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  Subjects -> BIOLOGY (Total: 3003 journals)
    - BIOCHEMISTRY (237 journals)
    - BIOENGINEERING (108 journals)
    - BIOLOGY (1427 journals)
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BIOLOGY (1427 journals)

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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]
  • Kv10.1 potassium channel: from the brain to the tumors
    • Authors: V. Cázares-Ordoñez, L.A. Pardo
      Pages: 531 - 536
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 5, Page 531-536, October 2017.
      The KCNH1 gene encodes the Kv10.1 (Eag1) ion channel, a member of the EAG (ether-à-go-go) family of voltage-gated potassium channels. Recent studies have demonstrated that KCHN1 mutations are implicated in Temple–Baraitser and Zimmermann–Laband syndromes and other forms of developmental deficits that all present with mental retardation and epilepsy, suggesting that Kv10.1 might be important for cognitive development in humans. Although the Kv10.1 channel is mainly expressed in the mammalian brain, its ectopic expression occurs in 70% of human cancers. Cancer cells and tumors expressing Kv10.1 acquire selective advantages that favor cancer progression through molecular mechanisms that involve several cellular pathways, indicating that protein–protein interactions may be important for Kv10.1 influence in cell proliferation and tumorigenesis. Several studies on transcriptional and post-transcriptional regulation of Kv10.1 expression have shown interesting mechanistic insights about Kv10.1 role in oncogenesis, increasing the importance of identifying the cellular factors that regulate Kv10.1 expression in tumors.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-14T07:00:00Z
      DOI: 10.1139/bcb-2017-0062
       
  • Can mesenchymal stem cells pretreated with platelet-rich plasma modulate
           tissue remodeling in a rat with burned skin'
    • Authors: Hanan Hosni Ahmed, Laila Ahmed Rashed, Sohair Mahfouz, Rania Elsayed Hussein, Marwa Alkaffas, Shaimaa Mostafa, Azza Abusree
      Pages: 537 - 548
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 5, Page 537-548, October 2017.
      Our aim was to study the effect of platelet-rich plasma (PRP) on the proliferation of bone-marrow-derived mesenchymal stem cells (BM-MSCs) and to investigate their roles in the healing of experimental burn injury and the possible mechanism of action. Our work was divided into in-vitro and in-vivo studies. The in-vitro study included untreated MSCs and MSCs treated with PRP. Levels of TGF-β and cell proliferation were assessed. In the in-vivo study, 72 rats were distributed equally among 6 groups: control, burn, burn with MSCs, burn with PRP, burn with both MSCs and PRP, and burn with MSCs pretreated with PRP. On the 7th and 20th day after injury, the serum levels of transforming growth factor beta (TGF-β) and tumor necrosis factor alpha (TNF-α), as well as interleukin-10 (IL-10) levels in skin tissue were measured by ELISA; histopathology and gene expression of MMP-1, TIMP-2, Ang-1, Ang-2, and vimentin by real-time PCR were performed in all groups. In vitro: proliferation of MSCs and TGF-β increased in the PRP-treated group compared with the control group. In vivo: Ang-1, Ang-2, and vimentin were upregulated, whereas MMP-1 and TIMP-2 were downregulated. TGF-β and IL-10 were increased, whereas TNF-α was decreased in all treated groups with more significance in MSCs and PRP on day 20. Histopathology of burn skin was improved in all treated groups, particularly in MSCs pretreated with PRP 20 days post-burn.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-17T07:00:00Z
      DOI: 10.1139/bcb-2016-0224
       
  • Anti-angiogenic effect of chebulagic acid involves inhibition of the
           VEGFR2- and GSK-3β-dependent signaling pathways
    • Authors: A.P. Athira, C.S. Abhinand, K. Saja, A. Helen, P. Reddanna, P.R. Sudhakaran
      Pages: 563 - 570
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 5, Page 563-570, October 2017.
      Inhibition of angiogenesis is a useful strategy to prevent cancer growth by targeting new vessels that grow to nourish actively proliferating tumor cells. Endothelial cells can use a number of different pathways to cause angiogenesis, and each step in these pathways can be targeted. The use of multi-targeted drugs is gaining much importance in this scenario. Our previous results have shown that chebulagic acid (a benzopyran tannin present in the fruits of Terminalia chebula) has anti-angiogenic properties. Thus, this study was designed to examine the molecular mechanism for the anti-angiogenic effects of chebulagic acid. Results from our investigations using molecular docking studies and human umbilical vein endothelial cells in culture suggested that chebulagic acid inhibits both GSK-3β-dependent β-catenin phosphorylation (an important mediator of VE-cadherin–β-catenin signaling) and VEGFR2 phosphorylation, which is an important step in VEGF signaling. Chebulagic acid inhibits angiogenesis by blocking both the VEGF–VEGFR2 complex and cell–cell contact dependent downstream signaling pathways.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-03T07:00:00Z
      DOI: 10.1139/bcb-2016-0132
       
  • Tamoxifen inhibits mitochondrial membrane damage caused by disulfiram
    • Authors: Natalia Pavón, Mabel Buelna-Chontal, Francisco Correa, Belem Yoval-Sánchez, Javier Belmont, Luz Hernández-Esquivel, José S. Rodríguez-Zavala, Edmundo Chávez
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      In this work, we studied the protective effects of tamoxifen (TAM) on disulfiram (Dis)-induced mitochondrial membrane insult. The results indicate that TAM circumvents the inner membrane leakiness manifested as Ca2+ release, mitochondrial swelling, and collapse of the transmembrane electric gradient. Furthermore, it was found that TAM prevents inactivation of the mitochondrial enzyme aconitase and detachment of cytochrome c from the inner membrane. Interestingly, TAM also inhibited Dis-promoted generation of hydrogen peroxide. Given that TAM is an antioxidant molecule, it is plausible that its protection may be due to the inhibition of Dis-induced oxidative stress.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-06-08T07:00:00Z
      DOI: 10.1139/bcb-2017-0027
       
  • Interaction between miR-572 and PPP2R2C, and their effects on the
           proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC)
           cells
    • Authors: Lei Yan, Kerui Cai, Jun Liang, Haifeng Liu, Yang Liu, Jinqiu Gui
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      We investigated the how miR-572 regulates PPP2R2C, and studied the effects of miR-572 and PPP2R2C on proliferation and migration as well as invasion of nasopharyngeal carcinoma (NPC) cells. NPC tissues and normal tissues were collected, and the expressions of miR-572 and PPP2R2C were detected by real-time PCR. Western blot was applied to detect the expression of PPP2R2C protein. The target relationship between miR-572 and PPP2R2C was confirmed by dual luciferase reporter gene assay. MTT assay and flow cytometry were applied to investigate the viability and apoptosis levels of NPC cells. Transwell as well as wound healing assays were used, respectively, to detect the invasiveness and migration of NPC cells. MiR-572 was highly expressed in NPC tissues as well as NPC cells, and there was lower expression of PPP2R2C in NPC tissues compared with normal samples. MiR-572 could bind to the 3′ UTR of PPP2R2C and decrease its expression. Over-expressed miR-572 and decreased PPP2R2C expression could both inhibit proliferation and invasion and induce apoptosis of NPC cells. Thus, miR-572 promotes the proliferation and invasion of NPC by directly down-regulating PPP2R2C.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-19T07:00:00Z
      DOI: 10.1139/bcb-2016-0237
       
  • Characterization of an ionic liquid-tolerant β-xylosidase from a
           marine-derived fungal endophyte
    • Authors: Anindita Sengupta, Angela Zabala, Si Yu Tan, Arthur Broadstock, Trichur S. Suryanarayanan, Venkat Gopalan
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Ionic liquids (ILs) are used in lignocellulosic biomass (LCB) pretreatment because of their ability to disrupt the extensive hydrogen-bonding network in cellulose and hemicellulose, and thereby decrease LCB recalcitrance to subsequent enzymatic degradation. However, this approach necessitates the development of cellulases and hemicellulases that can tolerate ∼20% (w/v) IL, an amount that either co-precipitates with the sugar polymers after the initial pretreatment or is typically used in single-pot biomass deconstructions. By investigating the secretomes from 4 marine-derived fungal endophytes, we identified a β-xylosidase derived from Trichoderma harzianum as the most promising in terms of tolerating 1-ethyl-3-methylimidazolium-dimethyl phosphate (EMIM-DMP), an IL. When tested with p-nitrophenyl-β-d-xyloside, this extracellular xylosidase retained ∼50% activity even in 1.2 mol·L–1 (20% w/v) EMIM-DMP after incubation for 48 h. When tested on the natural substrate xylobiose, there was ∼85% of the initial activity in 1.2 mol·L–1 EMIM-DMP after incubation for 9 h and ∼80% after incubation for 48 h. Despite previous findings associating thermostability and IL tolerance, our findings related to the mesophilic T. harzianum β-xylosidase(s) emphasize the need to include the marine habitat in the bioprospecting dragnet for identification of new IL-tolerant LCB-degrading enzymes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-19T07:00:00Z
      DOI: 10.1139/bcb-2017-0053
       
  • MiR-301b promotes the proliferation, mobility, and
           epithelial-to-mesenchymal transition of bladder cancer cells by targeting
           EGR1
    • Authors: Lei Yan, Yan Wang, Jun Liang, Zhixin Liu, Xiaodong Sun, Kerui Cai
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      We investigated the role of miR-301b in the modulation of the proliferation, migration, and invasion of bladder cancer (BLCA) cells. The expression of miR-301b and EGR1 (early growth response gene 1) mRNA were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). A dual-luciferase reporter gene system was used to identify the target relationship between miR-301b and EGR1. Cell proliferation, cell cycle, and apoptosis were analyzed by MTT assay, colony-forming assay, and flow cytometry, respectively. Cell motility and invasiveness were assessed by wound healing and Transwell assays. The expression of proteins involved in epithelial-to-mesenchymal transition (EMT) and EGR1 were determined by Western blot. Our results showed that miR-301b was up-regulated while EGR1 was down-regulated in BLCA tissues compared with adjacent normal tissues. The proliferation, migration, and invasiveness of T24 cells (a kind of human BLCA cell) were suppressed by decreasing miR-301b expression or increasing EGR1 expression. In addition, miR-301b promoted EMT signaling by influencing the expression of related proteins. In conclusion, miR-301b promotes the proliferation, migration, and aggressiveness of human BLCA cells by inhibiting the expression of EGR1.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-18T07:00:00Z
      DOI: 10.1139/bcb-2016-0232
       
  • TLR2 affects CD86 expression and inflammatory response in burn injury mice
           through regulation of p38
    • Authors: Li Li, Gang Xu, Chenwang Duan
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The aim of this study was to assess the effects of TLR2–p38–CD86 signaling pathways on the inflammatory response in a mouse model of burn injury. Wild-type (TLR2+/+) and mutant-type (TLR2−/−) mice were obtained, and a mouse burn injury model was constructed. Tissue samples were examined with hematoxylin and eosin staining and the transferase mediated nick end labeling (TUNEL) method. Macrophages were treated with TLR2 agonist and p38 inhibitor. The expression levels of TLR2, p38, CD86, IL-1β, and TNF-α were quantified by RT-qPCR, Western blot, and ELISA. When compared with the sham group, the burn group had a significantly higher rate of apoptosis as well as higher expressions of TLR2, p38, CD86, IL-1β, and TNF-α. Inhibiting TLR2 was shown to significantly reduce the expressions of p-p38, CD86, IL-1β, and TNF-α. In the results of in-vitro experiments, TLR2 agonist increased the expression of p-p38, CD86, IL-1β, and TNF-α, whereas a p38 inhibitor was shown to reduce the expression of CD86, IL-1β, and TNF-α. Our results suggest that the TLR2–p38–CD86 signaling pathway plays a vital role in inflammation associated with burn injury.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-01T07:00:00Z
      DOI: 10.1139/bcb-2016-0210
       
  • 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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