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Journal Cover Biochemistry and Cell Biology
  [SJR: 0.859]   [H-I: 76]   [14 followers]  Follow
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
   Published by NRC Research Press Homepage  [21 journals]
  • Modulation of amyloid assembly by glycosaminoglycans: from mechanism to
           biological significance
    • Authors: Noé Quittot, Mathew Sebastiao, Steve Bourgault
      Pages: 329 - 337
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 329-337, June 2017.
      Glycosaminoglycans (GAGs) are long and unbranched polysaccharides that are abundant in the extracellular matrix and basement membrane of multicellular organisms. These linear polyanionic macromolecules are involved in many physiological functions from cell adhesion to cellular signaling. Interestingly, amyloid fibrils extracted from patients afflicted with protein misfolding diseases are virtually always associated with GAGs. Amyloid fibrils are highly organized nanostructures that have been historically associated with pathological states, such as Alzheimer’s disease and systemic amyloidoses. However, recent studies have identified functional amyloids that accomplish crucial physiological roles in almost all living organisms, from bacteria to insects and mammals. Over the last 2 decades, numerous reports have revealed that sulfated GAGs accelerate and (or) promote the self-assembly of a large diversity of proteins, both inherently amyloidogenic and non-aggregation prone. Despite the fact that many studies have investigated the molecular mechanism(s) by which GAGs induce amyloid assembly, the mechanistic elucidation of GAG-mediated amyloidogenesis still remains the subject of active research. In this review, we expose the contribution of GAGs in amyloid assembly, and we discuss the pathophysiological and functional significance of GAG-mediated fibrillization. Finally, we propose mechanistic models of the unique and potent ability of sulfated GAGs to hasten amyloid fibril formation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-01T08:00:00Z
      DOI: 10.1139/bcb-2016-0236
  • Structural evaluations of tau protein conformation: methodologies and
    • Authors: Nicole L. Zabik, Matthew M. Imhof, Sanela Martic-Milne
      Pages: 338 - 349
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 338-349, June 2017.
      Protein-misfolding diseases are based on a common principle of aggregation initiated by intra- and inter-molecular contacts. The structural and conformational changes induced by biochemical transformations such as post-translational modifications (PTMs), often lead to protein unfolding and misfolding. Thus, these order-to-disorder or disorder-to-order transitions may regulate cellular function. Tau, a neuronal protein, regulates microtubule (MT) structure and overall cellular integrity. However, misfolded tau modified by PTMs results in MT destabilization, toxic tau aggregate formation, and ultimately cell death, leading to neurodegeneration. Currently, the lack of structural information surrounding tau severely limits understanding of neurodegeneration. This minireview focuses on the current methodologies and approaches aimed at probing tau conformation and the role of conformation in various aspects of tau biochemistry. The recent applications of nuclear magnetic resonance, mass spectrometry, Förster resonance electron transfer, and molecular dynamics simulations toward structural analysis of conformational landscapes of tau will be described. The strategies developed for structural evaluation of tau may significantly improve our understanding of misfolding diseases.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-09T08:00:00Z
      DOI: 10.1139/bcb-2016-0227
  • Interactions of U24 from Roseolovirus with WW domains: canonical vs
    • Authors: Yurou Sang, Rui Zhang, A. Louise Creagh, Charles A. Haynes, Suzana K. Straus
      Pages: 350 - 358
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 350-358, June 2017.
      U24 is a C-terminal membrane-anchored protein found in both human herpes virus type 6 and 7 (HHV-6 and HHV-7), with an N-terminal segment that is rich in prolines (PPxY motif in both HHV-6A and 7; PxxP motif in HHV-6A). Previous work has shown that U24 interacts strongly with Nedd4 WW domains, in particular, hNedd4L-WW3*. It was also shown that this interaction depends strongly on the nature of the amino acids that are upstream from the PY motif in U24. In this contribution, data was obtained from pull-downs, isothermal titration calorimetry, and NMR to further determine what modulates U24:WW domain interactions. Specifically, 3 non-canonical WW domains from human Smad ubiquitination regulatory factor (Smurf), namely hSmurf2-WW2, hSmurf2-WW3, and a tandem construct hSmurf2-WW2 + 3, were studied. Overall, the interactions between U24 and these Smurf WW domains were found to be weaker than those in U24:Nedd4 WW domain pairs, suggesting that U24 function is tightly linked to specific E3 ubiqitin ligases.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-17T07:00:00Z
      DOI: 10.1139/bcb-2016-0250
  • Use of substitute Nonidet P-40 nonionic detergents in intracellular
           tubulin polymerization assays for screening of microtubule targeting
    • Authors: S. Sinha, J.J. Field, J.H. Miller
      Pages: 379 - 384
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 379-384, June 2017.
      Shell Chemical Company Nonidet P-40 has been used for decades in many biochemical assays as a nonionic, nondenaturing detergent; however, Shell no longer manufactures this product. Four commercially available substitutes were investigated and their activities titrated in an intracellular tubulin polymerization assay. Although claimed by the supply companies to be identical to the Shell Nonidet P-40, all four substitutes were about 10-fold more potent and needed to be diluted accordingly. As microtubule targeting drugs are a major class of anticancer agent, and many researchers use the intracellular tubulin polymerization assay, this information is important to help troubleshoot assay development with the new substitutes. As the Shell Nonidet P-40 has been used in many biochemical buffers, these results will be of general interest to the biochemical, cell, and molecular research community.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0141
  • Lactoferrin interacts with SPLUNC1 to attenuate lipopolysaccharide-induced
           inflammation of human nasal epithelial cells via down-regulated
           MEK1/2-MAPK signaling
    • Authors: Yung-An Tsou, Yu-Tong Tung, Tsu-Fang Wu, Gary Ro-Lin Chang, Han-Chien Chen, Chia-Der Lin, Chih-Ho Lai, Hsiao-Ling Chen, Chuan-Mu Chen
      Pages: 394 - 399
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 394-399, June 2017.
      The short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is an important innate material in the upper airway, and lactoferrin (LF) aids the innate functions in humans. In this study, a nasal epithelial model was used to investigate how LF modulates SPLUNC1 to reduce the inflammatory process mediated by lipopolysaccharide (LPS). The inflammation of human RPMI-2650 cells was induced with LPS to evaluate SPLUNC1 expression after treating the cells with bovine LF (bLF). The interaction pathway between LF and SPLUNC1 in LPS-induced inflammation was further investigated. Our study reveals that the addition of bLF results in the recovery of SPLUNC1 expression in nasal epithelial cells under LPS-induced inflammation. MAPK is involved in the main pathway for the SPLUNC1 and bLF interaction. Decreased SPLUNC1 function could be recovered by addition of bLF. The MEK1/2–MAPK signaling pathway is crucial for the SPLUNC1 and bLF interaction. Therefore, LF could support SPLUNC1 in the innate immunity recovery process.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-08T08:00:00Z
      DOI: 10.1139/bcb-2016-0047
  • Differential effect of hypoxia and acidity on lung cancer cell and
           fibroblast metabolism
    • Authors: Alexandra Giatromanolaki, Maria Liousia, Stella Arelaki, Dimitra Kalamida, Stamatia Pouliliou, Achilleas Mitrakas, Avgi Tsolou, Efthimios Sivridis, Michael Koukourakis
      Pages: 428 - 436
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 428-436, June 2017.
      This study examined the metabolic response of lung cancer cells and normal lung fibroblasts to hypoxia and acidity. GLUT1 and HXKII mRNA/protein expression was up-regulated under hypoxia in the MRC5 fibroblasts and in the A549 and H1299 lung cancer cell lines, indicating intensified glucose absorption and glycolysis. Under hypoxia, the LDHA mRNA and LDH5 protein levels increased in the cancer cells but not in the fibroblasts. Acidity suppressed the above-mentioned hypoxia effect. PDH-kinase-1 (PDK1 mRNA and protein) and inactive phosphorylated-PDH protein levels were induced under hypoxia in the cancer cells, whereas these were reduced in the MRC5 lung fibroblasts. In human tissue sections, the prevalent expression patterns supported the contrasting metabolic behavior of cancer cells vs. tumor fibroblasts. The monocarboxylate/lactate transporter 1 (MCT1) was up-regulated in all the cell lines under hypoxic conditions, but it was suppressed under acidic conditions. The mitochondrial DNA (mtDNA) content per cell decreased significantly in the A549 cancer cell line under hypoxia, but it increased in the MRC5 fibroblasts. Taking into account these findings, we suggest that, under hypoxia, cancer cells intensify the anaerobic direction in glycolysis, while normal fibroblasts prefer to seek energy by intensifying the aerobic use of the available oxygen.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-24T08:00:00Z
      DOI: 10.1139/bcb-2016-0197
  • MicroRNA-181 inhibits proliferation and promotes apoptosis of chondrocytes
           in osteoarthritis by targeting PTEN
    • Authors: Xiao-Feng Wu, Zi-Hui Zhou, Jian Zou
      Pages: 437 - 444
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 437-444, June 2017.
      Objective: To investigate the effects of microRNA-181 (miR-181) on the proliferation and apoptosis of chondrocytes in osteoarthritis (OA) by targeting PTEN. Methods: The chondrocytes in logarithmic growth phase were selected and divided into 6 test groups: the normal, blank, negative control, miR-181 mimic, miR-181 inhibitor, and miR-181 inhibitor + PTEN-siRNA groups. Reverse transcription qPCR was used to detect the expressions of miR-181 and PTEN mRNA. MTT assay and flow cytometry were performed to detect cell proliferation and apoptosis. The protein expressions of PARP and caspase-3 and the activity of MMP-2 and MMP-9 were detected by Western blotting and gelatin zymography assay. Results: The miR-181 mimic group showed increased miR-181 expression and decreased PTEN expression compared with the other 5 groups. Also, by comparison with the other 5 groups, the cell proliferation rate declined and the rate of cell apoptosis was elevated in the miR-181 mimic group. The MiR-181 mimic group showed remarkably increased protein expression of caspase-3 and PARP compared with the other 5 groups. The activity of MMP-2 and MMP-9 was higher in the miR-181 mimic group than the other 5 groups. Conclusion: MiR-181 could up-regulate the expressions of caspase-3, PARP, MMP-2, and MMP-9, and thereby inhibit cell proliferation and promote apoptosis of chondrocytes in OA by targeting PTEN.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-25T08:00:00Z
      DOI: 10.1139/bcb-2016-0078
  • Ceruloplasmin-derived peptide is the strongest regulator of oxidative
           stress and leukotriene synthesis in neutrophils
    • Authors: Ekaterina A. Golenkina, Alexey D. Livenskyi, Galina M. Viryasova, Yulia M. Romanova, Galina F. Sud’ina, Alexey V. Sokolov
      Pages: 445 - 449
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 445-449, June 2017.
      Ceruloplasmin, an acute-phase protein, can affect the activity of leukocytes through its various enzymatic activities and protein–protein interactions (with lactoferrin, myeloperoxidase, eosinophil peroxidase, serprocidins, and 5-lipoxygenase (5-LOX), among others). However, the molecular mechanisms of ceruloplasmin activity are not clearly understood. In this study, we tested the ability of two synthetic peptides, RPYLKVFNPR (883–892) (P1) and RRPYLKVFNPRR (882–893) (P2), corresponding to the indicated fragments of the ceruloplasmin sequence, to affect neutrophil activation. Leukotriene (LT) B4 is the primary eicosanoid product of polymorphonuclear leukocytes (PMNLs, neutrophils). We studied leukotriene synthesis in PMNLs upon interaction with Salmonella enterica serovar Typhimurium. Priming of neutrophils with phorbol 12-myristate 13-acetate (PMA) elicited the strong regulatory function of P2 peptide as a superoxide formation inducer and leukotriene synthesis inhibitor. Ceruloplasmin-derived P2 peptide appeared to be a strong inhibitor of 5-LOX product synthesis under conditions of oxidative stress.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0180
  • Method comparison for analyzing wound healing rates
    • Authors: Prabhpreet K. Dhillon, Xinyin Li, Jurgen T. Sanes, Oluwafemi S. Akintola, Bingyun Sun
      Pages: 450 - 454
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 450-454, June 2017.
      Wound healing scratch assay is a frequently used method to characterize cell migration, which is an important biological process in the course of development, tissue repair, and immune response for example. The measurement of wound healing rate, however, varies among different studies. Here we summarized these measurements into three types: (I) direct rate average; (II) regression rate average; and (III) average distance regression rate. Using Chinese hamster ovary (CHO) cells as a model, we compared the three types of analyses on quantifying the wound closing rate, and discovered that type I & III measurements are more resistant to outliers, and type II analysis is more sensitive to outliers. We hope this study can help researchers to better use this simple yet effective assay.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-30T08:00:00Z
      DOI: 10.1139/bcb-2016-0163
  • GNG11 (G-protein subunit γ 11) suppresses cell growth with induction of
           reactive oxygen species and abnormal nuclear morphology in human SUSM-1
    • Authors: Yuki Takauji, Ikuru Kudo, Atsuki En, Ryo Matsuo, Mohammad Nazir Hossain, Kazuhiko Nakabayashi, Kensuke Miki, Michihiko Fujii, Dai Ayusawa
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Enforced expression of GNG11, G-protein subunit γ 11, induces cellular senescence in normal human diploid fibroblasts. We here examined the effect of the expression of GNG11 on the growth of immortalized human cell lines, and found that it suppressed the growth of SUSM-1 cells, but not of HeLa cells. We then compared these two cell lines to understand the molecular basis for the action of GNG11. We found that expression of GNG11 induced the generation of reactive oxygen species (ROS) and abnormal nuclear morphology in SUSM-1 cells but not in HeLa cells. Increased ROS generation by GNG11 would likely be caused by the down-regulation of the antioxidant enzymes in SUSM-1 cells. We also found that SUSM-1 cells, even under normal culture conditions, showed higher levels of ROS and higher incidence of abnormal nuclear morphology than HeLa cells, and that abnormal nuclear morphology was relevant to the increased ROS generation in SUSM-1 cells. Thus, SUSM-1 and HeLa cells showed differences in the regulation of ROS and nuclear morphology, which might account for their different responses to the expression of GNG11. Thus, SUSM-1 cells may provide a unique system to study the regulatory relationship between ROS generation, nuclear morphology, and G-protein signaling.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-04-05T07:00:00Z
      DOI: 10.1139/bcb-2016-0248
  • Vitellogenin receptor selectively endocytoses female-specific and
           highly-expressed hemolymph proteins in the silkworm, Bombyx mori
    • Authors: Chaoshan Han, Enxiang Chen, Guanwang Shen, Zhixin Peng, Yinying Xu, Haiyan Zhang, Hongling Liu, Yandi Zhang, Jinxin Wu, Ying Lin, Qingyou Xia
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      VgR, a member of the LDLR family, functions to transport vitellogenin into the ovaries to protome ovarian growth and embryonic development. In insects, the only widely accepted ligand of VgR is Vg. Recently, BmVgR has been shown to interact with BmSP1 in vitro. Therefore, in this study, we evaluated whether BmVgR could transport BmSP1 into certain cells. Although BmVgR could combine with BmVg and BmSP1, BmVgR did not affect the amount of BmSP1 taken up by Sf9 cells. Parallel immunofluorescence showed that most BmVg and BmVgR were localized in the inner oocyte membrane, showing tissue localization similar to that of BmVg labeled with pHrodo Red absorbed by the ovaries on day 2 of pupation. Although BmSP1 showed localization similar to BmVgR during the same phase, little BmSP1 was present in the ovary. Additionally, BmSP1 did not exist in ovaries when the ovaries contained BmVgR on day 5 of pupation, suggesting that BmSP1 in the ovaries was not endocytosed by BmVgR. In summary, BmVgR could facilitate uptake of BmVg by developing oocytes, but did not modulate in the transport of BmSP1.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-04-04T07:00:00Z
      DOI: 10.1139/bcb-2016-0255
  • Contribution of PPARγ in modulation of acrolein-induced inflammatory
           signaling in gp91phox knock-out mice
    • Authors: Zivar Yousefipour, Neha Chug, Katarzyna Marek, Alicia Nesbary, Joseph Mathew, Kasturi Ranganna, Mohammad A. Newaz
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Oxidative stress and inflammation are major contributors to acrolein toxicity. Peroxisome proliferator activated receptor gamma (PPARγ) has antioxidant and anti-inflammatory effects. We investigated the contribution of PPARγ ligand GW1929 to the attenuation of oxidative stress in acrolein-induced insult. Male gp91phox knock-out (KO) mice were treated with acrolein (0.5 mg·(kg body mass)–1 by intraperitoneal injection for 7 days) with or without GW1929 (GW; 0.5 mg·(kg body mass)–1·day–1, orally, for 10 days). The livers were processed for further analyses. Acrolein significantly increased 8-isoprostane and reduced PPARγ activity (P < 0.05) in the wild type (WT) and KO mice. GW1929 reduced 8-isoprostane (by 32% and 40% in WT and KO mice, respectively) and increased PPARγ activity (by 81% and 92% in WT and KO, respectively). Chemokine activity was increased (by 63%) in acrolein-treated WT mice, and was reduced by GW1929 (by 65%). KO mice exhibited higher xanthine oxidase (XO). Acrolein increased XO and COX in WT mice and XO in KO mice. GW1929 significantly reduced COX in WT and KO mice and reduced XO in KO mice. Acrolein significantly reduced the total antioxidant status in WT and KO mice (P < 0.05), which was improved by GW1929 (by 75% and 74%). The levels of NF-κB were higher in acrolein-treated WT mice. GW1929 reduced NF-κB levels (by 51%) in KO mice. Acrolein increased CD36 in KO mice (by 43%), which was blunted with GW1929. Data confirms that the generation of free radicals by acrolein is mainly through NAD(P)H, but other oxygenates play a role too. GW1929 may alleviate the toxicity of acrolein by attenuating NF-κB, COX, and CD36.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-04-04T07:00:00Z
      DOI: 10.1139/bcb-2016-0198
  • Indication for differential sorting of the rat v-SNARE splice isoforms
           VAMP-1a and -1b
    • Authors: Fiona R. Rodepeter, Susanne Wiegand, Hans-Georg Lüers, Gabriel A. Bonaterra, Anson W. Lowe, Michael Bette, Ralf Jacob, Robert Mandic
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins are essential constituents of the intracellular trafficking machinery. The variable C-terminus in the 2 rat VAMP-1 splice isoforms VAMP-1a and -1b potentially acts as a sorting signal, because similar changes at the C-terminal end of a human VAMP-1 splice isoform resulted in its sorting to mitochondria. To evaluate the differences in the subcellular localization of these two v-SNARE proteins, VAMP-1a and -1b proteins tagged with green fluorescent protein (GFP) and red fluorescent protein (RFP) were expressed in HeLa, COS-7, and MDCK cells and evaluated by conventional confocal as well as total internal reflection fluorescence microscopy. Regions consistent with the endoplasmic reticulum and Golgi apparatus demonstrated a major overlap of both signals. In the periphery, vesicular structures were observed that mainly expressed one of the 2 isoforms. Within our experimental settings, we could not observe sorting of any of the 2 isoforms to mitochondria or peroxisomes, whereas both isoforms were found expressed in a minor subset of singular vesicles, which sporadically appeared to co-localize with the exocyst marker EXOC3/Sec6. Because vesicular structures were seen that expressed only one of the two splice variants, it is possible that VAMP-1a and VAMP-1b are sorted to distinct cellular compartments that require further characterization.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-17T07:00:00Z
      DOI: 10.1139/bcb-2016-0184
  • Genetic variants of interferon-gamma and its mRNA expression and
           inflammatory parameters in the pathogenesis of vitiligo
    • Authors: Rehab A. Karam, Haidy E. Zidan, Mohamed H. Khater
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Although genetics plays an essential role in the pathogenesis of vitiligo, vitiligo pathogenesis is still unclear. Our aim was to investigate the role of IFN-γ expression and polymorphism in vitiligo susceptibility and whether intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor (TNF)-α, and TNF-β play a role in vitiligo pathogenesis as important inflammatory parameters. Eighty-five patients with vitiligo and 90 controls were investigated for IFN-γ gene expression by quantitative real-time PCR and genotyped for IFN-γ +874T/A (rs2430561) and IFN-γ +2109A/G (rs1861494) gene polymorphisms by sequence-specific primer (SSP)-PCR and PCR-restriction fragment length polymorphism (RFLP), respectively. Serum levels of inflammatory parameters were measured using ELISA. Frequencies of the +874 TT genotype and T allele were significantly higher in patients with active vitiligo than in stable patients (P = 0.01 and 0.03, respectively). Calculation of odds ratio suggested a 1.7-fold increased risk of vitiligo in individuals having the TA haplotype. We observed overexpression of IFN-γ mRNA with elevated serum levels of IFN-γ, ICAM-1, TNF-α, and TNF-β in patients with vitiligo when compared with the control group (P = 0.001, for all). In addition, these levels were elevated in patients with active vitiligo compared with stable patients with vitiligo (P = 0.008, 0.006, 0.01, 0.01, and 0.03, respectively), which suggests the involvement of these cytokines in disease activity. In conclusion, IFN-γ is a promising immunological marker in vitiligo pathogenesis.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-08T08:00:00Z
      DOI: 10.1139/bcb-2016-0228
  • A modified method for isolating mouse islets of an adequate quality,
           quantity, and purity
    • Authors: Jiejie Xu, Baogang Peng, Caiyun Zhang, Jiwei Xu, Yi Ma, Xinjun Lu
      Pages: 1 - 4
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Mouse islets are widely used in diabetes research. Thus an adequate quality, quantity, and purity of islets are needed for high-quality investigations. We performed a combination of filtration and density gradient separation and optimized many steps in the islet isolation procedure, including perfusion, digestion, and purification. Our results show that an increased quality, quantity, and purity of isolated islets can be achieved using these modifications. Moreover, this method can guarantee maximal recovery and purity of the isolated islets and is easy to perform with practice.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-03T08:00:00Z
      DOI: 10.1139/bcb-2016-0204
  • Osthole prevents cerebral ischemia–reperfusion injury via the Notch
           signaling pathway
    • Authors: Junhong Guan, Xiangtai Wei, Shengtao Qu, Tao Lv, Qiang Fu, Ye Yuan
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Stroke is a common cerebrovascular disease in aging populations, and constitutes the second highest principle cause of mortality and the principle cause of permanent disability, and ischemic stroke is the primary form. Osthole is a coumarin derivative extracted from the fruits of Cnidium monnieri (L.) Cusson. In this study, we established a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) in vivo and found that MCAO/R caused cerebral infarction, hippocampus neuronal injury and apoptosis, and also activated the Notch 1 signaling pathway. However, treatment with osthole further enhanced the activity of Notch 1 signaling and reduced the cerebral infarction as well as the hippocampus neuronal injury and apoptosis induced by MCAO/R in a dose-dependent manner. The same results were observed in a primary neuronal oxygen glucose deficiency/reperfusion (OGD/R) model in vitro, and the effect of osthole could be blocked by an inhibitor of Notch 1 signaling, N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine tert-butyl ester (DAPT). Therefore, we demonstrated that osthole injection prevented rat ischemia–reperfusion injury via activating the Notch 1 signaling pathway in vivo and in vitro in a dose-dependent manner, which may be significant for clinical treatment of ischemic stroke.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-03T08:00:00Z
      DOI: 10.1139/bcb-2016-0233
  • Histone H3.3 regulates mitotic progression in mouse embryonic fibroblasts
    • Authors: Aysegul Ors, Christophe Papin, Bertrand Favier, Yohan Roulland, Defne Dalkara, Mehmet Ozturk, Ali Hamiche, Stefan Dimitrov, Kiran Padmanabhan
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      H3.3 is a histone variant that marks transcription start sites as well as telomeres and heterochromatic sites on the genome. The presence of H3.3 is thought to positively correlate with the transcriptional status of its target genes. Using a conditional genetic strategy against H3.3B, combined with short hairpin RNAs against H3.3A, we essentially depleted all H3.3 gene expression in mouse embryonic fibroblasts. Following nearly complete loss of H3.3 in the cells, our transcriptomic analyses show very little impact on global gene expression or on the localization of histone variant H2A.Z. Instead, fibroblasts displayed slower cell growth and an increase in cell death, coincident with large-scale chromosome misalignment in mitosis and large polylobed or micronuclei in interphase cells. Thus, we conclude that H3.3 may have an important under-explored additional role in chromosome segregation, nuclear structure, and the maintenance of genome integrity.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-01T08:00:00Z
      DOI: 10.1139/bcb-2016-0190
  • Comparison of the effects of nobiletin and letrozole on the activity and
           expression of aromatase in the MCF-7 breast cancer cell line
    • Authors: Seyedeh Tayebeh Rahideh, Mohammad Keramatipour, Mitra Nourbakhsh, Fariba Koohdani, Mostafa Hoseini, Saeed Talebi, Farzad Shidfar
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Nobiletin (NOB) is one of the polymethoxyflavones mainly found in citrus fruits. Aromatase or cytochrome P450 (CYP19) enzyme catalyzes the last and rate-limiting step in estrogen biosynthesis. This study was carried out to investigate the effect of NOB on the activity and expression of aromatase, and to compare this property with letrozole (LET) as aromatase inhibitor in the MCF-7 breast cancer cell line. Cell viability was assessed with 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assays. Aromatase enzyme activity based on the conversion of androgenic substrate testosterone into 17β-estradiol was determined. CYP19 gene expression was measured by quantitative real-time PCR. MTT assays demonstrated that NOB at a concentration of 100 μmol/L decreased cell viability in a time-dependent manner (P < 0.05). NOB significantly inhibited aromatase at the concentration of 0.1 μmol/L (P = 0.013), whereas other concentrations had no effect. Treatment with 10 μmol/L and 1 μmol/L of NOB for 48 h significantly increased (P = 0.001) and decreased (P = 0.02) relative aromatase expression, respectively. The combination of LET and NOB had no effect on aromatase. This study showed for the first time that NOB decreases the activity and expression of aromatase at low concentrations in MCF-7 breast cancer cells.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-01T08:00:00Z
      DOI: 10.1139/bcb-2016-0206
  • An aqueous extract from Moringa oleifera leaves ameliorates hepatotoxicity
           in alloxan-induced diabetic rats
    • Authors: Mabrouk Attia Abd Eldaim, Ahmed Shaban Abd Elrasoul, Samy Ahmed Abd Elaziz
      Pages: 524 - 530
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      This study was carried out to evaluate the possible mechanisms through which an aqueous extract from MO leaves demonstrates hepatoprotective effects in alloxan-induced diabetic rats. Eighty albino rats were assigned to 4 groups. The control group was orally administered sterile saline. The second group was injected with alloxan (150 mg/kg body mass (b.m.)) by intraperitoneal injection (i.p.). The third group was given MO (250 mg/kg b.m.) orally, daily. The fourth group was injected with alloxan, as for the second group, and administrated an aqueous extract of MO leaves, as for the third group. Alloxan induced degenerative changes in hepatic and pancreatic tissues, increased hepatic lipid peroxidation, and increased gene expression of PC and caspase 3. However, it decreased the activities of hepatic SOD and CAT, and gene expression of GS. In contrast, the MO extract prevented changes to the histoarchitecture of hepatic and pancreatic tissues and normalized the reduced hepatic levels of glutathione, as well as the activities of SOD and CAT, and the gene expression of GS, while reducing blood glucose levels, hepatic lipid peroxidation, and the gene expression of PC and caspase 3. This study indicated that an aqueous extract of MO leaves can be a potent antioxidant and used as an hepatoprotective agent.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-04-19T07:00:00Z
      DOI: 10.1139/bcb-2016-0256
  • Potential regulatory mechanisms of lncRNA in diabetes and its
    • Pages: 361 - 367
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 361-367, June 2017.
      Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides without protein-coding potential. Although these molecules were initially considered as “junk products” of transcription without biological relevance, recent advances in research have shown that lncRNA plays an important role, not only in cellular processes such as proliferation, differentiation, and metabolism, but also in the pathological processes of cancers, diabetes, and neurodegenerative diseases. In this review, we focus on the potential regulatory roles of lncRNA in diabetes and the complications associated with diabetes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-21T08:00:00Z
      DOI: 10.1139/bcb-2016-0110
  • Functional assessment of MeCP2 in Rett syndrome and cancers of breast,
           colon, and prostate
    • Pages: 368 - 378
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 368-378, June 2017.
      Ever since the first report that mutations in methyl-CpG-binding protein 2 (MeCP2) causes Rett syndrome (RTT), a severe neurological disorder in females world-wide, there has been a keen interest to gain a comprehensive understanding of this protein. While the classical model associated with MeCP2 function suggests its role in gene suppression via recruitment of co-repressor complexes and histone deacetylases to methylated CpG-sites, recent discoveries have brought to light its role in transcription activation, modulation of RNA splicing, and chromatin compaction. Various post-translational modifications (PTMs) of MeCP2 further increase its functional versatility. Involvement of MeCP2 in pathologies other than RTT, such as tumorigenesis however, remains poorly explored and understood. This review provides a survey of the literature implicating MeCP2 in breast, colon and prostate cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0154
  • PRPS1 silencing reverses cisplatin resistance in human breast cancer cells
    • Pages: 385 - 393
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 385-393, June 2017.
      PRPS1 (phosphoribosyl pyrophosphate synthetase 1), which drives the nucleotide biosynthesis pathway, modulates a variety of functions by providing central building blocks and cofactors for cell homeostasis. As tumor cells often display abnormal nucleotide metabolism, dysregulated de-novo nucleotide synthesis has potential impacts in cancers. We now report that PRPS1 is specifically and highly expressed in chemoresistant (CR) cancer cells derived from cisplatin-resistant human breast cancer cell lines SK-BR-3 and MCF-7. The inhibition of PRPS1 activity in CR cells by genetic silencing reduces cell viability and increases apoptosis in vitro, both of which can be further potentiated by cisplatin treatment. Significantly, such down-regulation of PRPS1 in CR cells when administered to nude mice enhanced the survival of those animals, as demonstrated by decreased tumor growth. Knockdown of PRPSI may cause these effects by potently inducing autonomous activation of caspase-3 and inhibiting the proliferation in the engrafted CR tumors. As a result, cisplatin sensitivity in a xenograft model of CR cancer cells can be restored by the down-regulation of PRPS1. Thus, PRPS1 inhibition may afford a therapeutic approach to relapsed patients with breast cancer, resistant to chemotherapy.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-03T07:00:00Z
      DOI: 10.1139/bcb-2016-0106
  • Diosmin attenuates radiation-induced hepatic fibrosis by boosting PPAR-γ
           expression and hampering miR-17-5p-activated canonical Wnt–β-catenin
    • Pages: 400 - 414
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 400-414, June 2017.
      Background: Liver fibrosis is one of the major complications from upper right quadrant radiotherapy. MicroRNA-17-5p (miR-17-5p) is hypothesized to act as a regulator of hepatic stellate cell (HSCs) activation by activation of the canonical Wnt–β-catenin pathway. Diosmin (Dios), a citrus bioflavonoid, is known to possess potent antioxidant, anti-inflammatory, and anti-apoptotic properties. Purpose: To explore the molecular mechanisms that underlie radiation-induced liver fibrosis, and to evaluate the possible influence of Dios on the miR-17-5p–Wnt–β-catenin signaling axis during fibrogenesis provoked by irradiation (IRR) in rats. Also, the effect of Dios on hepatic peroxisome proliferator activated receptor-γ (PPAR-γ) expression as a regulator for HSC activation was considered. Methods: We administered 100 mg·(kg body mass)–1·day–1 (per oral) of Dios were administered to IRR-exposed rats (overall dose of 12 Gy on 6 fractions of 2 Gy each) for 6 successive weeks. Results: Data analysis revealed that Dios treatment mitigated oxidative stress, enhanced antioxidant defenses, alleviated hepatic inflammatory responses, abrogated pro-fibrogenic cytokines, and stimulated PPAR-γ expression. Dios treatment repressed the miR-17-5p activated Wnt–β-catenin signaling induced by IRR. Moreover, Dios treatment restored the normal hepatic architecture and reversed pathological alterations induced by IRR. Conclusion: We hypothesize that the stimulation of PPAR-γ expression and interference with miR-17-5p activated Wnt–β-catenin signaling mediates the antifibrotic properties of Dios.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-21T08:00:00Z
      DOI: 10.1139/bcb-2016-0142
  • Chronic intermittent hypoxia disturbs insulin secretion and causes
           pancreatic injury via the MAPK signaling pathway
    • Pages: 415 - 420
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 415-420, June 2017.
      Obstructive sleep apnea (OSA) is a breathing disorder during sleep, with a most prominent character of chronic intermittent hypoxia (CIH), which induces the generation of reactive oxygen species (ROS) that damages multiple tissues and causes metabolic disorders. In this study, we established a rat model of varying OSA with different grades of CIH (12.5% O2, 10% O2, 7.5% O2, and 5% O2) for 12 weeks, and found that CIH stimulated insulin secretion, reduced the insulin:proinsulin ratio in pancreatic tissue, and caused pancreatic tissue lesions and cell apoptosis in a dose-dependent manner. Moreover, CIH promoted the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and activated mitogen-activated protein kinase (MAPK) family members, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, depending on the O2 concentration. In summary, CIH disturbed insulin secretion, and caused inflammation, lesions, and cell apoptosis in pancreatic tissue via the MAPK signaling pathway, which may be of great significance for clinical treatment of OSA and type 2 diabetes mellitus (T2DM).
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-28T08:00:00Z
      DOI: 10.1139/bcb-2016-0167
  • Temporo-spacial microanatomical distribution of the murine
           sodium-dependent ascorbic acid transporters Slc23a1 and Slc23a2 in the
           kidney throughout development
    • Pages: 421 - 427
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 421-427, June 2017.
      The two membrane transporters Slc23a1 and Slc23a2 mediate ascorbic acid uptake into cells. We recently determined the key role of Slc23a1 in renal re-absorption of ascorbic acid in a knockout mouse model. However, the renal spatial and temporal expression patterns of murine Slc23a1 and Slc23a2 are not defined. This study utilizes database evidence combined with experimental confirmation via in-situ hybridization to define the spatial and temporal expression of Slc23a1 in the murine kidney. Slc23a1 is expressed in the early proximal tubule, but not in its precursors during embryonic development, and exclusive proximal tubular expression persists throughout the animal’s lifetime. In contrast, Slc23a2 is uniformly expressed in metabolic cell types such as stromal cells. The expression patterns appear to be conserved from rodent lineages to humans.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-12-20T08:00:00Z
      DOI: 10.1139/bcb-2015-0090
  • PANC-1 cells proliferative response to ionizing radiation is related to
           GSK-3β phosphorylation
    • Authors: Nora A. Mohamad, Graciela P. Cricco, Claudia M. Cocca, Elena S. Rivera, Rosa M. Bergoc, Gabriela A. Martín
      Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Radiotherapy may be used to treat pancreatic cancer and relieve pain. We have previously reported that histamine modulates pancreatic adenocarcinoma PANC-1 cell proliferation. This work was aimed to evaluate whether histamine improves radiosensitivity of PANC-1 cells in relation to phosphorylation/inhibition of glycogen synthase kinase-3β (GSK-3β). Immediately after γ irradiation, intracellular hydrogen peroxide was markedly decreased together with a rapid increase in catalase activity. Although histamine diminished catalase activity in nonirradiated cells, it only partially hindered the increase observed in irradiated cells and could not modify radiosensitivity. In control cells, a high expression of total and a very low expression of phosphorylated/inactive GSK-3β were found. An increment in reactive oxygen species levels produced an augmentation in GSK-3β phosphorylation and suppressed cell proliferation. In both control and histamine-treated irradiated cells, the rise in catalase activity lowered reactive oxygen species levels and only a small increase in phosphorylated GSK-3β was detected. Alternatively, 3-aminotriazole, an irreversible inhibitor of catalase, reduced the survival fraction in irradiated control cells along with an increment in phosphorylated GSK-3β. These results suggest that upon irradiation, early catalase activation may be responsible for keeping GSK-3β active conceding cells a survival advantage toward cytotoxic effects of ionizing radiation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2012-11-25T03:55:27Z
      DOI: 10.1139/bcb-2012-032
  • Utp22p acts in concert with Utp8p to channel aminoacyl-tRNA from the
           nucleolus to the nuclear tRNA export receptor Los1p but not Msn5p
    • Authors: Manoja B.K. Eswara, Ashley Clayton, Dev Mangroo
      Pages: 1 - 19
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Utp8p is an essential nucleolar protein that channels aminoacyl-tRNAs from aminoacyl-tRNA synthetases in the nucleolus to the nuclear tRNA export receptors located in the nucleoplasm and nuclear pore complex in Saccharomyces cerevisiae. Utp8p is also part of the U3 snoRNA-associated protein complex involved in 18S rRNA biogenesis in the nucleolus. We report that Utp22p, which is another member of the U3 snoRNA-associated protein complex, is also an intranuclear component of the nuclear tRNA export machinery. Depletion of Utp22p results in nuclear retention of mature tRNAs derived from intron-containing and intronless precursors. Moreover, Utp22p copurifies with the nuclear tRNA export receptor Los1p, the aminoacyl-tRNA synthetase Tys1p and Utp8p, but not with the RanGTPase Gsp1p and the nuclear tRNA export receptor Msn5p. Utp22p interacts directly with Utp8p and Los1p in a tRNA-independent manner in vitro. Utp22p also interacts directly with Tys1p, but this binding is stimulated when Tys1p is bound to tRNA. However, Utp22p, unlike Utp8p, does not bind tRNA saturably. These data suggest that Utp22p recruits Utp8p to aminoacyl-tRNA synthetases in the nucleolus to collect aminoacyl-tRNA and then accompanies the Utp8p–tRNA complex to deliver the aminoacyl-tRNAs to Los1p but not Msn5p. It is possible that Nrap/Nol6, the mammalian orthologue of Utp22p, plays a role in channelling aminoacyl-tRNA to the nuclear tRNA export receptor exportin-t.
      Citation: Biochemistry and Cell Biology
      PubDate: 2012-11-20T01:45:45Z
      DOI: 10.1139/bcb-2012-034
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