Full antagonist of the IL-7 receptor suppresses chronic inflammation in non-human primate models by controlling antigen-specific memory T cells

Volume 2 (2018)

Cover: This month in Cell Stress: Kinase signaling in the innate immune system. Fluorescence microscopic depiction of immune cell responses within the CNS upon chronic pain. Images by Centre for Nanoscale BioPhotonics (CNBP) licensed under the CC BY 2.0 license. Image modified by Cell Stress. The cover is published under the CC BY 4.0 license.

SKP2 and OTUD1 govern non-proteolytic ubiquitination of YAP that promotes YAP nuclear localization and activity

Fan Yao1, Zhenna Xiao1,2, Yutong Sun3 and Li Ma1,2

YAP and its paralog TAZ are key effectors of the evolutionarily conserved Hippo signaling pathway, a pathway that regulates organ size, tissue homeostasis, and tumorigenesis. In human cells, MST1/2 (mammalian

T lymphocytes against solid malignancies: winning ways to defeat tumours

Ignazio Caruana1,§, Luca Simula1,2,§, Franco Locatelli1,# and Silvia Campello2,3, #

INTRODUCTION When a tumour mass starts growing in the body, T lymphocytes are activated inside secondary lymphoid organs (SLOs) and mount an immune response against immuno-stimulating tumour antigens presented by

Irreversible impact of chronic hepatitis C virus infection on human natural killer cell diversity

Benedikt Strunz1, Julia Hengst1,2, Heiner Wedemeyer2,3,4 and Niklas K. Björkström1

Due to the fact that infection with HCV nearly always becomes chronic, we first investigated the imprint of the persisting infection on the NK cell compartment. To overcome shortcomings of

GFI1’s role in DNA repair suggests implications for tumour cell response to treatment

Charles Vadnais1 and Tarik Möröy1,2,3

GFI1 was discovered over 20 years ago and a large body of experimental evidence defines its function as a DNA binding transcriptional repressor. Since GFI1 does not possess any enzymatic

Mitochondrial dysfunction and its role in tissue-specific cellular stress

David Pacheu-Grau1, Robert Rucktäschel1 and Markus Deckers1

Mitochondrial bioenergetics require the coordination of two different and independent genomes. Mutations in either genome will affect mitochondrial functionality and produce different sources of cellular stress. Depending on the kind of defect and stress, different tissues and organs will be affected, leading to diverse pathological conditions. There is no curative therapy for mitochondrial diseases, nevertheless, there are strategies described that fight the various stress forms caused by the malfunctioning organelles. Here, we will revise the main kinds of stress generated by mutations in mitochondrial genes and outline several ways of fighting this stress.

Alzheimer’s disease: amyloid-based pathogenesis and potential therapies

Yixiu Zhou1, Yuhui Sun2, Quan-Hong Ma2 and Yaobo Liu2

INTRODUCTION Alzheimer’s disease (AD) is one of the most prevalent forms of dementia; in 2015, for example, AD affected ~46.8 million people worldwide. It is estimated that this number will

Foie gras and liver regeneration: a fat dilemma

Maria Agnese Della Fazia1 and Giuseppe Servillo1

The liver has a unique ability of regenerating after injuries or partial loss of its mass. The mechanisms responsible for liver regeneration – mostly occurring when the hepatic tissue is damaged or functionally compromised by metabolic stress – have been studied in considerable detail over the last few decades, because this phenomenon has both basic-biology and clinical relevance. More specifically, recent interest has been focusing on the widespread occurrence of abnormal nutritional habits in the Western world that result in an increased prevalence of non-alcoholic fatty liver disease (NAFLD). NAFLD is closely associated with insulin resistance and dyslipidemia, and it represents a major clinical challenge. The disease may progress to steatohepatitis with persistent inflammation and progressive liver damage, both of which will compromise regeneration under conditions of partial hepatectomy in surgical oncology or in liver transplantation procedures. Here, we analyze the impact of ER stress and SIRT1 in lipid metabolism and in fatty liver pathology (...)

Amelioration of obesity-induced diabetes by a novel autophagy enhancer

Hyejin Lim1 and Myung-Shik Lee1

Our screening system was a convenient high throughput assay of autophagic flux rather than cumulative autophagy levels, and the index of autophagic activity was calculated as the ratio of the

Epigenetic mechanisms behind cellular sensitivity to DNA damage

Amanda K. Williamson1, Zijing Zhu1 and Zhi-Min Yuan1

INTRODUCTION Epigenetics is the regulation of gene expression independent of the gene sequence itself via the interactions between DNA and proteins called histones [cite]10.4161/epi.24042[/cite]. In the nucleus, DNA is highly

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The emerging role of minor intron splicing in neurological disorders

Daniel Jutzi 1,2,+, Maureen V. Akinyi 3,+, Jonas Mechtersheimer1,2,+, Mikko J. Frilander3 and Marc-David Ruepp1,4

INTRODUCTION Pre-mRNA splicing is an essential step in eukaryotic gene expression. It is predominantly a co-transcriptional process during which the non-coding introns are excised from precursor mRNA (pre-mRNA) molecules and

A new way to regulate inflammation: selective autophagic degradation of IKKγ mediated by ANGPTL8

Yu Zhang1, Ling Zheng2 and Kun Huang1

Activation of transcription factor nuclear factor-κB (NF-κB) is one of the central events in inflammation and immunity. In resting cells, the activity of NF-κB is inhibited by its binding partner,

Rejuvenation of the aged neuromuscular junction by exercise

Tabita Kreko-Pierce1,2 and Benjamin A. Eaton1,2

Age-dependent declines in muscle function are observed across species. The loss of mobility resulting from the decline in muscle function represents an important health issue and a key determinant of quality of life for the elderly. It is believed that changes in the structure and function of the neuromuscular junction are important contributors to the observed declines in motor function with increased age. Numerous studies indicate that the aging muscle is an important contributor to the deterioration of the neuromuscular junction but the cellular and molecular mechanisms driving the degeneration of the synapse remain incompletely described. Importantly, growing data from both animal models and humans indicate that exercise can rejuvenate the neuromuscular junction and improve motor function. In this review we will focus on the role of muscle-derived neurotrophin signaling in the rejuvenation of the aged neuromuscular junction in response to exercise.

Salmonella Typhimurium infection: Type I Interferons integrate cellular networks to disintegrate macrophages

Nirmal Robinson1,2

Salmonella enterica serovar Typhimurium (S. Typhimurium) are facultative intracellular bacteria that effectively evade innate immune defense mechanisms using a plethora of pathogenic principles encoded in their pathogenicity islands namely Salmonella

Centriolar satellites prevent uncontrolled degradation of centrosome proteins: a speculative review

Nicolas Lecland1 and Andreas Merdes1

INTRODUCTION Centrosomes are cytoplasmic structures that serve as primary microtubule organizing centers in a large variety of animal cells. They consist of a pair of cylindrically shaped centrioles, surrounded by

miR34a: a master regulator in the pathogenesis of bronchopulmonary dysplasia

Pragnya Das1, Mansoor Ali Syed1,2, Dilip Shah1, Vineet Bhandari1,3,*

BPD has been getting more attention as neonatologists from across the world are getting better in saving the lives of premature neonates. This has mobilized intense research to fill the

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Intravital imaging tumor screen used to identify novel metastasis-blocking therapeutic targets

Konstantin Stoletov1, Lian Willetts1, Perrin H. Beatty1 and John D. Lewis1

INTRODUCTION Currently, many cancer patients undergo chemotherapy, which is aimed at mitigating the risk of future metastasis. These treatments, however, have numerous system-wide off-target effects that negatively impact the patients’

Therapeutic anti-tumor immunity directed against neo-epitopes by intratumor delivery of mRNA encoding MLKL

Lien Van Hoecke1,2 and Xavier Saelens1,2,3

We have developed a potentially generic treatment method to induce tumor antigen-specific cellular immunity based on the transient intra-tumor expression of the necroptosis-inducing factor MLKL (Figure 1). Importantly, we have

Red blood cell extracellular vesicles as robust carriers of RNA-based therapeutics

Chanh Tin Pham1, Xin Zhang1, Austin Lam1, Minh TN Le1

The emerging RNA-based therapeutics are renowned for a wide array of druggable targets, which are difficult to achieve by conventional therapies, with high specificity and great versatility. RNA-based drugs function

New insights into the role of soluble E-cadherin in tumor angiogenesis

Maggie K.S. Tang1, Philip P. Ip2 and Alice S.T. Wong1

Ovarian cancer, the leading cause of death among all gynecological malignancies, is a highly aggressive disease with a propensity for metastasis. Due to the discreet anatomical location, by the time

SKP2 and OTUD1 govern non-proteolytic ubiquitination of YAP that promotes YAP nuclear localization and activity

Fan Yao1, Zhenna Xiao1,2, Yutong Sun3 and Li Ma1,2

YAP and its paralog TAZ are key effectors of the evolutionarily conserved Hippo signaling pathway, a pathway that regulates organ size, tissue homeostasis, and tumorigenesis. In human cells, MST1/2 (mammalian

T lymphocytes against solid malignancies: winning ways to defeat tumours

Ignazio Caruana1,§, Luca Simula1,2,§, Franco Locatelli1,# and Silvia Campello2,3, #

INTRODUCTION When a tumour mass starts growing in the body, T lymphocytes are activated inside secondary lymphoid organs (SLOs) and mount an immune response against immuno-stimulating tumour antigens presented by

Irreversible impact of chronic hepatitis C virus infection on human natural killer cell diversity

Benedikt Strunz1, Julia Hengst1,2, Heiner Wedemeyer2,3,4 and Niklas K. Björkström1

Due to the fact that infection with HCV nearly always becomes chronic, we first investigated the imprint of the persisting infection on the NK cell compartment. To overcome shortcomings of

GFI1’s role in DNA repair suggests implications for tumour cell response to treatment

Charles Vadnais1 and Tarik Möröy1,2,3

GFI1 was discovered over 20 years ago and a large body of experimental evidence defines its function as a DNA binding transcriptional repressor. Since GFI1 does not possess any enzymatic

Mitochondrial dysfunction and its role in tissue-specific cellular stress

David Pacheu-Grau1, Robert Rucktäschel1 and Markus Deckers1

Mitochondrial bioenergetics require the coordination of two different and independent genomes. Mutations in either genome will affect mitochondrial functionality and produce different sources of cellular stress. Depending on the kind of defect and stress, different tissues and organs will be affected, leading to diverse pathological conditions. There is no curative therapy for mitochondrial diseases, nevertheless, there are strategies described that fight the various stress forms caused by the malfunctioning organelles. Here, we will revise the main kinds of stress generated by mutations in mitochondrial genes and outline several ways of fighting this stress.

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Astrocytes, emerging stars of energy homeostasis

Simonetta Camandola1

INTRODUCTION The brain is the organ responsible for the centralized control of the other organs’ functions and, in higher vertebrates, of reasoning. Such tasks are achieved thanks to the interconnections

Base editors: a powerful tool for generating animal models of human diseases

Zongyang Lu1,2 and Xingxu Huang1,3

BASE EDITORS: A NOVEL GENOME ENGINEERING TOOL Genetically engineered mouse models of human diseases have long been used in understanding the underlying mechanisms of the clinically relevant genetic disorders. In

Unweaving the role of nuclear Lamins in neural circuit integrity

Samantha L. Deal1 and Shinya Yamamoto1,2,3,4

Structural integrity of the nuclear membrane is essential for the homeostasis of eukaryotic cells. Critical components of this process are Lamins or type-V intermediate filament proteins that form a meshwork

Alzheimer’s disease: amyloid-based pathogenesis and potential therapies

Yixiu Zhou1, Yuhui Sun2, Quan-Hong Ma2 and Yaobo Liu2

INTRODUCTION Alzheimer’s disease (AD) is one of the most prevalent forms of dementia; in 2015, for example, AD affected ~46.8 million people worldwide. It is estimated that this number will

Membrane closure in stress induced-autophagosome formation

Eiji Morita1

Autophagy (macroautophagy) is a bulk degradation system that sequesters cytoplasmic components by generating double-layered isolation membranes and delivering these isolated contents to the lysosomes [cite]10.1146/annurev-cellbio-092910-154005[/cite]. Though this pathway was originally

Centriolar satellites prevent uncontrolled degradation of centrosome proteins: a speculative review

Nicolas Lecland1 and Andreas Merdes1

INTRODUCTION Centrosomes are cytoplasmic structures that serve as primary microtubule organizing centers in a large variety of animal cells. They consist of a pair of cylindrically shaped centrioles, surrounded by

Novel role of the SIRT4-OPA1 axis in mitochondrial quality control

Alexander Lang1 and Roland P. Piekorz1

Aging is defined by various molecular and cellular hallmarks, among them stem cell exhaustion, genomic instability, altered proteostasis, cellular senescence, and mitochondrial dysfunction [cite]10.1016/j.cell.2013.05.039[/cite]. Mitochondrial defects are considered major drivers