IUBMB Life

Cover image for Vol. 68 Issue 9

Edited By: Angelo Azzi and William J. Whelan

Impact Factor: 2.653

ISI Journal Citation Reports © Ranking: 2015: 108/187 (Cell Biology); 145/289 (Biochemistry & Molecular Biology)

Online ISSN: 1521-6551

Associated Title(s): Biochemistry and Molecular Biology Education, Biotechnology and Applied Biochemistry, BioFactors

Featured

  • MicroRNA-106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer

    MicroRNA‐106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer

    Up-regulation of miR-106b induced cell migration, invasion, and proliferation of breast cancer in vitro. The ability of migration and invasion was compared in MCF-7 and MDA-MB-231 cells with miR-NC or miR-106b mimics based on wound healing (A, B) and transwell assays (C). The proliferation capacity was tested in the cell lines including MCF-7 and MDA-MB-231 transfected with miR-NC or miR-106b mimics by clone formation (D) and CCK8 assays (E, F). Each experiment was independently repeated at least three times. Data was presented as the mean ± SD (*P < 0.05) compared with the control group.

  • Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt-Rac1-FAK-JNK and ERK signaling pathways

    Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

    Effect of bFGF on melanocyte migration. (A) Treatment with different concentrations of bFGF for 24 h showed no effect on melanocyte proliferation by MTT assay. (B, C) Melanocyte migration after different concentrations of bFGF treated within 24 h by transwell assay. (D) F-actin was labeled by FITC-conjugated phalloidin 24 h after wounding with or without bFGF treatment. The increased magnitude of lamellipodia formation in the migration cells were denoted with arrowheads. The experiments were repeated three times. Bar = 50 μm. Data were presented as mean ± SEM (n = 3). **P < 0.01 and ***P < 0.001 compared with control group.

  • Mutant p53 and mTOR/PKM2 regulation in cancer cells

    Mutant p53 and mTOR/PKM2 regulation in cancer cells

    Schematic representation of the regulation of the mTOR/PKM2 axis in p53 mutated cancer cells.

  • Epigenomic maintenance through dietary intervention can facilitate DNA repair process to slow down the progress of premature aging

    Epigenomic maintenance through dietary intervention can facilitate DNA repair process to slow down the progress of premature aging

    Appropriate nutraceutical intervention slows down premature aging by decreasing DNA damage and promoting epigenomic stability through facilitation of DNA repair mechanisms. DNA damage is caused by various exogenous and endogenous factors, age-related chromatin changes and DNA repair deficiency. Once DNA damage is detected, appropriate DNA damage responses (DDRs) are elicited. DDRs inhibit factors causing DNA damage as well as initiate repair mechanisms. DNA damage signals the activation of DNA repair enzymes, which when deficient results in accumulation of DNA damage. This disturbs the genomic stability and leads to disturbances in the physiology. This also causes epigenomic disturbances, thereby culminating in accelerated or premature aging and finally an early death. Nutrients/nutrient formulations like Amalaki rasayana, DHA, resveratrol, curcumin, etc. and neurotrophic factors like BDNF, NGF and IGF-1 provide a coherent cellular microenvironment which is conducive to genomic and epigenomic stability. Such epigenomic maintenance could bring about positive impact directly by inhibiting DNA damage or indirectly via initiating DNA repair mechanisms.

  • Bioconversion of anhydrosugars: Emerging concepts and strategies

    Bioconversion of anhydrosugars: Emerging concepts and strategies

    a) Ribbon diagram of AnmK (PDB: 3QBW) superimposed on LGK in the closed state (PDB: 4ZLU). AnmK is shown in gray while the two monomeric subunits of LGK are shown in maroon and cyan. The nucleotide and sugar substrates are shown as sphere representations in green and yellow, respectively; b) For comparison of closed and open conformations, AnmK in the open state is shown (PDB: 4MO5).

  • Uncoupling proteins of invertebrates: A review

    Uncoupling proteins of invertebrates: A review

    Phylogenetic analysis based on the known or predicted protein sequences of UCPs with a particular emphasis on phylogenetic associations within the UCP4 clade. Based on available annotations, the presence of conserved domains and BLASTp similarity, the UCP4 clade was manually retrieved from an UniProt database. The UCP4 clade is split into clade I, which contains only B and C isoforms found in Drosophila and the monarch butterfly, while the other, clade II, includes A isoforms and all other insect UCP4s. The sequences were aligned using the ClustalW tool in Geneious and the evolutionary model was selected with ProtTest 3.1. Considering the large number of studied proteins, we applied FastTree 2.1.7 software to construct the approximate maximum-likelihood tree (JTT + G model, other settings default). KMCP, kidney mitochondrial carrier family; DCP/FACP, dicarboxylate carrier proteins.

  • MicroRNA‐106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer
  • Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways
  • Mutant p53 and mTOR/PKM2 regulation in cancer cells
  • Epigenomic maintenance through dietary intervention can facilitate DNA repair process to slow down the progress of premature aging
  • Bioconversion of anhydrosugars: Emerging concepts and strategies
  • Uncoupling proteins of invertebrates: A review

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IUBMB Joint Virtual Issue on Cancer Therapies

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We’re pleased to present a new Joint Virtual Issue on Cancer Therapies in celebration of the IUBMB 2015 Miami Winter Symposium, featuring articles from Biofactors, Biotechnologyand Applied Biochemistry, and IUBMB Life.

2015 IUBMB Life Young Investigator Award

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On behalf of the IUBMB, IUBMB Life, and Wiley, it is with great pleasure and honor that we announce Yang Chao as the recipient of the 2015 IUBMB Life - Wiley Young Investigator Award for his article, Aquaporin-4 knockdown ameliorates hypoxic-ischemic cerebral edema in newborn piglets.

Yang Chao, M. D. is an attending physician in Department of Radiology at Dalian Medical University of China, His research interest is in molecular imaging and neuroimaging. The winning article Aquaporin-4 knockdown ameliorates hypoxic-ischemic cerebral edema in newborn piglets is main part of his doctoral thesis under guidance of professor Bian Jie. Yang Chao will be honored with the 2015 IUBMB Life - Wiley Young Investigator Award at the 23rd International Union for Biochemistry and Molecular Biology (IUBMB) Congress and 44th Annual Meeting of the Brazilian Society for Biochemistry and Molecular Biology in Foz do Iguaçu, Brazil from August 24th to 28th, 2015, and his award-winning article will be FREELY available online through the conference.

Please join us in congratulating Mr. Yang Chao as the recipient of the annual IUBMB Life– Wiley Young Investigator Award!

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