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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/28304405/the-erbb3-receptor-tyrosine-kinase-negatively-regulates-paneth-cells-by-pi3k-dependent-suppression-of-atoh1
#1
Dana Almohazey, Yuan-Hung Lo, Claire V Vossler, Alan J Simmons, Jonathan J Hsieh, Edie B Bucar, Michael A Schumacher, Kathryn E Hamilton, Ken S Lau, Noah F Shroyer, Mark R Frey
Paneth cells (PCs), a secretory population located at the base of the intestinal crypt, support the intestinal stem cells (ISC) with growth factors and participate in innate immunity by releasing antimicrobial peptides, including lysozyme and defensins. PC dysfunction is associated with disorders such as Crohn's disease and necrotizing enterocolitis, but the specific pathways regulating PC development and function are not fully understood. Here we tested the role of the neuregulin receptor ErbB3 in control of PC differentiation and the ISC niche...
March 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28304404/interactions-between-th1-cells-and-tregs-affect-regulation-of-hepatic-fibrosis-in-biliary-atresia-through-the-ifn-%C3%AE-stat1-pathway
#2
Jie Wen, Ying Zhou, Jun Wang, Jie Chen, Wenbo Yan, Jin Wu, Junkai Yan, Kejun Zhou, Yongtao Xiao, Yang Wang, Qiang Xia, Wei Cai
Regulatory T cells (Tregs) and CD4(+) T helper (Th) cells have important roles in bile duct injury of biliary atresia (BA). However, their impacts on liver fibrosis are undefined. Between 2013 and 2016, 146 patients with various stages of BA were enrolled in this study. Peripheral blood, liver biopsy and lymph node samples were collected. Flow cytometry, magnetic cell sorting and immunostaining were used to characterize lymphocytes from BA patients. Deficiency of Tregs was observed along with increased Th1, Th2 and Th17 frequencies in the peripheral blood and livers of BA patients...
March 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28282038/spata2-more-than-a-missing-link
#3
Lisa Schlicher, Prisca Brauns-Schubert, Florian Schubert, Ulrich Maurer
The assembly of the TNFR1 signalling complex (TNF-RSC) depends on K63- and M1-linked ubiquitylation, promoting the recruitment of complex constituents and the stability of the complex. Ubiquitylation is a dynamic process, controlled by E3 ubiquitin ligases as well as deubiquitinases, such as CYLD and OTULIN. A novel molecule, SPATA2, which is crucial for recruiting and activating the deubiquitinase CYLD within the TNF-RSC, has now been identified by four different studies. Loss of SPATA2 was shown to result in increased TNF-, but also NOD2-mediated proinflammatory signalling...
March 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28282037/sk2-channels-regulate-mitochondrial-respiration-and-mitochondrial-ca-2-uptake
#4
Birgit Honrath, Lina Matschke, Tammo Meyer, Lena Magerhans, Fabiana Perocchi, Goutham K Ganjam, Hans Zischka, Cornelius Krasel, Albert Gerding, Barbara M Bakker, Moritz Bünemann, Stefan Strack, Niels Decher, Carsten Culmsee, Amalia M Dolga
Mitochondrial calcium ([Ca(2+)]m) overload and changes in mitochondrial metabolism are key players in neuronal death. Small conductance calcium-activated potassium (SK) channels provide protection in different paradigms of neuronal cell death. Recently, SK channels were identified at the inner mitochondrial membrane, however, their particular role in the observed neuroprotection remains unclear. Here, we show a potential neuroprotective mechanism that involves attenuation of [Ca(2+)]m uptake upon SK channel activation as detected by time lapse mitochondrial Ca(2+) measurements with the Ca(2+)-binding mitochondria-targeted aequorin and FRET-based [Ca(2+)]m probes...
March 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28282036/heterarchy-of-transcription-factors-driving-basal-and-luminal-cell-phenotypes-in-human-urothelium
#5
Carl Fishwick, Janet Higgins, Lawrence Percival-Alwyn, Arianna Hustler, Joanna Pearson, Sarah Bastkowski, Simon Moxon, David Swarbreck, Chris D Greenman, Jennifer Southgate
Cell differentiation is affected by complex networks of transcription factors that co-ordinate re-organisation of the chromatin landscape. The hierarchies of these relationships can be difficult to dissect. During in vitro differentiation of normal human uro-epithelial cells, formaldehyde-assisted isolation of regulatory elements (FAIRE-seq) and RNA-seq was used to identify alterations in chromatin accessibility and gene expression changes following activation of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) as a differentiation-initiating event...
March 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28234359/non-apoptotic-functions-of-bcl-2-family-proteins
#6
REVIEW
Atan Gross, Samuel G Katz
The BCL-2 family proteins are major regulators of the apoptosis process, but the mechanisms by which they regulate this process are only partially understood. It is now well documented that these proteins play additional non-apoptotic roles that are likely to be related to their apoptotic roles and to provide important clues to cracking their mechanisms of action. It seems that these non-apoptotic roles are largely related to the activation of cellular survival pathways designated to maintain or regain cellular survival, but, if unsuccessful, will switch over into a pro-apoptotic mode...
February 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28234358/ampk-improves-gut-epithelial-differentiation-and-barrier-function-via-regulating-cdx2-expression
#7
Xiaofei Sun, Qiyuan Yang, Carl J Rogers, Min Du, Mei-Jun Zhu
Impairment in gut epithelial integrity and barrier function is associated with many diseases. The homeostasis of intestinal barrier is based on a delicate regulation of epithelial proliferation and differentiation. AMP-activated protein kinase (AMPK) is a master regulator of energy metabolism, and cellular metabolites are intrinsically involved in epigenetic modifications governing cell differentiation. We aimed to evaluate the regulatory role of AMPK on intestinal epithelial development and barrier function...
February 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28234357/pathogen-response-like-recruitment-and-activation-of-neutrophils-by-sterile-immunogenic-dying-cells-drives-neutrophil-mediated-residual-cell-killing
#8
Abhishek D Garg, Lien Vandenberk, Shentong Fang, Tekele Fasche, Sofie Van Eygen, Jan Maes, Matthias Van Woensel, Carolien Koks, Niels Vanthillo, Norbert Graf, Peter de Witte, Stefaan Van Gool, Petri Salven, Patrizia Agostinis
Innate immune sensing of dying cells is modulated by several signals. Inflammatory chemokines-guided early recruitment, and pathogen-associated molecular patterns-triggered activation, of major anti-pathogenic innate immune cells like neutrophils distinguishes pathogen-infected stressed/dying cells from sterile dying cells. However, whether certain sterile dying cells stimulate innate immunity by partially mimicking pathogen response-like recruitment/activation of neutrophils remains poorly understood. We reveal that sterile immunogenic dying cancer cells trigger (a cell autonomous) pathogen response-like chemokine (PARC) signature, hallmarked by co-release of CXCL1, CCL2 and CXCL10 (similar to cells infected with bacteria or viruses)...
February 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28234356/metacaspases-versus-caspases-in-development-and-cell-fate-regulation
#9
REVIEW
E A Minina, N S Coll, H Tuominen, P V Bozhkov
Initially found to be critically involved in inflammation and apoptosis, caspases have since then been implicated in the regulation of various signaling pathways in animals. How caspases and caspase-mediated processes evolved is a topic of great interest and hot debate. In fact, caspases are just the tip of the iceberg, representing a relatively small group of mostly animal-specific enzymes within a broad family of structurally related cysteine proteases (family C14 of CD clan) found in all kingdoms of life...
February 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28234355/the-emerging-role-of-rnas-in-dna-damage-repair
#10
REVIEW
Ben R Hawley, Wei-Ting Lu, Ania Wilczynska, Martin Bushell
Many surveillance and repair mechanisms exist to maintain the integrity of our genome. All of the pathways described to date are controlled exclusively by proteins, which through their enzymatic activities identify breaks, propagate the damage signal, recruit further protein factors and ultimately resolve the break with little to no loss of genetic information. RNA is known to have an integral role in many cellular pathways, but, until very recently, was not considered to take part in the DNA repair process...
February 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#11
Ivana Celardo, Susann Lehmann, Ana C Costa, Samantha Hy Loh, L Miguel Martins
Neurons rely on mitochondria as their preferred source of energy. Mutations in PINK1 and PARKIN cause neuronal death in early-onset Parkinson's disease (PD), thought to be due to mitochondrial dysfunction. In Drosophila pink1 and parkin mutants, mitochondrial defects lead to the compensatory upregulation of the mitochondrial one-carbon cycle metabolism genes by an unknown mechanism. Here we uncover that this branch is triggered by the activating transcription factor 4 (ATF4). We show that ATF4 regulates the expression of one-carbon metabolism genes SHMT2 and NMDMC as a protective response to mitochondrial toxicity...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211873/the-p53-family-members-have-distinct-roles-during-mammalian-embryonic-development
#12
Jeanine L Van Nostrand, Margot E Bowen, Hannes Vogel, Maria Barna, Laura D Attardi
The p53 tumor suppressor is a member of a multi-protein family, including the p63 and p73 transcription factors. These proteins can bind to the same consensus sites in DNA and activate the same target genes, suggesting that there could be functional redundancy between them. Indeed, double mutant mice heterozygous for any two family member-encoding genes display enhanced cancer phenotypes relative to single heterozygous mutants. However, whether the family members play redundant roles during embryonic development has remained largely unexplored...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211872/rictor-mtorc2-deficiency-enhances-keratinocyte-stress-tolerance-via-mitohormesis
#13
Beatrice Tassone, Stefania Saoncella, Francesco Neri, Ugo Ala, Davide Brusa, Mark A Magnuson, Paolo Provero, Salvatore Oliviero, Chiara Riganti, Enzo Calautti
How metabolic pathways required for epidermal tissue growth and remodeling influence the ability of keratinocytes to survive stressful conditions is still largely unknown. The mechanistic target of rapamycin complex 2 (mTORC2) regulates growth and metabolism of several tissues, but its functions in epidermal cells are poorly defined. Rictor is an adaptor protein essential for mTORC2 activity. To explore the roles of mTORC2 in the epidermis, we have conditionally deleted rictor in mice via K14-Cre-mediated homologous recombination and found that its deficiency causes moderate tissue hypoplasia, reduced keratinocyte proliferation and attenuated hyperplastic response to TPA...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211871/expression-level-is-a-key-determinant-of-e2f1-mediated-cell-fate
#14
Igor Shats, Michael Deng, Adam Davidovich, Carolyn Zhang, Jungeun S Kwon, Dinesh Manandhar, Raluca Gordân, Guang Yao, Lingchong You
The Rb/E2F network has a critical role in regulating cell cycle progression and cell fate decisions. It is dysfunctional in virtually all human cancers, because of genetic lesions that cause overexpression of activators, inactivation of repressors, or both. Paradoxically, the downstream target of this network, E2F1, is rarely strongly overexpressed in cancer. E2F1 can induce both proliferation and apoptosis but the factors governing these critical cell fate decisions remain unclear. Previous studies have focused on qualitative mechanisms such as differential cofactors, posttranslational modification or state of other signaling pathways as modifiers of the cell fate decisions downstream of E2F1 activation...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211870/non-apoptotic-functions-of-caspases-in-myeloid-cell-differentiation
#15
REVIEW
Stéphanie Solier, Michaela Fontenay, William Vainchenker, Nathalie Droin, Eric Solary
Subtle caspase activation is associated with the differentiation of several myeloid lineages. A tightly orchestrated dance between caspase-3 activation and the chaperone HSP70 that migrates to the nucleus to protect the master regulator GATA-1 from cleavage transiently occurs in basophilic erythroblasts and may prepare nucleus and organelle expel that occurs at the terminal phase of erythroid differentiation. A spatially restricted activation of caspase-3 occurs in maturing megakaryocytes to promote proplatelet maturation and platelet shedding in the bloodstream...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211869/non-apoptotic-cell-death-in-animal-development
#16
REVIEW
Lena M Kutscher, Shai Shaham
Programmed cell death (PCD) is an important process in the development of multicellular organisms. Apoptosis, a form of PCD characterized morphologically by chromatin condensation, membrane blebbing, and cytoplasm compaction, and molecularly by the activation of caspase proteases, has been extensively investigated. Studies in Caenorhabditis elegans, Drosophila, mice, and the developing chick have revealed, however, that developmental PCD also occurs through other mechanisms, morphologically and molecularly distinct from apoptosis...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186506/epigenetic-regulation-of-hdac1-sumoylation-as-an-endogenous-neuroprotection-against-a%C3%AE-toxicity-in-a-mouse-model-of-alzheimer-s-disease
#17
Chih Chieh Tao, Wei Lun Hsu, Yun Li Ma, Sin Jhong Cheng, Eminy Hy Lee
Amyloid-β (Aβ) produces neurotoxicity in the brain and causes neuronal death, but the endogenous defense mechanism that is activated on Aβ insult is less well known. Here we found that acute Aβ increases the expression of PIAS1 and Mcl-1 via activation of MAPK/ERK, and Aβ induction of PIAS1 enhances HDAC1 SUMOylation in rat hippocampus. Knockdown of PIAS1 decreases endogenous HDAC1 SUMOylation and blocks Aβ induction of Mcl-1. Sumoylated HDAC1 reduces it association with CREB, increases CREB binding to the Mcl-1 promoter and mediates Aβ induction of Mcl-1 expression...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186504/a-defective-dntp-pool-hinders-dna-replication-in-cell-cycle-reactivated-terminally-differentiated-muscle-cells
#18
Deborah Pajalunga, Elisa Franzolin, Martina Stevanoni, Sara Zribi, Nunzia Passaro, Aymone Gurtner, Samantha Donsante, Daniela Loffredo, Lidia Losanno, Vera Bianchi, Antonella Russo, Chiara Rampazzo, Marco Crescenzi
Terminally differentiated cells are defined by their inability to proliferate. When forced to re-enter the cell cycle, they generally cannot undergo long-term replication. Our previous work with myotubes has shown that these cells fail to proliferate because of their intrinsic inability to complete DNA replication. Moreover, we have reported pronounced modifications of deoxynucleotide metabolism during myogenesis. Here we investigate the causes of incomplete DNA duplication in cell cycle-reactivated myotubes (rMt)...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186503/a-novel-dlx3-pkc-integrated-signaling-network-drives-keratinocyte-differentiation
#19
Elisabetta Palazzo, Meghan D Kellett, Christophe Cataisson, Paul W Bible, Shreya Bhattacharya, Hong-Wei Sun, Anna C Gormley, Stuart H Yuspa, Maria I Morasso
Epidermal homeostasis relies on a well-defined transcriptional control of keratinocyte proliferation and differentiation, which is critical to prevent skin diseases such as atopic dermatitis, psoriasis or cancer. We have recently shown that the homeobox transcription factor DLX3 and the tumor suppressor p53 co-regulate cell cycle-related signaling and that this mechanism is functionally involved in cutaneous squamous cell carcinoma development. Here we show that DLX3 expression and its downstream signaling depend on protein kinase C α (PKCα) activity in skin...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186502/stat1-mediates-transmembrane-tnf-alpha-induced-formation-of-death-inducing-signaling-complex-and-apoptotic-signaling-via-tnfr1
#20
Yaping Jiang, Min Yu, Xuena Hu, Lu Han, Kun Yang, Hongping Ba, Zunyue Zhang, Bingjiao Yin, Xiang-Ping Yang, Zhuoya Li, Jing Wang
Tumor necrosis factor-alpha (TNF-α) exists in two forms: secretory TNF-α (sTNF-α) and transmembrane TNF-α (tmTNF-α). Although both forms of TNF-α induce tumor cell apoptosis, tmTNF-α is able to kill tumor cells that are resistant to sTNF-α-mediated cytotoxicity, indicating their differences in signal transduction. Here, we demonstrate that internalization of TNFR1 is crucial for sTNF-α- but not for tmTNF-α-induced apoptosis. sTNF-α induces binding of tumor necrosis factor receptor type 1-associated death domain protein (TRADD) to the death domain (DD) of TNFR1 and subsequent activation of nuclear factor kappa B (NF-κB), and the formation of death-inducing signaling complexes (DISCs) in the cytoplasm after internalization...
February 10, 2017: Cell Death and Differentiation
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