Special Issue "Modulators of Endoplasmic Reticulum Stress 2016"
Deadline for manuscript submissions: closed (31 December 2016)
Prof. Dr. Masato Matsuoka
Department of Hygiene and Public Health 1, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan
Website | E-Mail
Phone: 81 3 5269 7418
Interests: cell survival and death; signal transduction; endoplasmic reticulum stress; cellular stress response; neurotoxicants; toxic metals; fluoride
The accumulation of unfolded proteins in the lumen of endoplasmic reticulum (ER) causes ER stress and induces the unfolded protein response (UPR). The UPR alleviates stress by inhibiting protein synthesis, and by promoting the expression of molecular chaperones and other factors involved in ER-associated protein degradation (ERAD). Under cellular stress, the ER activates three branches of the UPR: (i) the protein kinase RNA-activated-like ER kinase–eukaryotic translation initiation factor 2 alpha (PERK-eIF2α) pathway, (ii) the inositol-requiring enzyme 1–X-box binding protein 1 (IRE1-XBP1) pathway, and (iii) the activating transcription factor 6 (ATF6) pathway. However, if ER stress is prolonged and severe, the UPR can result in cell death through the activation of apoptotic pathways. Accumulating evidence indicates that the ER stress is involved in the pathogenesis of not only the protein misfolding disorders such as neurodegenerative disease, but also in the cytotoxicity of drugs, environmental pollutants, and industrial chemicals. Thus, the determination of the modulators that activate or inhibit ER stress signaling pathways is an important field of research. The articles in this special issue will address research aspects related to the inducers or modulators of ER stress in the biological, toxicological, and medical fields.
Prof. Dr. Masato Matsuoka
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. International Journal of Molecular Sciences is an international peer-reviewed open access monthly journal published by MDPI.
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- endoplasmic reticulum stress
- unfolded protein response
- molecular chaperones
- signal transduction
- cell survival and death
- protein misfolding disorders
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Neuroprotection Strategy in Retinal Degeneration: Suppressing ER Stress-Induced Cell Death via Inhibition of mTOR Signal
Authors: Bin Fan, Ying-Jian Sun, Shu-Yan Liu, Lin Che, Guang-Yu Li
Affiliation: Department of Ophthalmology, Second Hospital of JiLin University, ChangChun 130041, China
Abstract: Retina is specialized sensory organ essential for light detection and visual formation in the human eye. Retinal neurons dysfunction and death cause vision loss in many eye diseases such as retinitis pigmentosa and achromatopsia. Endoplasmic reticulum (ER) stress plays an important role in the development and pathology of retinal degeneration diseases. However, mammalian target of rapamycin (mTOR) kinase, as a signaling node, controls many cellular processes including protein synthesis, translation, energy metabolism, apoptosis, autophagy and ER stress as well. mTOR complex 1 (mTORC1) operates both upstream and downstream of ER stress signals, which can either enhance or suppress ER stress-induced cell death. This review surveys our knowledge about the influence of mTOR signal on ER stress arising from misfolded proteins and genetic mutations in retinal degeneration diseases and highlights potential neuroprotection strategy and therapeutic implications.
Keywords: mTOR; ER stress; retinal degeneration; unfolded protein response; cell death; apoptosis
Title: ER Stress in Monogenic Endocrine Disorders
Authors: Daisuke Ariyasu 1, Yukihiro Hasegawa 2, Hiderou Yoshida 3
1 Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan
2 Department of Endocrinology and Metabolism, Tokyo Metropolitan Children’s Medical Center, Tokyo, Japan
3 Department of Biochemistry and Molecular Biology, Graduate School of Life Science, University of Hyogo, Hyogo, Japan
Abstract: Unfolded proteins, accumulated in the endoplasmic reticulum (ER), cause ER stress, which contributes to the development of endocrine disorders such as Ins2Akita diabetes, familial neurohypophysial diabetes insipidus, and Wolfram syndrome. Here, we summarize recent findings on monogenic endocrine disorders in which ER stress is involved. In particular, growth hormone deficiency, caused by heterozygous intron 3 splice-site mutations in the GH1 gene, was clarified to be one of the ER stress-related diseases, suggesting that the anterior pituitary gland is one of the organs which are vulnerable to ER stress.