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Special Issue "Structure, Interaction, Reaction, and Function of Biomolecules in Multimolecular Crowding Biosystems"

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 31 October 2019.

Special Issue Editors

Dr. Daisuke Miyoshi
E-Mail Website
Guest Editor
Konan University, Kobe, Japan
Tel. +81-78-303-1426
Interests: molecular crowding; nucleic acid structure; stability; function; ligand; photodynamic therapy; liquid–liquid phase separation
Dr. Akio Ojida
E-Mail Website
Guest Editor
Kyushu University, Fukuoka, Japan
Interests: chemical biology; chemical protein labeling; chemical probe; fluorescence imaging; drug discovery
Dr. Kazuhito Tabata
E-Mail Website
Guest Editor
The University of Tokyo, Tokyo, Japan
Interests: MEMS; micro-TAS; single molecule; reconstitution of cellular function; liposome; origin of life; synthetic biology; biophysics

Special Issue Information

Dear Colleagues,

The inside of living cells are surprisingly enriched with a great variety of biomolecules, from small ions, metabolites, and osmolytes, to macromolecular proteins, nucleic acids, and polysaccharides. These biomolecules occupy up to 40 % of the cellular volume, and constitute a multimolecular crowding biosysytem of cells. Biomolecule evolution has been done in order to optimize and maximize their structure, interaction, reaction, and function in the multimolecular crowding biosystems. Therefore, it is obvious that multimolecular crowding is critical, not only in order to unveil the property of biomolecules inside cells, but also to develop a functional molecule that maintains activity, even inside of the cells.

The aim of this Special Issue is to collect research papers, reviews, and communications concerning the physical, chemical, biological, and computational characterization of biomolecules; the detection and imaging of a target molecule; the modification and regulation of biomolecules; and the development of a functional molecule and a device, under molecular crowding, multimolecular crowding, and cellular environments. Moreover, studies on biological roles of multimolecular crowding and on the utilization of multimolecular crowding for applications are invited.

Dr. Daisuke Miyoshi
Dr. Akio Ojida
Dr. Kazuhito Tabata
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Chemical biology
  • Synthetic biology
  • Cell imaging
  • Computational chemistry
  • Bioorganic chemistry
  • Systems biology
  • Biomolecular chemistry
  • Molecular crowding
  • Ligands
  • Osmolytes
  • Metabolites
  • Gene expression
  • Enzyme activity
  • Single molecular analysis

Published Papers (3 papers)

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Research

Open AccessArticle
DMPK is a New Candidate Mediator of Tumor Suppressor p53-Dependent Cell Death
Molecules 2019, 24(17), 3175; https://doi.org/10.3390/molecules24173175 - 01 Sep 2019
Abstract
Tumor suppressor p53 plays an integral role in DNA-damage induced apoptosis, a biological process that protects against tumor progression. Cell shape dramatically changes when cells undergo apoptosis, which is associated with actomyosin contraction; however, it remains entirely elusive how p53 regulates actomyosin contraction [...] Read more.
Tumor suppressor p53 plays an integral role in DNA-damage induced apoptosis, a biological process that protects against tumor progression. Cell shape dramatically changes when cells undergo apoptosis, which is associated with actomyosin contraction; however, it remains entirely elusive how p53 regulates actomyosin contraction in response to DNA-damaging agents. To identify a novel p53 regulating gene encoding the modulator of myosin, we conducted DNA microarray analysis. We found that, in response to DNA-damaging agent doxorubicin, expression of myotonic dystrophy protein kinase (DMPK), which is known to upregulate actomyosin contraction, was increased in a p53-dependent manner. The promoter region of DMPK gene contained potential p53-binding sequences and its promoter activity was increased by overexpression of the p53 family protein p73, but, unexpectedly, not of p53. Furthermore, we found that doxorubicin treatment induced p73 expression, which was significantly attenuated by downregulation of p53. These data suggest that p53 induces expression of DMPK through upregulating p73 expression. Overexpression of DMPK promotes contraction of the actomyosin cortex, which leads to formation of membrane blebs, loss of cell adhesion, and concomitant caspase activation. Taken together, our results suggest the existence of p53-p73-DMPK axis which mediates DNA-damage induced actomyosin contraction at the cortex and concomitant cell death. Full article
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Open AccessArticle
Next Generation Sequencing-Based Transcriptome Predicts Bevacizumab Efficacy in Combination with Temozolomide in Glioblastoma
Molecules 2019, 24(17), 3046; https://doi.org/10.3390/molecules24173046 - 22 Aug 2019
Abstract
Glioblastoma (GBM), the most common and malignant brain tumor, is classified according to its isocitrate dehydrogenase (IDH) mutation status in the 2016 World Health Organization (WHO) brain tumor classification scheme. The standard treatment for GBM is maximal resection, radiotherapy, and Temozolomide (TMZ). Recently, [...] Read more.
Glioblastoma (GBM), the most common and malignant brain tumor, is classified according to its isocitrate dehydrogenase (IDH) mutation status in the 2016 World Health Organization (WHO) brain tumor classification scheme. The standard treatment for GBM is maximal resection, radiotherapy, and Temozolomide (TMZ). Recently, Bevacizumab (Bev) has been added to basic therapy for newly diagnosed GBM, and monotherapy for recurrent GBM. However, the effect of IDH1 mutation on the combination of Bev and TMZ is unknown. In this study, we performed transcriptomic analysis by RNA sequencing with next generation sequencing (NGS), a newly developed powerful method that enables the quantification of the expression level of genome-wide genes. Extracellular matrix and immune cell migration genes were mainly upregulated whereas cell cycle genes were downregulated in IDH1-mutant U87 cells but not in IDH1-wildtype U87 cells after adding Bev to TMZ. In vitro and in vivo studies were conducted for further investigations to verify these results, and the addition of Bev to TMZ showed a significant antitumor effect only in the IDH1-mutant GBM xenograft model. Further studies of gene expression profiling in IDH1 mutation gliomas using NGS will provide more genetic information and will lead to new treatments for this refractory disease. Full article
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Open AccessArticle
Inhibition of CpLIP2 Lipase Hydrolytic Activity by Four Flavonols (Galangin, Kaempferol, Quercetin, Myricetin) Compared to Orlistat and Their Binding Mechanisms Studied by Quenching of Fluorescence
Molecules 2019, 24(16), 2888; https://doi.org/10.3390/molecules24162888 - 08 Aug 2019
Abstract
The inhibition of recombinant CpLIP2 lipase/acyltransferase from Candida parapsiolosis was considered a key model for novel antifungal drug discovery and a potential therapeutic target for candidiasis. Lipases have identified recently as potent virulence factors in C. parapsilosis and some other yeasts. The inhibition [...] Read more.
The inhibition of recombinant CpLIP2 lipase/acyltransferase from Candida parapsiolosis was considered a key model for novel antifungal drug discovery and a potential therapeutic target for candidiasis. Lipases have identified recently as potent virulence factors in C. parapsilosis and some other yeasts. The inhibition effects of orlistat and four flavonols (galangin, kaempferol, quercetin and myricetin) characterized by an increasing degree of hydroxylation in B-ring, were investigated using ethyl oleate hydrolysis as the model reaction. Orlistat and kaempferol (14 µM) strongly inhibited CpLIP2 catalytic activity within 1 min of pre-incubation, by 90% and 80%, respectively. The relative potency of flavonols as inhibitors was: kaempferol > quercetin > myricetin > galangin. The results suggested that orlistat bound to the catalytic site while kaempferol interacted with W294 on the protein lid. A static mechanism of interactions between flavonols and CpLIP2 lipase was confirmed by fluorescence quenching analyses, indicating that the interactions were mainly driven by hydrophobic bonds and electrostatic forces. From the Lehrer equation, fractions of tryptophan accessibility to the quencher were evaluated, and a relationship with the calculated number of binding sites was suggested. Full article
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