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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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/28186505/n-glycosylation-of-mouse-trail-r-and-human-trail-r1-enhances-trail-induced-death
#8
Florent Dufour, Thibault Rattier, Sarah Shirley, Gaelle Picarda, Andrei Alexandru Constantinescu, Aymeric Morlé, Al Batoul Zakaria, Guillaume Marcion, Sebastien Causse, Eva Szegezdi, Dirk Michael Zajonc, Renaud Seigneuric, Gilles Guichard, Tijani Gharbi, Fabien Picaud, Guillaume Herlem, Carmen Garrido, Pascal Schneider, Chris Alan Benedict, Olivier Micheau
APO2L/TRAIL (TNF-related apoptosis-inducing ligand) induces death of tumor cells through two agonist receptors, TRAIL-R1 and TRAIL-R2. We demonstrate here that N-linked glycosylation (N-glyc) plays also an important regulatory role for TRAIL-R1-mediated and mouse TRAIL receptor (mTRAIL-R)-mediated apoptosis, but not for TRAIL-R2, which is devoid of N-glycans. Cells expressing N-glyc-defective mutants of TRAIL-R1 and mouse TRAIL-R were less sensitive to TRAIL than their wild-type counterparts. Defective apoptotic signaling by N-glyc-deficient TRAIL receptors was associated with lower TRAIL receptor aggregation and reduced DISC formation, but not with reduced TRAIL-binding affinity...
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
#9
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
#10
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
#11
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
https://www.readbyqxmd.com/read/28186501/intrinsic-repair-protects-cells-from-pore-forming-toxins-by-microvesicle-shedding
#12
Matthew Romero, Michelle Keyel, Guilan Shi, Pushpak Bhattacharjee, Robyn Roth, John E Heuser, Peter A Keyel
Pore-forming toxins (PFTs) are used by both the immune system and by pathogens to disrupt cell membranes. Cells attempt to repair this disruption in various ways, but the exact mechanism(s) that cells use are not fully understood, nor agreed upon. Current models for membrane repair include (1) patch formation (e.g., fusion of internal vesicles with plasma membrane defects), (2) endocytosis of the pores, and (3) shedding of the pores by blebbing from the cell membrane. In this study, we sought to determine the specific mechanism(s) that cells use to resist three different cholesterol-dependent PFTs: Streptolysin O, Perfringolysin O, and Intermedilysin...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186500/evi2b-is-a-c-ebp%C3%AE-target-gene-required-for-granulocytic-differentiation-and-functionality-of-hematopoietic-progenitors
#13
Polina Zjablovskaja, Miroslava Kardosova, Petr Danek, Pavla Angelisova, Touati Benoukraf, Alexander A Wurm, Tomas Kalina, Stephanie Sian, Martin Balastik, Ruud Delwel, Tomas Brdicka, Daniel G Tenen, Gerhard Behre, Fréderic Fiore, Bernard Malissen, Vaclav Horejsi, Meritxell Alberich-Jorda
Development of hematopoietic populations through the process of differentiation is critical for proper hematopoiesis. The transcription factor CCAAT/enhancer binding protein alpha (C/EBPα) is a master regulator of myeloid differentiation, and the identification of C/EBPα target genes is key to understand this process. Here we identified the Ecotropic Viral Integration Site 2B (EVI2B) gene as a direct target of C/EBPα. We showed that the product of the gene, the transmembrane glycoprotein EVI2B (CD361), is abundantly expressed on the surface of primary hematopoietic cells, the highest levels of expression being reached in mature granulocytes...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28186499/downregulation-of-lnc-spry1-mediates-tgf-%C3%AE-induced-epithelial-mesenchymal-transition-by-transcriptional-and-posttranscriptional-regulatory-mechanisms
#14
Cristina Rodríguez-Mateo, Belén Torres, Gabriel Gutiérrez, José A Pintor-Toro
Long non-coding RNAs (lncRNAs) are a class of regulatory genes that participate in a wide range of biological processes, including proliferation, differentiation and development, as well as in a broad spectrum of diseases. Although the role of lncRNAs in TGF-β-induced epithelial-to-mesenchymal transition (EMT) has been well established, little is known about the role of lncRNAs as immediate-early regulators of EMT. Here lnc-Spry1 is identified as an immediate-early regulator of EMT that is downregulated by TGF-β...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28157210/modulation-of-macrophage-antitumor-potential-by-apoptotic-lymphoma-cells
#15
Jorine J L P Voss, Catriona A Ford, Sofia Petrova, Lynsey Melville, Margaret Paterson, John D Pound, Pam Holland, Bruno Giotti, Tom C Freeman, Christopher D Gregory
In aggressive non-Hodgkin's lymphoma (NHL), constitutive apoptosis of a proportion of the tumor cell population can promote net tumor growth. This is associated with the accumulation of tumor-associated macrophages (TAMs) that clear apoptotic cells and exhibit pro-oncogenic transcriptional activation profiles characteristic of reparatory, anti-inflammatory and angiogenic programs. Here we consider further the activation status of these TAMs. We compare their transcriptomic profile with that of a range of other macrophage types from various tissues noting especially their expression of classically activated (IFN-γ and LPS) gene clusters - typically antitumor - in addition to their previously described protumor phenotype...
February 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28157209/autophagy-induced-by-damps-facilitates-the-inflammation-response-in-lungs-undergoing-ischemia-reperfusion-injury-through-promoting-traf6-ubiquitination
#16
Xingguang Liu, Hao Cao, Jian Li, Bo Wang, Peng Zhang, Xu Dong Zhang, Zhongmin Liu, Hongbin Yuan, Zhenzhen Zhan
Lung ischemia-reperfusion (I/R) injury remains one of the most common complications after various cardiopulmonary surgeries. The inflammation response triggered by the released damage-associated molecular patterns (DAMPs) aggravates lung tissue damage. However, little is known about the role of autophagy in the pathogenesis of lung I/R injury. Here, we report that a variety of inflammation-related and autophagy-associated genes are rapidly upregulated, which facilitate the inflammation response in a minipig lung I/R injury model...
February 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28157208/rnf20-and-histone-h2b-ubiquitylation-exert-opposing-effects-in-basal-like-versus-luminal-breast-cancer
#17
Ohad Tarcic, Roy Z Granit, Ioannis S Pateras, Hadas Masury, Bella Maly, Yaara Zwang, Yosef Yarden, Vassilis G Gorgoulis, Eli Pikarsky, Ittai Ben-Porath, Moshe Oren
Breast cancer subtypes display distinct biological traits that influence their clinical behavior and response to therapy. Recent studies have highlighted the importance of chromatin structure regulators in tumorigenesis. The RNF20-RNF40 E3 ubiquitin ligase complex monoubiquitylates histone H2B to generate H2Bub1, while the deubiquitinase (DUB) USP44 can remove this modification. We found that RNF20 and RNF40 expression and global H2Bub1 are relatively low, and USP44 expression is relatively high, in basal-like breast tumors compared with luminal tumors...
February 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28106886/loss-of-menin-in-osteoblast-lineage-affects-osteocyte-osteoclast-crosstalk-causing-osteoporosis
#18
Peng Liu, Sooyeon Lee, Jeanette Knoll, Alexander Rauch, Susanne Ostermay, Julia Luther, Nicole Malkusch, Ulf H Lerner, Mario M Zaiss, Mona Neven, Rainer Wittig, Martina Rauner, Jean-Pierre David, Philippe Bertolino, Chang X Zhang, Jan P Tuckermann
During osteoporosis bone formation by osteoblasts is reduced and/or bone resorption by osteoclasts is enhanced. Currently, only a few factors have been identified in the regulation of bone integrity by osteoblast-derived osteocytes. In this study, we show that specific disruption of menin, encoded by multiple endocrine neoplasia type 1 (Men1), in osteoblasts and osteocytes caused osteoporosis despite the preservation of osteoblast differentiation and the bone formation rate. Instead, an increase in osteoclast numbers and bone resorption was detected that persisted even when the deletion of Men1 was restricted to osteocytes...
January 20, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28106885/c-flipl-enhances-anti-apoptotic-akt-functions-by-modulation-of-gsk3%C3%AE-activity
#19
C Quintavalle, M Incoronato, L Puca, M Acunzo, C Zanca, G Romano, M Garofalo, M Iaboni, C M Croce, G Condorelli
No abstract text is available yet for this article.
January 20, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28106884/excess-reactive-oxygen-species-production-mediates-monoclonal-antibody-induced-human-embryonic-stem-cell-death-via-oncosis
#20
Ji Yun Zheng, Heng Liang Tan, Paul Thomas Matsudaira, Andre Choo
Antibody-mediated cell killing has significantly facilitated the elimination of undesired cells in therapeutic applications. Besides the well-known Fc-dependent mechanisms, pathways of antibody-induced apoptosis were also extensively studied. However, with fewer studies reporting the ability of antibodies to evoke an alternative form of programmed cell death, oncosis, the molecular mechanism of antibody-mediated oncosis remains underinvestigated. In this study, a monoclonal antibody (mAb), TAG-A1 (A1), was generated to selectively kill residual undifferentiated human embryonic stem cells (hESC) so as to prevent teratoma formation upon transplantation of hESC-derived products...
January 20, 2017: Cell Death and Differentiation
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