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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/28430185/phospholipase-c%C3%AE-1-regulates-p38-mapk-activity-and-skin-barrier-integrity
#1
Kaori Kanemaru, Yoshikazu Nakamura, Kengo Totoki, Takatsugu Fukuyama, Madoka Shoji, Hisae Kaneko, Kanako Shiratori, Atsuko Yoneda, Takafumi Inoue, Yoichiro Iwakura, Kenji Kabashima, Kiyoko Fukami
Keratinocytes undergo a unique type of programmed cell death known as cornification, which leads to the formation of the stratum corneum (SC), the main physical barrier of the epidermis. A defective epidermal barrier is a hallmark of the two most common inflammatory skin disorders, psoriasis, and atopic dermatitis. However, the detailed molecular mechanisms of skin barrier formation are not yet fully understood. Here, we showed that downregulation of phospholipase C (PLC) δ1, a Ca(2+)-mobilizing and phosphoinositide-metabolizing enzyme abundantly expressed in the epidermis, impairs the barrier functions of the SC...
April 21, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28430184/the-ubiquitin-ligase-lin41-trim71-targets-p53-to-antagonize-cell-death-and-differentiation-pathways-during-stem-cell-differentiation
#2
Duong Thi Thuy Nguyen, Daniel Richter, Geert Michel, Sibylle Mitschka, Waldemar Kolanus, Elisa Cuevas, F Gregory Wulczyn
Rapidity and specificity are characteristic features of proteolysis mediated by the ubiquitin-proteasome system. Therefore, the UPS is ideally suited for the remodeling of the embryonic stem cell proteome during the transition from pluripotent to differentiated states and its inverse, the generation of inducible pluripotent stem cells. The Trim-NHL family member LIN41 is among the first E3 ubiquitin ligases to be linked to stem cell pluripotency and reprogramming. Initially discovered in C. elegans as a downstream target of the let-7 miRNA, LIN41 is now recognized as a critical regulator of stem cell fates as well as the timing of neurogenesis...
April 21, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28430183/neuroprotectin-d1-upregulates-iduna-expression-and-provides-protection-in-cellular-uncompensated-oxidative-stress-and-in-experimental-ischemic-stroke
#3
Ludmila Belayev, Pranab K Mukherjee, Veronica Balaszczuk, Jorgelina M Calandria, Andre Obenaus, Larissa Khoutorova, Sung-Ha Hong, Nicolas G Bazan
Ring finger protein 146 (Iduna) facilitates DNA repair and protects against cell death induced by NMDA receptor-mediated glutamate excitotoxicity or by cerebral ischemia. Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived lipid mediator, promotes cell survival under uncompensated oxidative stress (UOS). Our data demonstrate that NPD1 potently upregulates Iduna expression and provides remarkable cell protection against UOS. Iduna, which was increased by the lipid mediator, requires the presence of the poly(ADP-ribose) (PAR) sites...
April 21, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28409774/dr5-and-caspase-8-are-dispensable-in-er-stress-induced-apoptosis
#4
Jason A Glab, Marcel Doerflinger, Christina Nedeva, Irvin Jose, George W Mbogo, James C Paton, Adrienne W Paton, Andrew J Kueh, Marco J Herold, David Cs Huang, David Segal, Gabriella Brumatti, Hamsa Puthalakath
The endoplasmic reticulum (ER) stress response constitutes cellular reactions triggered by a wide variety of stimuli that disturb folding of proteins, often leading to apoptosis. ER stress-induced apoptotic cell death is thought to be an important contributor to many human pathological conditions. The molecular mechanism of this apoptosis process has been highly controversial with both the receptor and the mitochondrial pathways being implicated. Using knockout mouse models and RNAi-mediated gene silencing in cell lines, our group and others had demonstrated the importance of the mitochondrial apoptotic pathway in ER stress-induced cell death, particularly the role of the pro-apoptotic BH3-only BCL-2 family members, BIM and PUMA...
April 14, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28409773/the-making-of-a-mammalian-peroxisome-version-2-0-mitochondria-get-into-the-mix
#5
Michael Schrader, Luca Pellegrini
A recent report from the Laboratory of Heidi McBride (McGill University) presents a role for mitochondria in the de novo biogenesis of peroxisomes in mammalian cells. Peroxisomes are essential organelles responsible for a wide variety of biochemical functions, from the generation of bile to plasmalogen synthesis, reduction of peroxides, and the oxidation of very-long-chain fatty acids. Like mitochondria, peroxisomes proliferate primarily through growth and division of pre-existing peroxisomes. However, unlike mitochondria, peroxisomes do not fuse; further, and perhaps most importantly, they can also be born de novo, a process thought to occur through the generation of pre-peroxisomal vesicles that originate from the endoplasmic reticulum...
April 14, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28387757/gfi1-downregulation-promotes-inflammation-linked-metastasis-of-colorectal-cancer
#6
Wenjing Xing, Yun Xiao, Xinliang Lu, Hongyan Zhu, Xiangchuan He, Wei Huang, Elsa S Lopez, Jerry Wong, Huanyu Ju, Linlu Tian, Fengmin Zhang, Hongwei Xu, Sheng Dian Wang, Xia Li, Michael Karin, Huan Ren
Inflammation is frequently associated with initiation, progression, and metastasis of colorectal cancer (CRC). Here, we unveil a CRC-specific metastatic programme that is triggered via the transcriptional repressor, GFI1. Using data from a large cohort of clinical samples including inflammatory bowel disease and CRC, and a cellular model of CRC progression mediated by cross-talk between the cancer cell and the inflammatory microenvironment, we identified GFI1 as a gating regulator responsible for a constitutively activated signalling circuit that renders CRC cells competent for metastatic spread...
April 7, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28387756/pore-forming-toxin-mediated-ion-dysregulation-leads-to-death-receptor-independent-necroptosis-of-lung-epithelial-cells-during-bacterial-pneumonia
#7
Norberto González-Juarbe, Kelley Margaret Bradley, Anukul Taranath Shenoy, Ryan Paul Gilley, Luis Felipe Reyes, Cecilia Anahí Hinojosa, Marcos Ignacio Restrepo, Peter Herman Dube, Molly Ann Bergman, Carlos Javier Orihuela
We report that pore-forming toxins (PFTs) induce respiratory epithelial cell necroptosis independently of death receptor signaling during bacterial pneumonia. Instead, necroptosis was activated as a result of ion dysregulation arising from membrane permeabilization. PFT-induced necroptosis required RIP1, RIP3 and MLKL, and could be induced in the absence or inhibition of TNFR1, TNFR2 and TLR4 signaling. We detected activated MLKL in the lungs from mice and nonhuman primates experiencing Serratia marcescens and Streptococcus pneumoniae pneumonia, respectively...
April 7, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28387755/transglutaminases-factor-xiii-a-and-tg2-regulate-resorption-adipogenesis-and-plasma-fibronectin-homeostasis-in-bone-and-bone-marrow
#8
Aisha Mousa, Cui Cui, Aimei Song, Vamsee D Myneni, Huifang Sun, Jin Jin Li, Monzur Murshed, Gerry Melino, Mari T Kaartinen
Appropriate bone mass is maintained by bone-forming osteoblast and bone-resorbing osteoclasts. Mesenchymal stem cell (MSC) lineage cells control osteoclastogenesis via expression of RANKL and OPG (receptor activator of nuclear factor κB ligand and osteoprotegerin), which promote and inhibit bone resorption, respectively. Protein crosslinking enzymes transglutaminase 2 (TG2) and Factor XIII-A (FXIII-A) have been linked to activity of myeloid and MSC lineage cells; however, in vivo evidence has been lacking to support their function...
April 7, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362433/il-2-prevents-deletion-of-developing-t-regulatory-cells-in-the-thymus
#9
Daniel Y Hu, Rushika C Wirasinha, Christopher C Goodnow, Stephen R Daley
In the thymus, strongly self-reactive T cells may undergo apoptotic deletion or differentiate into Foxp3+ T-regulatory (T-reg) cells. Mechanisms that partition T cells into these two fates are unclear. Here, we show that IL-2 signalling is required to prevent deletion of CD4+ CD8- CCR7+ Helios+ thymocytes poised to upregulate Foxp3. The deletion prevented by IL-2 signalling is Foxp3 independent and occurs later in thymocyte development than the deletion that is prevented by Card11 signalling. Our results distinguish two bottlenecks at which strongly self-reactive thymocytes undergo deletion or progress to the next stage of T-reg differentiation; Card11 regulates the first bottleneck and IL-2 regulates the second...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362432/regulation-of-transcriptional-activators-by-dna-binding-domain-ubiquitination
#10
Vivien Landré, Bhindu Revi, Maria Gil Mir, Chandra Verma, Ted R Hupp, Nick Gilbert, Kathryn L Ball
Ubiquitin is a key component of the regulatory network that maintains gene expression in eukaryotes, yet the molecular mechanism(s) by which non-degradative ubiquitination modulates transcriptional activator (TA) function is unknown. Here endogenous p53, a stress-activated transcription factor required to maintain health, is stably monoubiquitinated, following pathway activation by IR or Nutlin-3 and localized to the nucleus where it becomes tightly associated with chromatin. Comparative structure-function analysis and in silico modelling demonstrate a direct role for DNA-binding domain (DBD) monoubiquitination in TA activation...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362431/killers-creating-new-life-caspases-drive-apoptosis-induced-proliferation-in-tissue-repair-and-disease
#11
Caitlin E Fogarty, Andreas Bergmann
Apoptosis is a carefully orchestrated and tightly controlled form of cell death, conserved across metazoans. As the executioners of apoptotic cell death, cysteine-dependent aspartate-directed proteases (caspases) are critical drivers of this cellular disassembly. Early studies of genetically programmed cell death demonstrated that the selective activation of caspases induces apoptosis and the precise elimination of excess cells, thereby sculpting structures and refining tissues. However, over the past decade there has been a fundamental shift in our understanding of the roles of caspases during cell death-a shift precipitated by the revelation that apoptotic cells actively engage with their surrounding environment throughout the death process, and caspases can trigger a myriad of signals, some of which drive concurrent cell proliferation regenerating damaged structures and building up lost tissues...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362430/cyld-a20-and-otulin-deubiquitinases-in-nf-%C3%AE%C2%BAb-signaling-and-cell-death-so-similar-yet-so-different
#12
REVIEW
Marie Lork, Kelly Verhelst, Rudi Beyaert
Polyubiquitination of proteins has a pivotal role in the regulation of numerous cellular functions such as protein degradation, DNA repair and cell signaling. As deregulation of these processes can result in pathological conditions such as inflammatory diseases, neurodegeneration or cancer, tight regulation of the ubiquitin system is of tremendous importance. Ubiquitination by E3 ubiquitin ligases can be counteracted by the activity of several deubiquitinating enzymes (DUBs). CYLD, A20 and OTULIN have been implicated as key DUBs in the negative regulation of NF-κB transcription factor-mediated gene expression upon stimulation of cytokine receptors, antigen receptors and pattern recognition receptors, by removing distinct types of polyubiquitin chains from specific NF-κB signaling proteins...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362429/pu-1-supports-trail-induced-cell-death-by-inhibiting-nf-%C3%AE%C2%BAb-mediated-cell-survival-and-inducing-dr5-expression
#13
Aladin Haimovici, Magali Humbert, Elena A Federzoni, Deborah Shan-Krauer, Thomas Brunner, Steffen Frese, Thomas Kaufmann, Bruce E Torbett, Mario P Tschan
The hematopoietic Ets-domain transcription factor PU.1/SPI1 orchestrates myeloid, B- and T-cell development, and also supports hematopoietic stem cell maintenance. Although PU.1 is a renowned tumor suppressor in acute myeloid leukemia (AML), a disease characterized by an accumulation of immature blast cells, comprehensive studies analyzing the role of PU.1 during cell death responses in AML treatment are missing. Modulating PU.1 expression in AML cells, we found that PU.1 supports tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis via two mechanisms: (a) by repressing NF-κB activity via a novel direct PU...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362428/%C3%AE-133p53-represses-p53-inducible-senescence-genes-and-enhances-the-generation-of-human-induced-pluripotent-stem-cells
#14
Izumi Horikawa, Kye-Yoon Park, Kazunobu Isogaya, Yukiharu Hiyoshi, Han Li, Katsuhiro Anami, Ana I Robles, Abdul M Mondal, Kaori Fujita, Manuel Serrano, Curtis C Harris
p53 functions to induce cellular senescence, which is incompatible with self-renewal of pluripotent stem cells such as induced pluripotent stem cells (iPSC) and embryonic stem cells (ESC). However, p53 also has essential roles in these cells through DNA damage repair for maintaining genomic integrity and high sensitivity to apoptosis for eliminating severely damaged cells. We hypothesized that Δ133p53, a physiological inhibitory p53 isoform, is involved in the balanced regulation of self-renewing capacity, DNA damage repair and apoptosis...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28362427/anti-apoptotic-proteins-bcl-2-mcl-1-and-a1-summate-collectively-to-maintain-survival-of-immune-cell-populations-both-in-vitro-and-in-vivo
#15
Emma M Carrington, Yifan Zhan, Jamie L Brady, Jian-Guo Zhang, Robyn M Sutherland, Natasha S Anstee, Robyn L Schenk, Ingela B Vikstrom, Rebecca B Delconte, David Segal, Nicholas D Huntington, Philippe Bouillet, David M Tarlinton, David Cs Huang, Andreas Strasser, Suzanne Cory, Marco J Herold, Andrew M Lew
Survival of various immune cell populations has been proposed to preferentially rely on a particular anti-apoptotic BCL-2 family member, for example, naive T cells require BCL-2, while regulatory T cells require MCL-1. Here we examined the survival requirements of multiple immune cell subsets in vitro and in vivo, using both genetic and pharmacological approaches. Our findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins rather than by a single anti-apoptotic protein...
March 31, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28338659/intercellular-cannibalism-fuels-tumor-growth
#16
Ernesto Pérez, Andreas Bergmann
No abstract text is available yet for this article.
March 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28338656/focal-adhesion-kinase-depletion-reduces-human-hepatocellular-carcinoma-growth-by-repressing-enhancer-of-zeste-homolog-2
#17
Daniela Gnani, Ilaria Romito, Simona Artuso, Marco Chierici, Cristiano De Stefanis, Nadia Panera, Annalisa Crudele, Sara Ceccarelli, Elena Carcarino, Valentina D'Oria, Manuela Porru, Ezio Giorda, Karin Ferrari, Luca Miele, Erica Villa, Clara Balsano, Diego Pasini, Cesare Furlanello, Franco Locatelli, Valerio Nobili, Rossella Rota, Carlo Leonetti, Anna Alisi
Hepatocellular carcinoma (HCC) is the most common type of liver cancer in humans. The focal adhesion tyrosine kinase (FAK) is often over-expressed in human HCC and FAK inhibition may reduce HCC cell invasiveness. However, the anti-oncogenic effect of FAK knockdown in HCC cells remains to be clarified. We found that FAK depletion in HCC cells reduced in vitro and in vivo tumorigenicity, by inducing G2/M arrest and apoptosis, decreasing anchorage-independent growth, and modulating the expression of several cancer-related genes...
March 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28338655/evolution-of-caspase-mediated-cell-death-and-differentiation-twins-separated-at-birth
#18
REVIEW
Ryan A V Bell, Lynn A Megeney
The phenotypic and biochemical similarities between caspase-mediated apoptosis and cellular differentiation are striking. They include such diverse phenomenon as mitochondrial membrane perturbations, cytoskeletal rearrangements and DNA fragmentation. The parallels between the two disparate processes suggest some common ancestry and highlight the paradoxical nature of the death-centric view of caspases. That is, what is the driving selective pressure that sustains death-inducing proteins throughout eukaryotic evolution? Plausibly, caspase function may be rooted in a primordial non-death function, such as cell differentiation, and was co-opted for its role in programmed cell death...
March 24, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28304405/the-erbb3-receptor-tyrosine-kinase-negatively-regulates-paneth-cells-by-pi3k-dependent-suppression-of-atoh1
#19
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
#20
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
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