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  Subjects -> BIOLOGY (Total: 2603 journals)
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BIOLOGY (1322 journals)            First | 6 7 8 9 10 11 12 13 | Last

Mechanisms of Ageing and Development     Hybrid Journal   (Followers: 1)
Mechanisms of Development     Hybrid Journal   (Followers: 4)
m├ędecine/sciences     Full-text available via subscription   (Followers: 1)
Medical and Biological Engineering and Computing     Hybrid Journal   (Followers: 2)
Medical and Biological Sciences     Open Access  
Medical Engineering & Physics     Hybrid Journal   (Followers: 9)
Membrane Protein Transport     Full-text available via subscription   (Followers: 3)
Memoirs of the Association of Australasian Palaeontologists     Full-text available via subscription   (Followers: 2)
Metabolic Engineering     Hybrid Journal   (Followers: 6)
Metabolites     Open Access   (Followers: 1)
Metabolomics     Hybrid Journal   (Followers: 5)
Metallomics     Full-text available via subscription  
Methods     Hybrid Journal   (Followers: 11)
Methods in Cell Biology     Full-text available via subscription   (Followers: 7)
Methods in Cell Science     Hybrid Journal   (Followers: 3)
Methods in Ecology and Evolution     Partially Free   (Followers: 14)
Micologia Aplicada Internacional     Open Access  
Microarrays     Open Access  
Micron     Hybrid Journal  
Mitochondrial DNA     Hybrid Journal   (Followers: 3)
Mitochondrion     Hybrid Journal   (Followers: 3)
Modelling and Simulation in Engineering     Open Access   (Followers: 4)
Modelling and Simulation in Materials Science and Engineering     Hybrid Journal   (Followers: 7)
Molecular & Cellular Proteomics     Full-text available via subscription   (Followers: 7)
Molecular & Cellular Toxicology     Hybrid Journal   (Followers: 2)
Molecular and Biochemical Parasitology     Hybrid Journal   (Followers: 2)
Molecular and Cellular Biochemistry     Hybrid Journal   (Followers: 4)
Molecular and Cellular Biology     Full-text available via subscription   (Followers: 16)
Molecular Based Mathematical Biology     Open Access  
Molecular Biology     Hybrid Journal   (Followers: 10)
Molecular Biology and Evolution     Hybrid Journal   (Followers: 153)
Molecular Biology International     Open Access   (Followers: 3)
Molecular Biology of the Cell     Partially Free   (Followers: 15)
Molecular Biology Reports     Hybrid Journal   (Followers: 4)
Molecular Brain     Open Access   (Followers: 2)
Molecular Breeding     Hybrid Journal   (Followers: 6)
Molecular Cell     Full-text available via subscription   (Followers: 34)
Molecular Ecology     Hybrid Journal   (Followers: 16)
Molecular Ecology Resources     Hybrid Journal   (Followers: 8)
Molecular Genetics and Metabolism     Hybrid Journal   (Followers: 6)
Molecular Immunology     Hybrid Journal   (Followers: 13)
Molecular Membrane Biology     Hybrid Journal   (Followers: 1)
Molecular Neurobiology     Hybrid Journal   (Followers: 3)
Molecular Pain     Open Access  
Molecular Plant-Microbe Interactions     Partially Free   (Followers: 5)
Molecular Reproduction & Development     Hybrid Journal   (Followers: 7)
Molecular Therapy - Nucleic Acids     Open Access  
Molecules and Cells     Hybrid Journal   (Followers: 1)
Momona Ethiopian Journal of Science     Open Access   (Followers: 2)
Monoclonal Antibodies in Immunodiagnosis and Immunotherapy     Hybrid Journal  
Monographs of the Western North American Naturalist     Full-text available via subscription   (Followers: 1)
Moscow University Physics Bulletin     Hybrid Journal  
Movement Ecology     Open Access   (Followers: 4)
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis     Hybrid Journal   (Followers: 2)
Mutation Research/Genetic Toxicology and Environmental Mutagenesis     Hybrid Journal   (Followers: 8)
Mutation Research/Reviews in Mutation Research     Hybrid Journal   (Followers: 4)
Mycological Progress     Hybrid Journal   (Followers: 1)
Mycopathologia     Hybrid Journal   (Followers: 1)
Mycorrhiza     Hybrid Journal   (Followers: 5)
Mycoscience     Hybrid Journal   (Followers: 1)
Mycotoxin Research     Hybrid Journal   (Followers: 4)
NAMMCO Scientific Publications     Open Access  
Nano Reviews     Open Access   (Followers: 15)
Nano Today     Hybrid Journal   (Followers: 11)
Nanoscale Research Letters     Open Access   (Followers: 4)
Natural Hazards     Hybrid Journal   (Followers: 207)
Natural History     Full-text available via subscription   (Followers: 4)
Natural Product Research: Formerly Natural Product Letters     Hybrid Journal   (Followers: 1)
Natural Science     Open Access   (Followers: 9)
Nature     Full-text available via subscription   (Followers: 2227)
Nature Cell Biology     Full-text available via subscription   (Followers: 222)
Nature China     Full-text available via subscription   (Followers: 5)
Nature Digest     Full-text available via subscription   (Followers: 4)
Nature Protocols     Full-text available via subscription   (Followers: 40)
Nature Reviews Molecular Cell Biology     Full-text available via subscription   (Followers: 201)
Nature Structural & Molecular Biology     Full-text available via subscription   (Followers: 172)
Naturwissenschaften     Hybrid Journal   (Followers: 4)
Nematology     Hybrid Journal   (Followers: 2)
Nematropica     Open Access  
NeoBiota     Open Access   (Followers: 2)
Neotropical Ichthyology     Open Access  
Nepal Journal of Science and Technology     Open Access  
Neurobiology of Aging     Hybrid Journal   (Followers: 3)
Neurobiology of Disease     Hybrid Journal   (Followers: 3)
NeuroImmune Biology     Full-text available via subscription  
Neuroinformatics     Hybrid Journal   (Followers: 2)
Neuropeptides     Hybrid Journal   (Followers: 2)
Neuropsychobiology     Full-text available via subscription   (Followers: 3)
New Biotechnology     Hybrid Journal   (Followers: 4)
New Journal of Physics     Open Access   (Followers: 7)
New Phytologist     Hybrid Journal   (Followers: 11)
New Zealand Journal of Marine and Freshwater Research     Hybrid Journal   (Followers: 4)
Nigerian Journal of Basic and Applied Sciences     Open Access   (Followers: 2)
Nigerian Journal of Parasitology     Full-text available via subscription   (Followers: 1)
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  

  First | 6 7 8 9 10 11 12 13 | Last

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]
  • Ganglioside GM3 is required for caffeic acid phenethyl ester-induced
           megakaryocytic differentiation of human chronic myelogenous leukemia K562
           cells Ganglioside GM3 is required for caffeic acid phenethyl ester-induced
           megakaryocytic differentiation of human chronic myelogenous leukemia K562
           cells
    • Pages: 243 - 249
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 243-249, August 2014. The human chronic myelogenous cell line K562 has been used extensively as a model for the study of leukemia differentiation. We show here that treatment of K562 cells with caffeic acid phenethyl ester (CAPE) induced a majority of cells to differentiate towards the megakaryocytic lineage. Microscopy analysis showed that K562 cells treated with CAPE exhibited characteristic features of physiological megakaryocytic differentiation, including the presence of vacuoles and demarcation membranes. Differentiation of K562 cells treated with CAPE was also accompanied by a net increase in megakaryocytic markers. The transcriptional activity of lactosylceramide α-2,3-sialyltransferase (GM3 synthase) and synthesis of ganglioside GM3 were increased by CAPE treatment. The promoter analysis of GM3 synthase demonstrated that CAPE induced the expression of GM3 synthase mRNA via activation of the cAMP response element-binding protein (CREB), transcription factor in nucleus. Interestingly, the inhibition of ganglioside GM3 synthesis by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propranol (D-PDMP) and GM3 synthase-siRNA blocked the CAPE-induced expression of the megakaryocytic markers and differentiation of K562 cells. Taken together, these results suggest that CAPE induces ganglioside GM3-mediated megakaryocytic differentiation of human chronic myelogenous cells.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 13 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0015
       
  • Mechanism of a novel missense mutation, p.V174M, of the human connexin31
           (GJB3) in causing nonsyndromic hearing loss Mechanism of a novel missense
           mutation, p.V174M, of the human connexin31 (GJB3) in causing nonsyndromic
           hearing loss
    • Pages: 251 - 257
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 251-257, August 2014. Hearing loss is the most common sensory disorder, worldwide. In a recent study, we have identified a missense mutation, p.V174M, in the connexin 31 encoded by the GJB3 gene, in a patient with nonsyndromic hearing loss. However, the functional change in the CX31V174M mutant remains unknown. This study compared the intracellular distribution and assembly of the mutant CX31V174M with that of the wild-type (WT) CX31 in HeLa cells, and it examined the effect that the mutant protein had on those cells. A fluorescent localization assay of WT CX31 showed the typical punctuate pattern of a gap junction channel between the neighboring expression cells. Conversely, the p.V174M missense mutation resulted in the accumulation of the mutant protein in the lysosomes rather than in the cytoplasmic membrane. Moreover, dye transfer experiments have also demonstrated that the CX31V174M mutant did not form functional gap junction channels, probably due to the incorrect assembly or the altered properties of the CX31 channels. In addition, we found that CX31V174M-transfection can cause cell death by MTT assay. CX31V174M co-expressed with either CX31WT or CX26WT studies, suggested the impairment of the ability of CX26WT proteins to intracellular trafficking and targeting to the plasma membrane, but did not influence the trafficking of CX31WT. Based on these findings, we suggest that the CX31V174M mutant may have an effect on the formation and function of the gap junction, and CX31V174M has a trans-dominant negative effect on the function of wild types CX26. These results provide a novel molecular explanation for the role that GJB3 plays in hearing loss.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 15 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2013-0126
       
  • Comparison of the adipogenesis in intramuscular and subcutaneous
           adipocytes from Bamei and Landrace pigs Comparison of the adipogenesis in
           intramuscular and subcutaneous adipocytes from Bamei and Landrace pigs
    • Pages: 259 - 267
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 259-267, August 2014. Fat deposition is a complex process involving proliferation, differentiation, and lipogenesis of adipocytes. Bamei and Landrace are considered to represent fat- and lean-type pig breeds. Subcutaneous (SC) and intramuscular (IM) pre-adipocytes were cultured to compare the proliferation and lipogenesis in these breeds. The differentiated adipocytes were exposed to glucose or insulin to evaluate their effects on lipogenesis and lipogenic gene expression. Pre-adipocytes proliferated dramatically faster in SC vs. IM cells, and in Bamei vs. Landrace breeds. Lipogenesis and lipogenic gene expression had a greater increase in Bamei than in Landrace, and in SC vs. IM in the process of differentiation. Glucose markedly promoted lipogenesis and lipogenic gene expression in differentiated adipocytes. The stimulation of high-glucose levels on lipogenesis and ChREBP and lipogenic gene expression was higher in SC than IM adipocytes, and in Bamei vs. Landrace. Insulin largely increased SREBP-1c expression, however it modestly stimulated lipogenesis and lipogenic gene expression, and there was no difference between cell populationsor between breeds. These data demonstrated that regional and varietal differences obviously existed in the development of porcine adipocytes. The proliferation and differentiation capacity of pre-adipocytes, and the adipocyte lipogenesis stimulated by glucose, are stronger in Bamei than Landrace, and in SC vs. IM adipocytes independent of breed.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 22 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0019
       
  • Small expression tags enhance bacterial expression of the first three
           transmembrane segments of the apelin receptor Small expression tags
           enhance bacterial expression of the first three transmembrane segments of
           the apelin receptor
    • Pages: 269 - 278
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 269-278, August 2014. G-protein coupled receptors (GPCRs) are inherently dynamic membrane protein modulators of various important cellular signaling cascades. The apelin receptor (AR or APJ) is a class A GPCR involved in numerous physiological processes, implicated in angiogenesis during tumour formation and as a CD4 co-receptor for entry of human immunodeficiency virus type 1 (HIV-1) to cells. Due to the lack of efficient methods to produce full-length GPCRs enriched with nuclear magnetic resonance (NMR) active 15N, 13C, and (or) 2H isotopes, small GPCR fragments typically comprising 1–2 transmembrane segments are frequently studied using NMR spectroscopy. Here, we report successful overexpression of transmembrane segments 1–3 of AR (AR_TM1-3) in the C41(DE3) strain of Escherichia coli using an AT-rich gene tag previously reported to enhance cell-free expression yields. The resulting protein, with 6 additional N-terminal residues due to the expression tag, was purified using high-performance liquid chromatography (HPLC). Far UV circular dichroism spectropolarimetry demonstrates that AR_TM1-3 has the predicted ∼40% α-helical character in membrane-mimetic environments. 1H-15N HSQC NMR experiments imply amenability to high-resolution NMR structural characterization and stability in solution for weeks. Notably, this small expression tag approach may also be generally applicable to other membrane proteins that are difficult to express in E. coli.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 23 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0009
       
  • A novel role of transient receptor potential mucolipin1 (TRPML1) in
           protecting against imidazole-induced cytotoxicity A novel role of
           transient receptor potential mucolipin1 (TRPML1) in protecting against
           imidazole-induced cytotoxicity
    • Pages: 279 - 286
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 279-286, August 2014. Lysosomotropic amines cause serious side effects such as cytoplasmic vacuolation and cell death. TRPML1 (also known as mucolipin1), a member of the transient receptor potential (TRP) protein family, may regulate fusion/fission of vesicles along the endocytic pathway and some aspects of lysosomal ion homeostasis. Nevertheless, it is still unknown whether TRPML1 is involved in death of mammalian cells induced by lysosomotropic agents. In this study, imidazole was used as a model to investigate the role of TRPML1 in the cytotoxicity of lysosomotropic agents. Overexpression of wild-type TRPML1 inhibited imidazole-induced vacuole formation and cell death in human endometrial adenocarcinoma (HEC-1B) cells. In contrast, siRNA-mediated TRPML1 knockdown increased the cell death induced by imidazole. Bafilomycin A1 raises the pH of acidic organelles and therefore suppresses accumulation of weak bases in them. Similarly, lysosomal pH was raised in TRPML1-overexpressing cells; therefore, we inferred that TRPML1 protected against imidazole toxicity by regulating the pH of acidic organelles. We concluded that TRPML1 had a novel role in protecting against lysosomotropic amine toxicity.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 28 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0044
       
  • Differential nuclear shape dynamics of invasive andnon-invasive breast
           cancer cells are associated with actin cytoskeleton organization and
           stability Differential nuclear shape dynamics of invasive andnon-invasive
           breast cancer cells are associated with actin cytoskeleton organization
           and stability
    • Pages: 287 - 295
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 287-295, August 2014. Cancer cells often exhibit characteristic aberrations in their nuclear architecture, which are indicative of their malignant potential. In this study, we have examined the nuclear and cytoskeletal composition, attachment configuration dynamics, and osmotic or drug treatment response of invasive (Hs578T and MDA-MB-231) and non-invasive (MCF-10A and MCF-7) breast cancer cell lines. Unlike MCF-10A and MCF-7, Hs578T and MDA-MB-231 cells showed extensive nuclear elasticity and deformability and displayed distinct kinetic profiles during substrate attachment. The nuclear shape of MCF-10A and MCF-7 cells remained almost unaffected upon detachment, hyperosmotic shock, or cytoskeleton depolymerization, while Hs578T and MDA-MB-231 revealed dramatic nuclear contour malformations following actin reorganization.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 17 Jun 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2013-0120
       
  • Inhibition of HDAC increases the senescence induced by natural polyphenols
           in glioma cells Inhibition of HDAC increases the senescence induced by
           natural polyphenols in glioma cells
    • Pages: 297 - 304
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 297-304, August 2014. Cellular senescence is an irreversible block of cellular division, and induction of senescence is being considered for treatment of many cancer types, mainly those resistant to classical pro-apoptotic therapies. Resveratrol (Rsv) and quercetin (Quer), two natural polyphenols, are able to induce senescence in different cancer models, including gliomas, the most common and aggressive primary brain tumor. These polyphenols modulate the activity of several proteins involved in cell growth and death in cancer cells, including histone deacetylases (HDAC), but the role of HDAC in senescence induced by Rsv and Quer is unclear. The HDAC inhibitor sodium butyrate (NaB) potentiated the pro-senescent effect of Rsv and Quer in human and rat glioma cell lines but not in normal rat astrocytes. Furthermore, the increment of Quer-induced senescence by NaB was accompanied by an increase of reactive oxygen species levels and an increment of the number of cells with nuclear abnormalities. Altogether, these data support a positive role of HDAC inhibition on the senescence induced by these polyphenols, and therefore co-treatment of HDAC inhibitors and polyphenols emerges as a potential alternative for gliomas.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 23 Jun 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0022
       
  • Involvement of ERK1/2, p38 MAPK, and PI3K/Akt signaling pathways in the
           regulation of cell cycle progression by PTHrP in colon adenocarcinoma
           cells Involvement of ERK1/2, p38 MAPK, and PI3K/Akt signaling pathways in
           the regulation of cell cycle progression by PTHrP in colon adenocarcinoma
           cells
    • Pages: 305 - 315
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 305-315, August 2014. Parathyroid hormone-related peptide (PTHrP) is distributed in most fetal and adult tissues, and its expression correlates with the severity of colon carcinoma. Recently we obtained evidence that in Caco-2 cells, a cell line from human colorectal adenocarcinoma, exogenous PTHrP increases the number of live cells, via ERK1/2, p38 MAPK, and PI3-kinase and induces the expression of cyclin D1, a cell cycle regulatory protein. In this study, we further investigated the role of PTHrP in the regulation of the cell cycle progression in these intestinal cells. Flow cytometry analysis revealed that PTHrP treatment diminishes the number of cells in the G0/G1 phase and increases the number in both S and G2/M phases. The hormone increases the expression of CDK6 and diminishes the amount of negative cell cycle regulators p27Kip1, p15INK4B, and p53. However, PTHrP does not modify the expression of cyclin D3, CDK4, and p16INK4A. In addition, inhibitors of ERK1/2 (PD98059), p38 MAPK (SB203580), and PI3Kinase (LY294002) reversed PTHrP response in Caco-2 cells. Taken together, our results suggest that PTHrP positively modulates cell cycle progression and changes the expression of proteins involved in cell cycle regulation via ERK1/2, p38 MAPK, and PI3K signaling pathways in Caco-2 cells.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 25 Jun 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2013-0106
       
  • Dual cross-linking ribonucleoprotein immunoprecipitation assay Dual
           cross-linking ribonucleoprotein immunoprecipitation assay
    • Pages: 317 - 319
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 4, Page 317-319, August 2014. Ribonucleoprotein immunoprecipitation (RIP) is an antibody-based method to detect RNA–protein interactions in situ. In the assay, UV cross-linking is commonly used to preserve RNA–protein interactions for subsequent target identification. UV light is a zero-length cross linker and thus identifies proteins directly bound to RNAs. Here, we describe a dual cross-linking RIP method that involves sequential protein–protein cross-linking step with a protein–protein cross-linker, followed by protein–RNA fixation by UV irradiation. In this way, proteins that indirectly bound to RNA can be analyzed.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 22 May 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0028
       
  • 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
       
  • 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 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 Characterization of human mutations in
           phosphorylatable amino acids of the cytosolic regulatory tail of SLC9A11
    • 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 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
       
  • Ser9-phosphorylated GSK3β induced by 14-3-3ζ actively
           antagonizes cell apoptosis in a NF-κB dependent manner
           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 Breaking the cycle: the role of omega-3
           polyunsaturated fatty acids in inflammation-driven cancers1
    • 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 Lessons
           from a red squirrel, mentors, and the pathway to success1
    • 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,
           Sec61-channelopathies Protein transport into the human ER and related
           diseases, Sec61-channelopathies
    • 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 Import of ribosomal
           proteins into yeast mitochondria1
    • 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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