlines key (patho)physiological actions of the AR, addresses what is known about signal transduction downstream of AR activation, and concludes by discussing unique properties of the endogenous peptidic ligands of the AR.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 20 Aug 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0072
  • Interaction between 2 extracellular loops influences the activity of the
           cystic fibrosis transmembrane conductance regulator chloride channel
    • Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles. Activity of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is thought to be controlled by cytoplasmic factors. However, recent evidence has shown that overall channel activity is also influenced by extracellular anions that interact directly with the extracellular loops (ECLs) of the CFTR protein. Very little is known about the structure of the ECLs or how substances interacting with these ECLs might affect CFTR function. We used patch-clamp recording to investigate the accessibility of cysteine-reactive reagents to cysteines introduced throughout ECL1 and 2 key sites in ECL4. Furthermore, interactions between ECL1 and ECL4 were investigated by the formation of disulfide crosslinks between cysteines introduced into these 2 regions. Crosslinks could be formed between R899C (in ECL4) and a number of sites in ECL1 in a manner that was dependent on channel activity, suggesting that the relative orientation of these 2 loops changes on activation. Formation of these crosslinks inhibited channel function, suggesting that relative movement of these ECLs is important to normal channel function. Implications of these findings for the effects of mutations in the ECLs that are associated with cystic fibrosis and interactions with extracellular substances that influence channel activity are discussed.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 20 Aug 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0066
  • Profibrogenic phenotype in caveolin-1 deficiency via differential
           regulation of STAT-1/3 proteins
    • Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Fibrosis underlies the pathogenesis of several human diseases, which can lead to severe injury of vital organs. We previously demonstrated that caveolin-1 expression is reduced in experimental fibrosis and that caveolin-1 exerts antiproliferative and antifibrotic effects in lung fibrosis models. The signal transducers and activators of transcription (STAT) proteins, STAT1 and STAT3, can be activated simultaneously. STAT1 can inhibit cell growth and promote apoptosis while STAT3 inhibits apoptosis. Here, we show that caveolin-1-deficient (cav-1−/−) lung fibroblasts display dramatically upregulated STAT3 activation in response to platelet-derived growth factor-BB and transforming growth factor-β stimuli, whereas STAT1 activation is undetectable. Downregulation of protein tyrosine phosphatase-1B played a role in the preferential activation of STAT3 in cav-1−/− fibroblasts. Genetic deletion of STAT3 by siRNA modulated the expression of genes involved in cell proliferation and fibrogenesis. Basal expression of α-smooth muscle actin was prominent in cav-1−/− liver and kidney, consistent with deposition of collagen in these organs. Collectively, we demonstrate that the antiproliferative and antifibrogenic properties of caveolin-1 in vitro are mediated by the balance between STAT1 and STAT3 activation. Deregulated STAT signaling associated with caveolin-1 deficiency may be relevant to proliferative disorders such as tissue fibrosis.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 06 Aug 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0075
  • Functional interdependence of NHE1 and merlin in human melanoma cells
    • Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles. Upregulation of the Na+/H+ exchanger isoform 1 (NHE1) has been correlated with tumor malignancy. In contrast, moesin-radixin-ezrin–like protein (merlin) is a tumor suppressor that protects from cancerogenesis. Merlin is highly related to the members of the ezrin, radixin, and moesin (ERM) protein family that are directly attached to and functionally linked with NHE1. In addition, merlin inhibits the MAPK cascade and the Rho-GTPases known to activate NHE1 activity. The present study investigates whether NHE1 expression and activity affect merlin or, conversely, whether merlin has an impact on NHE1 in human melanoma (MV3) cells. Indeed, features of merlin-deficient MV3 cells point to a functional link: merlin-deficient cells showed a decreased NHE1 expression and, paradoxically, an increase in NHE1 activity as measured upon cytosolic acidification (NH4Cl prepulse method). Loss of merlin also led to an elevated cell motility that could be further increased by NHE1 overexpression, whereas NHE1 overexpression alone had no effect on migration. In contrast, neither NHE1 expression nor its activity had an impact on merlin expression. These results suggest a novel tumor suppressor function of merlin in melanoma cells: the inhibition of the proto-oncogenic NHE1 activity, possibly including its downstream signaling pathways.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 06 Aug 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0041
  • Identification of a novel lysyl oxidase-like 2 alternative splicing
           isoform, LOXL2 Δe13, in esophageal squamous cell carcinoma
    • Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles. Lysyl oxidase-like 2 (LOXL2) participates in every stage of cancer progression and promotes invasion and metastasis. In this study, we identified a novel alternative splicing isoform of LOXL2, namely LOXL2 Δe13, which lacked exon 13. Deletion of exon 13 caused an open reading frame shift and produced a truncated protein. LOXL2 Δe13 was expressed ubiquitously in cell lines and tissues and was mainly localized to the cytoplasm. Although it showed impaired deamination enzymatic activity compared with full-length LOXL2, LOXL2 Δe13 promoted the cell mobility and invasion of esophageal squamous cell carcinoma (ESCC) cells to greater degrees. In further research on the mechanisms, gene expression profiling and signaling pathway analysis revealed that LOXL2 Δe13 induced the expression of MAPK8 without affecting the FAK, AKT, and ERK signaling pathways. RNAi-mediated knockdown of MAPK8 could block the cell migration promoted by LOXL2De13, but it had little effect on that of full-length LOXL2. Our data suggest that LOXL2 Δe13 modulates the effects of cancer cell migration and invasion through a different mechanism from that of full-length LOXL2 and that it may play a very important role in tumor carcinogenesis and progression.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 05 Aug 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0046
  • Computational study on the molecular mechanisms of drug resistance of
           Narlaprevir due to V36M, R155K, V36M+R155K, T54A, and A156T mutations of
           HCV NS3/4A protease
    • Pages: 1 - 13
      Abstract: Biochemistry and Cell Biology, e-First Articles. Narlaprevir is a novel NS3/4A protease inhibitor of hepatitis C virus (HCV), and it has been tested in a phase II clinical trial recently. However, distinct drug-resistance of Narlaprevir has been discovered. In our study, the molecular mechanisms of drug-resistance of Narlaprevir due to the mutations V36M, R155K, V36M+R155K, T54A, and A156T of NS3/4A protease have been investigated by molecular dynamics (MD) simulations, free energy calculations, and free energy decomposition analysis. The predicted binding free energies of Narlaprevir towards the wild-type and five mutants show that the mutations V36M, R155K, and T54A lead to low-level drug resistance and the mutations V36M+R155K and A156T lead to high-level drug resistance, which is consistent with the experimental data. The analysis of the individual energy terms indicates that the van der Waals contribution is important for distinguishing the binding affinities of these six complexes. These findings again show that the combination of different molecular modeling techniques is an efficient way to interpret the molecular mechanism of drug-resistance. Our work mainly elaborates the molecular mechanism of drug-resistance of Narlaprevir and further provides valuable information for developing novel, safer, and more potent HCV antiviral drugs in the near future.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 23 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0039
  • Characterization of human mutations in phosphorylatable amino acids of the
           cytosolic regulatory tail of SLC9A1
    • Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles. The NHE1 isoform of the mammalian Na+/H+ exchanger is a ubiquitous plasma membrane protein that regulates intracellular pH in cells by removing one intracellular proton in exchange for one extracellular sodium. Genetic defects in NHE1 have been shown to affect the growth and motor ability of mice, but mutations in humans have not been studied. NHE1 has a cytosolic C-terminal regulatory domain of approximately 300 amino acids. We investigated the functional effects of two human mutations found in the regulatory phosphorylatable amino acids Ser703 and Ser771. A Ser703Pro mutant protein had essentially the same activity, expression, and targeting as the wild type NHE1 protein. In contrast, the Ser771Pro protein had reduced activity and expression of NHE1 protein, though cell surface targeting was normal. In dual pulse assays the Ser771Pro mutant was not further activated by sustained intracellular acidosis but displayed an unusual activation by brief pulses of acidosis. The results demonstrate that the Ser771Pro human genetic mutation has significant and detrimental physiological effects on the activity of the NHE1 protein, SLC9A1.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 23 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0071
  • Diadenosine diphosphate (Ap2A) delays neutrophil apoptosis via the
           adenosine A2A receptor and cAMP/PKA pathway
    • Pages: 1 - 5
      Abstract: Biochemistry and Cell Biology, e-First Articles. Diadenosine polyphosphates have been shown to inhibit neutrophil apoptosis, but mechanisms of the antiapoptotic effect are not known. Diadenosine diphosphate (Ap2A) is the simplest naturally occurring diadenosine polyphosphate, and its effect on neutrophil apoptosis has not previously been investigated. Here we report that Ap2A delays spontaneous apoptosis of human neutrophils, and the effect is reversed by the adenosine A2A receptor antagonists SCH442416 and ZM241385. Ap2A induced an elevation of intracellular cAMP and the elevation was blocked by the adenosine A2A receptor antagonists. The antiapoptotic effect of Ap2A was abrogated by 2′,5′-dideoxyadenosine, an inhibitor of adenylyl cyclase, and Rp-8-Br-cAMPS, an inhibitor of type I cAMP-dependent protein kinase A (PKA). Together, these results demonstrate that Ap2A delays neutrophil apoptosis via the adenosine A2A receptor and cAMP/PKA signaling axis.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 18 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0059
  • Oroxylin A exerts anti-inflammatory activity on lipopolysaccharide-induced
           mouse macrophage via Nrf2/ARE activation
    • Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles. Regulating inflammation could be an important measure for the effective treatment of cancer. Here we examine the mechanisms by which oroxylin A inhibits inflammation in RAW264.7 cells. The results demonstrate that pretreatment with oroxylin A (50, 100, and 150 μmol/L) inhibited lipopolysaccharide (LPS)-induced mRNA and protein expression of COX-2 and iNOS. In addition, oroxylin A significantly increased the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and NADP(H):quinone oxidoreductase (NQO1), induced Nrf2 translocation to the nucleus and up-regulated antioxidant response element (ARE)-luciferase reporter activity. Moreover, oroxylin A inhibited Nrf2 ubiquitination and proteasome activity. Transfection with Nrf2 siRNA knocked down Nrf2 expression and partially reversed oroxylin A-mediated inhibition of LPS-induced COX-2 and iNOS expression. Importantly, we showed for the first time that Nrf2 plays an important role in oroxylin A-suppressed inflammation in RAW264.7 cells. Uncovering the effect of oroxylin A on the regulation of Nrf2 signaling may be beneficial for developing new therapeutic strategies against inflammatory diseases.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 17 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0030
  • Ser9-phosphorylated GSK3β induced by 14-3-3ζ actively
           antagonizes cell apoptosis in a NF-κB dependent manner
    • Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles. The activity of glycogen synthase kinase beta (GSK3β) is mainly regulated by its Ser9 phosphorylation. It has been believed for a long time that Ser9 phosphorylation regulates the functions of GSK3β through inhibition of its kinase activity. In this study, we have confirmed the interaction of Ser9-phosphorylated GSK3β with 14-3-3ζ by using GST pull-down assays. We show that 14-3-3ζ enhances Ser9 phosphorylation of GSK3β by PKC. Surprisingly, using a NF-κB luciferase reporter system, we find that Ser9-phosphorylation of GSK3β promoted by 14-3-3ζ is critical for the activation of NF-κB pathway, which may thwart the pro-apoptotic activity of GSK3β. Inhibition of either NF-κB or GSK3β significantly abolishes the anti-apoptotic effect of 14-3-3ζ and Ser9-phosphorylated GSK3β, suggesting that Ser9-phosphorylated GSK3β actively antagonizes cell apoptosis in a NF-κB dependent manner.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 17 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0065
  • Breaking the cycle: the role of omega-3 polyunsaturated fatty acids in
           inflammation-driven cancers
    • Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles. Chronic inflammation is a cyclical, self-stimulating process. Immune cells called to sites of inflammation release pro-inflammatory signaling molecules that stimulate activation of inducible enzymes and transcription factors. These enzymes and transcription factors then stimulate production of signaling molecules that attract more immune cells and induce more enzymatic and transcriptional activity, creating a perpetual loop of inflammation. This self-renewing pool of inflammatory stimuli makes for an ideal tumor microenvironment, and chronic inflammation has been linked to oncogenesis, tumor growth, tumor cell survival, and metastasis. Three protein pathways in particular, nuclear factor kappa B (NF-kB), cyclooxygenase (COX), and lipoxygenase (LOX), provide excellent examples of the cyclical, self-renewing nature of chronic inflammation-driven cancers. NF-kB is an inducible transcription factor responsible for the expression of a vast number of inflammation and cancer related genes. COX and LOX convert omega-6 (n-6) and omga-3 (n-3) polyunsaturated fatty acids (PUFA) into pro- and anti-inflammatory signaling molecules. These signaling molecules stimulate or repress activity of all three of these pathways. In this review, we will discuss the pro- and anti-inflammatory functions of these fatty acids and their role in chronic inflammation and cancer progression.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 08 Jul 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2013-0127
  • Lessons from a red squirrel, mentors, and the pathway to success
    • Pages: 1 - 4
      Abstract: Biochemistry and Cell Biology, e-First Articles. In this article I will review my personal career path starting with how a red squirrel got me interested in research, and the vital role that mentors played in my pathway to success — a pathway that taught me many lessons that I would like to share with the reader, particularly graduate students and post-doctoral fellows who are just starting down their own unique pathways.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 23 Jun 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0058
  • Protein transport into the human ER and related diseases,
    • Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles. Protein transport into the human endoplasmic reticulum (ER) is relevant to the biogenesis of most soluble and membrane proteins of organelles, which are involved in endo- or exo-cytsosis. It involves amino-terminal signal peptides in the precursor polypeptides and various transport components in the cytosol plus the ER, and can occur co- or post-translationally. The two mechanisms merge at the level of the ER membrane, specifically at the level of the heterotrimeric Sec61 complex, which forms a dynamic polypeptide-conducting channel in the ER membrane. Since the mammalian ER is also the main intracellular calcium storage organelle, and the Sec61 complex is calcium permeable, the Sec61 complex is tightly regulated in its equilibrium between the closed and open conformations, or “gated”, by ligands, such as signal peptides of the transport substrates and the ER lumenal Hsp70-type molecular chaperone BiP. Furthermore, BiP binding to the incoming polypeptide contributes to the efficiency and unidirectionality of transport. Recent insights into the structure and dynamic equilibrium of the Sec61 complex have various mechanistic as well as medical implications.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 27 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0043
  • Import of ribosomal proteins into yeast mitochondria
    • Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles. Mitochondrial ribosomes of baker’s yeast contain at least 78 protein subunits. All but one of these proteins are nuclear-encoded, synthesized on cytosolic ribosomes, and imported into the matrix for biogenesis. The import of matrix proteins typically relies on N-terminal mitochondrial targeting sequences that form positively charged amphipathic helices. Interestingly, the N-terminal regions of many ribosomal proteins do not closely match the characteristics of matrix targeting sequences, suggesting that the import processes of these proteins might deviate to some extent from the general import route. So far, the biogenesis of only two ribosomal proteins, Mrpl32 and Mrp10, was studied experimentally and indeed showed surprising differences to the import of other preproteins. In this review article we summarize the current knowledge on the transport of proteins into the mitochondrial matrix, and thereby specifically focus on proteins of the mitochondrial ribosome.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 20 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0029
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