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Stress Signalling and Cell Death
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Stress Signalling and Cell Death

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 13718

Special Issue Editor

Dr. Takuya Noguchi

E-Mail Website
Guest Editor
Department of Biopharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
Interests: apoptosis; signaling pathways; phosphorylation; signal transduction; cell signaling; reactive oxygen species; molecular cell biology; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Organisms are continuously exposed to various types of stress from the external and internal environments. In order to protect cells against such stresses, each cell is equipped with multiple signal transduction systems that elicit a wide range of cellular responses to adapt to or resist such stresses. These signal transduction systems are often described as “stress signaling”. Compelling evidence indicates that the dysregulation of stress signaling induces aberrant responses to stresses, which is responsible for various diseases. Programmed cell death (PCD) is perceived as a crucial event during development and tissue formation. As a stress response, PCD also plays a critical role in the elimination of cells suffering severe stress-induced damage to maintain homeostasis within multicellular organisms, and a number of stress-signaling pathways are involved in the regulation of PCD. In this Special Issue, studies of novel signalling mechanisms and pathological processes associated with PCD are welcome.

Dr. Takuya Noguchi
Guest Editor

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 submissions that pass pre-check are 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 semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (3 papers)

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Research

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11 pages, 4860 KiB  
Article
The E3 Ubiquitin-Protein Ligase RNF4 Promotes TNF-α-Induced Cell Death Triggered by RIPK1
by Tatsuya Shimada, Yuki Kudoh, Takuya Noguchi, Tomohiro Kagi, Midori Suzuki, Mei Tsuchida, Hiromu Komatsu, Miki Takahashi, Yusuke Hirata and Atsushi Matsuzawa
Int. J. Mol. Sci. 2021, 22(11), 5796; https://doi.org/10.3390/ijms22115796 - 28 May 2021
Cited by 5 | Viewed by 4161
Abstract
Receptor-interacting protein kinase 1 (RIPK1) is a key component of the tumor necrosis factor (TNF) receptor signaling complex that regulates both pro- and anti-apoptotic signaling. The reciprocal functions of RIPK1 in TNF signaling are determined by the state of the posttranslational modifications (PTMs) [...] Read more.
Receptor-interacting protein kinase 1 (RIPK1) is a key component of the tumor necrosis factor (TNF) receptor signaling complex that regulates both pro- and anti-apoptotic signaling. The reciprocal functions of RIPK1 in TNF signaling are determined by the state of the posttranslational modifications (PTMs) of RIPK1. However, the underlying mechanisms associated with the PTMs of RIPK1 are unclear. In this study, we found that RING finger protein 4 (RNF4), a RING finger E3 ubiquitin ligase, is required for the RIPK1 autophosphorylation and subsequent cell death. It has been reported that RNF4 negatively regulates TNF-α-induced activation of the nuclear factor-κB (NF-κB) through downregulation of transforming growth factor β-activated kinase 1 (TAK1) activity, indicating the possibility that RNF4-mediated TAK1 suppression results in enhanced sensitivity to cell death. However, interestingly, RNF4 was needed to induce RIPK1-mediated cell death even in the absence of TAK1, suggesting that RNF4 can promote RIPK1-mediated cell death without suppressing the TAK1 activity. Thus, these observations reveal the existence of a novel mechanism whereby RNF4 promotes the autophosphorylation of RIPK1, which provides a novel insight into the molecular basis for the PTMs of RIPK1. Full article
(This article belongs to the Special Issue Stress Signalling and Cell Death)
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Review

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22 pages, 10018 KiB  
Review
Impact of ER Stress and ER-Mitochondrial Crosstalk in Huntington’s Disease
by Shuvadeep Maity, Pragya Komal, Vaishali Kumar, Anshika Saxena, Ayesha Tungekar and Vaani Chandrasekar
Int. J. Mol. Sci. 2022, 23(2), 780; https://doi.org/10.3390/ijms23020780 - 11 Jan 2022
Cited by 18 | Viewed by 4110
Abstract
Accumulation of misfolded proteins is a common phenomenon of several neurodegenerative diseases. The misfolding of proteins due to abnormal polyglutamine (PolyQ) expansions are linked to the development of PolyQ diseases including Huntington’s disease (HD). Though the genetic basis of PolyQ repeats in HD [...] Read more.
Accumulation of misfolded proteins is a common phenomenon of several neurodegenerative diseases. The misfolding of proteins due to abnormal polyglutamine (PolyQ) expansions are linked to the development of PolyQ diseases including Huntington’s disease (HD). Though the genetic basis of PolyQ repeats in HD remains prominent, the primary molecular basis mediated by PolyQ toxicity remains elusive. Accumulation of misfolded proteins in the ER or disruption of ER homeostasis causes ER stress and activates an evolutionarily conserved pathway called Unfolded protein response (UPR). Protein homeostasis disruption at organelle level involving UPR or ER stress response pathways are found to be linked to HD. Due to dynamic intricate connections between ER and mitochondria, proteins at ER-mitochondria contact sites (mitochondria associated ER membranes or MAMs) play a significant role in HD development. The current review aims at highlighting the most updated information about different UPR pathways and their involvement in HD disease progression. Moreover, the role of MAMs in HD progression has also been discussed. In the end, the review has focused on the therapeutic interventions responsible for ameliorating diseased states via modulating either ER stress response proteins or modulating the expression of ER-mitochondrial contact proteins. Full article
(This article belongs to the Special Issue Stress Signalling and Cell Death)
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14 pages, 7809 KiB  
Review
The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis
by Shiyi Tan and Shi Chen
Int. J. Mol. Sci. 2021, 22(15), 8110; https://doi.org/10.3390/ijms22158110 - 28 Jul 2021
Cited by 35 | Viewed by 4189
Abstract
Silicosis remains one of the most severe pulmonary fibrotic diseases worldwide, caused by chronic exposure to silica dust. In this review, we have proposed that programmed cell death (PCD), including autophagy, apoptosis, and pyroptosis, is closely associated with silicosis progression. Furthermore, some autophagy, [...] Read more.
Silicosis remains one of the most severe pulmonary fibrotic diseases worldwide, caused by chronic exposure to silica dust. In this review, we have proposed that programmed cell death (PCD), including autophagy, apoptosis, and pyroptosis, is closely associated with silicosis progression. Furthermore, some autophagy, apoptosis, or pyroptosis-related signaling pathways or regulatory proteins have also been summarized to contribute greatly to the formation and development of silicosis. In addition, silicosis pathogenesis depends on the crosstalk among these three ways of PCD to a certain extent. In summary, more profound research on these mechanisms and effects may be expected to become promising targets for intervention or therapeutic methods of silicosis in the future. Full article
(This article belongs to the Special Issue Stress Signalling and Cell Death)
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