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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/28622300/the-als-linked-e102q-mutation-in-sigma-receptor-1-leads-to-er-stress-mediated-defects-in-protein-homeostasis-and-dysregulation-of-rna-binding-proteins
#1
Alice Dreser, Jan Tilmann Vollrath, Antonio Sechi, Sonja Johann, Andreas Roos, Alfred Yamoah, Istvan Katona, Saeed Bohlega, Dominik Wiemuth, Yuemin Tian, Axel Schmidt, Jörg Vervoorts, Marc Dohmen, Cordian Beyer, Jasper Anink, Eleonora Aronica, Dirk Troost, Joachim Weis, Anand Goswami
Amyotrophic lateral sclerosis (ALS) is characterized by the selective degeneration of motor neurons (MNs) and their target muscles. Misfolded proteins which often form intracellular aggregates are a pathological hallmark of ALS. Disruption of the functional interplay between protein degradation (ubiquitin proteasome system and autophagy) and RNA-binding protein homeostasis has recently been suggested as an integrated model that merges several ALS-associated proteins into a common pathophysiological pathway...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622299/a-circular-rna-promotes-tumorigenesis-by-inducing-c-myc-nuclear-translocation
#2
Qi Yang, William W Du, Nan Wu, Weining Yang, Faryal Mehwish Awan, Ling Fang, Jian Ma, Xiangmin Li, Yan Zeng, Zhenguo Yang, Jun Dong, Azam Khorshidi, Burton B Yang
Circular RNAs (circRNAs) are a subclass of noncoding RNAs widely expressed in mammalian cells. We report here the tumorigenic capacity of a circRNA derived from angiomotin-like1 (circ-Amotl1). Circ-Amotl1 is highly expressed in patient tumor samples and cancer cell lines. Single-cell inoculations using circ-Amotl1-transfected tumor cells showed a 30-fold increase in proliferative capacity relative to control. Agarose colony-formation assays similarly revealed a 142-fold increase. Tumor-take rate in nude mouse xenografts using 6-day (219 cells) and 3-day (9 cells) colonies were 100%, suggesting tumor-forming potential of every cell...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622298/tgf%C3%AE-pathway-limits-dedifferentiation-following-wnt-and-mapk-pathway-activation-to-suppress-intestinal-tumourigenesis
#3
Patrizia Cammareri, David F Vincent, Michael C Hodder, Rachel A Ridgway, Claudio Murgia, Max Nobis, Andrew D Campbell, Julia Varga, David J Huels, Chithra Subramani, Katie L H Prescott, Colin Nixon, Ann Hedley, Simon T Barry, Florian R Greten, Gareth J Inman, Owen J Sansom
Recent studies have suggested increased plasticity of differentiated cells within the intestine to act both as intestinal stem cells (ISCs) and tumour-initiating cells. However, little is known of the processes that regulate this plasticity. Our previous work has shown that activating mutations of Kras or the NF-κB pathway can drive dedifferentiation of intestinal cells lacking Apc. To investigate this process further, we profiled both cells undergoing dedifferentiation in vitro and tumours generated from these cells in vivo by gene expression analysis...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622297/p53-mediated-suppression-of-bip-triggers-bik-induced-apoptosis-during-prolonged-endoplasmic-reticulum-stress
#4
Ignacio López, Anne-Sophie Tournillon, Rodrigo Prado Martins, Konstantinos Karakostis, Laurence Malbert-Colas, Karin Nylander, Robin Fåhraeus
Physiological and pathological conditions that affect the folding capacity of the endoplasmic reticulum (ER) provoke ER stress and trigger the unfolded protein response (UPR). The UPR aims to either restore the balance between newly synthesized and misfolded proteins or if the damage is severe, to trigger cell death. However, the molecular events underlying the switch between repair and cell death are not well understood. The ER-resident chaperone BiP governs the UPR by sensing misfolded proteins and thereby releasing and activating the three mediators of the UPR: PERK, IRE1 and ATF6...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622296/bcl-2-family-integrating-stress-responses-at-the-er-to-control-cell-demise
#5
REVIEW
Philippe Pihán, Amado Carreras-Sureda, Claudio Hetz
In the last decade, the endoplasmic reticulum (ER) has emerged as a central organelle regulating the core mitochondrial apoptosis pathway. At the ER membrane, a variety of stress signals are integrated toward determining cell fate, involving a complex cross talk between key homeostatic pathways including the unfolded protein response, autophagy, calcium signaling and mitochondrial bioenergetics. In this context, key regulators of cell death of the BCL-2 and TMBIM/BI-1 family of proteins have relevant functions as stress rheostats mediated by the formation of distinct protein complexes that regulate the switch between adaptive and proapoptotic phases under stress...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622295/high-autophagic-flux-guards-esc-identity-through-coordinating-autophagy-machinery-gene-program-by-foxo1
#6
Pinglei Liu, Kun Liu, Haifeng Gu, Weixu Wang, Jiaqi Gong, Yingjie Zhu, Qian Zhao, Jiani Cao, Chunseng Han, Fei Gao, Quan Chen, Wei Li, Jianwei Jiao, Baoyang Hu, Qi Zhou, Tongbiao Zhao
Although much is known about transcriptional networks that control embryonic stem cell (ESC) self-renewal and differentiation, the metabolic regulation of ESC is less clear. Autophagy is a catabolic process that is activated under both stress and normal conditions to degrade damaged organelles and aggregated proteins, and thus plays pivotal roles in somatic and adult stem cell function. However, if and how ESCs harness autophagy to regulate stemness remains largely unknown. Recently, we have defined that autophagy is essential for mitochondrial homeostasis regulation in pluripotency acquirement and maintenance...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622294/hepatocyte-nuclear-factor-1b-is-a-novel-negative-regulator-of-white-adipocyte-differentiation
#7
Xin Wang, Hao Wu, Weihua Yu, Jiangzheng Liu, Jie Peng, Nai Liao, Jieling Zhang, Xiaodi Zhang, Chunxu Hai
Hepatocyte nuclear factor 1b (HNF1b) is a transcription factor belonging to the HNF family. We aimed to investigate the role of HNF1b in white adipocyte differentiation. The expression of HNF1b was reduced in white adipose tissue (WAT) of both diet-induced and genetic obese mice and decreased during the process of 3T3-L1 adipocyte differentiation. Downregulation of HNF1b enhanced 3T3-L1 adipocyte differentiation and upregulation of HNF1b inhibited this process. Upregulation of HNF1b inhibited peroxisome proliferator-activated receptor γ (PPARγ) and its target gene expression, while downregulation of HNF1b increased those genes expression...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622293/sumo-triggered-ubiquitination-of-nr4a1-controls-macrophage-cell-death
#8
Long Zhang, Feng Xie, Juan Zhang, Peter Ten Dijke, Fangfang Zhou
Nuclear receptor NR4A1 has been implicated as a key regulator in a wide range of pathophysiological responses. As an immediate early response gene, NR4A1 can be rapidly and potently induced by a variety of stimuli. Its induction is followed by its rapid degradation, but the mechanism by which NR4A1 is degraded remains poorly understood. Here we show that nuclear receptor NR4A1 is sumoylated by SUMO2/3. Upon poly-SUMO modification, NR4A1 can be targeted by the SUMO-dependent E3 ubiquitin ligase RNF4 for polyubiquitination and subsequent degradation...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622292/the-potential-of-erythrocytes-as-cellular-aging-models
#9
Lars Kaestner, Giampaolo Minetti
No abstract text is available yet for this article.
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622291/predicting-lung-cancer-recurrence-from-circulating-tumour-dna-commentary-on-phylogenetic-ctdna-analysis-depicts-early-stage-lung-cancer-evolution
#10
Daniel J Murphy, Kevin G Blyth
No abstract text is available yet for this article.
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622290/structural-basis-for-the-regulatory-interactions-of-proapoptotic-par-4
#11
Udaya K Tiruttani Subhramanyam, Jan Kubicek, Ulf B Eidhoff, Joerg Labahn
Par-4 is a unique proapoptotic protein with the ability to induce apoptosis selectively in cancer cells. The X-ray crystal structure of the C-terminal domain of Par-4 (Par-4CC), which regulates its apoptotic function, was obtained by MAD phasing. Par-4 homodimerizes by forming a parallel coiled-coil structure. The N-terminal half of Par-4CC contains the homodimerization subdomain. This structure includes a nuclear export signal (Par-4NES) sequence, which is masked upon dimerization indicating a potential mechanism for nuclear localization...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622289/microrna-26a-and-26b-inhibit-lens-fibrosis-and-cataract-by-negatively-regulating-jagged-1-notch-signaling-pathway
#12
Xiaoyun Chen, Wei Xiao, Weirong Chen, Xialin Liu, Mingxing Wu, Qu Bo, Yan Luo, Shaobi Ye, Yihai Cao, Yizhi Liu
Fibrosis is a chronic process involving development and progression of multiple diseases in various organs and is responsible for almost half of all known deaths. Epithelial-mesenchymal transition (EMT) is the vital process in organ fibrosis. Lens is an elegant biological tool to investigate the fibrosis process because of its unique biological properties. Using gain- and loss-of-function assays, and different lens fibrosis models, here we demonstrated that microRNA (miR)-26a and miR-26b, members of the miR-26 family have key roles in EMT and fibrosis...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574511/signalome-wide-rnai-screen-identifies-gba1-as-a-positive-mediator-of-autophagic-cell-death
#13
Santosh K Dasari, Shani Bialik, Smadar Levin-Zaidman, Vered Levin-Salomon, Alfred H Merrill, Anthony H Futerman, Adi Kimchi
Activating alternative cell death pathways, including autophagic cell death, is a promising direction to overcome the apoptosis resistance observed in various cancers. Yet, whether autophagy acts as a death mechanism by over consumption of intracellular components is still controversial and remains undefined at the ultrastructural and the mechanistic levels. Here we identified conditions under which resveratrol-treated A549 lung cancer cells die by a mechanism that fulfills the previous definition of autophagic cell death...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574510/rip4-inhibits-stat3-signaling-to-sustain-lung-adenocarcinoma-differentiation
#14
Jawahar Kopparam, Johanna Chiffelle, Paolo Angelino, Alessandra Piersigilli, Nadine Zangger, Mauro Delorenzi, Etienne Meylan
Loss of epithelial differentiation and extracellular matrix (ECM) remodeling are known to facilitate cancer progression and are associated with poor prognosis in patients with lung cancer. We have identified Receptor-interacting serine/threonine protein kinase 4 (RIP4) as a regulator of tumor differentiation in lung adenocarcinoma (AC). Bioinformatics analyses of human lung AC samples showed that poorly differentiated tumors express low levels of RIP4, whereas high levels are associated with better overall survival...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574509/mycn-amplified-neuroblastoma-requires-the-mrna-translation-regulator-eef2-kinase-to-adapt-to-nutrient-deprivation
#15
Alberto Delaidelli, Gian Luca Negri, Asad Jan, Brandon Jansonius, Amal El-Naggar, Jonathan K M Lim, Debjit Khan, Htoo Zarni Oo, Christopher J Carnie, Marc Remke, John M Maris, Gabriel Leprivier, Poul H Sorensen
MYC family proteins are implicated in many human cancers, but their therapeutic targeting has proven challenging. MYCN amplification in childhood neuroblastoma (NB) is associated with aggressive disease and high mortality. Novel and effective therapeutic strategies are therefore urgently needed for these tumors. MYC-driven oncogenic transformation impairs cell survival under nutrient deprivation (ND), a characteristic stress condition within the tumor microenvironment. We recently identified eukaryotic Elongation Factor 2 Kinase (eEF2K) as a pivotal mediator of the adaptive response of tumor cells to ND...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574508/caspase-involvement-in-autophagy
#16
REVIEW
Panagiotis Tsapras, Ioannis P Nezis
Caspases are a family of cysteine proteases widely known as the principal mediators of the apoptotic cell death response, but considerably less so as the contributors to the regulation of pathways outside cellular demise. In regards to autophagy, the modulatory roles of caspases have only recently begun to be adequately described. In contrast to apoptosis, autophagy promotes cell survival by providing energy and nutrients through the lysosomal degradation of cytoplasmic constituents. Under basal conditions autophagy and apoptosis cross-regulate each other through an elaborate network of interconnections which also includes the interplay between autophagy-related proteins (ATGs) and caspases...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574507/exploiting-tumour-addiction-with-a-serine-and-glycine-free-diet
#17
Ivano Amelio, Gerry Melino, Christian Frezza
No abstract text is available yet for this article.
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574506/role-of-atg5-dependent-cell-death-in-the-embryonic-development-of-bax-bak-double-knockout-mice
#18
Satoko Arakawa, Masatsune Tsujioka, Tatsushi Yoshida, Hajime Tajima-Sakurai, Yuya Nishida, Yosuke Matsuoka, Ikuyo Yoshino, Yoshihide Tsujimoto, Shigeomi Shimizu
Programmed cell death, which is required for the development and homeostasis of metazoans, includes mechanisms such as apoptosis, autophagic cell death, and necrotic (or type III) death. Members of the Bcl2 family regulate apoptosis, among which Bax and Bak act as a mitochondrial gateway. Although embryonic fibroblasts from Bax/Bak double-knockout (DKO) mice are resistant to apoptosis, we previously demonstrated that these cells die through an autophagy-dependent mechanism in response to various types of cellular stressors...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574505/the-small-molecule-that-packs-a-punch-ubiquitin-mediated-regulation-of-ripk1-fadd-caspase-8-complexes
#19
REVIEW
Rebecca Feltham, John Silke
The mechanisms that underpin the production of small molecules and cytokines that lead to inflammation or programmed cell death are intricately intertwined. So much so that some of the proteins that contribute to the transcriptional up regulation of cytokines can switch their role in the right circumstances to generate cell death-inducing complexes. This entwinement is reflected in the fact that inflammation helps an organism fight pathogens and that therefore pathogens are under an evolutionary pressure to interfere with this process...
June 2, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28574504/nox2-dependent-atm-kinase-activation-dictates-pro-inflammatory-macrophage-phenotype-and-improves-effectiveness-to-radiation-therapy
#20
Qiuji Wu, Awatef Allouch, Audrey Paoletti, Celine Leteur, Celine Mirjolet, Isabelle Martins, Laurent Voisin, Frédéric Law, Haithem Dakhli, Elodie Mintet, Maxime Thoreau, Zeinaf Muradova, Mélanie Gauthier, Olivier Caron, Fabien Milliat, David M Ojcius, Filippo Rosselli, Eric Solary, Nazanine Modjtahedi, Eric Deutsch, Jean-Luc Perfettini
Although tumor-associated macrophages have been extensively studied in the control of response to radiotherapy, the molecular mechanisms involved in the ionizing radiation-mediated activation of macrophages remain elusive. Here we show that ionizing radiation induces the expression of interferon regulatory factor 5 (IRF5) promoting thus macrophage activation toward a pro-inflammatory phenotype. We reveal that the activation of the ataxia telangiectasia mutated (ATM) kinase is required for ionizing radiation-elicited macrophage activation, but also for macrophage reprogramming after treatments with γ-interferon, lipopolysaccharide or chemotherapeutic agent (such as cisplatin), underscoring the fact that the kinase ATM plays a central role during macrophage phenotypic switching toward a pro-inflammatory phenotype through the regulation of mRNA level and post-translational modifications of IRF5...
June 2, 2017: Cell Death and Differentiation
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