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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/28914882/sirt3-sod2-maintains-osteoblast-differentiation-and-bone-formation-by-regulating-mitochondrial-stress
#1
Jing Gao, Zhihui Feng, Xueqiang Wang, Mengqi Zeng, Jing Liu, Shujun Han, Jie Xu, Lei Chen, Ke Cao, Jiangang Long, Zongfang Li, Weili Shen, Jiankang Liu
Recent studies have revealed robust metabolic changes during cell differentiation. Mitochondria, the organelles where many vital metabolic reactions occur, may play an important role. Here, we report the involvement of SIRT3-regulated mitochondrial stress in osteoblast differentiation and bone formation. In both the osteoblast cell line MC3T3-E1 and primary calvarial osteoblasts, robust mitochondrial biogenesis and supercomplex formation were observed during differentiation, accompanied by increased ATP production and decreased mitochondrial stress...
September 15, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28914881/microrna-200c-impairs-uterine-receptivity-formation-by-targeting-fut4-and-%C3%AE-1-3-fucosylation
#2
Qin Zheng, Dandan Zhang, Y U Yang, Xinyuan Cui, Jiaqi Sun, Caixia Liang, Huamin Qin, Xuesong Yang, Shuai Liu, Qiu Yan
Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by the specific fucosyltransferases. Fucosyltransferase IV (FUT4) is the key enzyme for the biosynthesis of α1,3-fucosylated glycans carried by glycoproteins, and the previous studies showed FUT4 expression changed dynamically during perimplantation...
September 15, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885620/oxidative-stress-induced-s100b-accumulation-converts-myoblasts-into-brown-adipocytes-via-an-nf-%C3%AE%C2%BAb-yy1-mir-133-axis-and-nf-%C3%AE%C2%BAb-yy1-bmp-7-axis
#3
Giulio Morozzi, Sara Beccafico, Roberta Bianchi, Francesca Riuzzi, Ilaria Bellezza, Ileana Giambanco, Cataldo Arcuri, Alba Minelli, Rosario Donato
Muscles of sarcopenic people show hypotrophic myofibers and infiltration with adipose and, at later stages, fibrotic tissue. The origin of infiltrating adipocytes resides in fibro-adipogenic precursors and nonmyogenic mesenchymal progenitor cells, and in satellite cells, the adult stem cells of skeletal muscles. Myoblasts and brown adipocytes share a common Myf5(+) progenitor cell: the cell fate depends on levels of bone morphogenetic protein 7 (BMP-7), a TGF-β family member. S100B, a Ca(2+)-binding protein of the EF-hand type, is expressed at relatively high levels in myoblasts from sarcopenic humans and exerts anti-myogenic effects via NF-κB-dependent inhibition of MyoD, a myogenic transcription factor acting upstream of the essential myogenic factor, myogenin...
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885619/powering-stem-cell-decisions-with-ubiquitin
#4
Achim Werner, Michael Rape
No abstract text is available yet for this article.
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885618/loss-of-bim-augments-resistance-of-atm-deficient-thymocytes-to-dna-damage-induced-apoptosis-but-does-not-accelerate-lymphoma-development
#5
Alex Rd Delbridge, Stephanie Grabow, Andreas Strasser
No abstract text is available yet for this article.
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885617/post-translational-regulation-of-p53-function-through-20s-proteasome-mediated-cleavage
#6
Hilla Solomon, Bastian Bräuning, Irit Fainer, Gili Ben-Nissan, Stav Rabani, Naomi Goldfinger, Oren Moscovitz, Zippora Shakked, Varda Rotter, Michal Sharon
The tumor suppressor p53 is a transcription factor that regulates the expression of a range of target genes in response to cellular stress. Adding to the complexity of understanding its cellular function is that in addition to the full-length protein, several p53 isoforms are produced in humans, harboring diverse expression patterns and functionalities. One isoform, Δ40p53, which lacks the first transactivation domain including the binding region for the negative regulator MDM2, was shown to be a product of alternative translation initiation...
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885616/myd88-is-an-essential-component-of-retinoic-acid-induced-differentiation-in-human-pluripotent-embryonal-carcinoma-cells
#7
Gomaa Sulaiman, Aoife Cooke, Brendan Ffrench, Claudia Gasch, Olayemi Azeez Abdullai, Kevin O'Connor, Salah Elbaruni, Gordon Blackshields, Cathy Spillane, Helen Keegan, Victoria McEneaney, Ronan Knittel, Annamarie Rogers, Ian B Jeffery, Brendan Doyle, Mark Bates, Charles d'Adhemar, Mathia Yc Lee, Eric L Campbell, Paul N Moynagh, Desmond G Higgins, Sharon O'Toole, Luke O'Neill, John J O'Leary, Michael F Gallagher
We have previously reported that myeloid differentiation primary response gene 88 (MyD88) is downregulated during all-trans retinoic acid (RA)-induced differentiation of pluripotent NTera2 human embryonal carcinoma cells (hECCs), whereas its maintained expression is associated with RA differentiation resistance in nullipotent 2102Ep hECCs. MyD88 is the main adapter for toll-like receptor (TLR) signalling, where it determines the secretion of chemokines and cytokines in response to pathogens. In this study, we report that loss of MyD88 is essential for RA-facilitated differentiation of hECCs...
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28885615/necroptosis-in-microglia-contributes-to-neuroinflammation-and-retinal-degeneration-through-tlr4-activation
#8
Zijing Huang, Tian Zhou, Xiaowei Sun, Yingfeng Zheng, Bing Cheng, Mei Li, Xialin Liu, Chang He
Inflammation has emerged to be a critical mechanism responsible for neural damage and neurodegenerative diseases. Microglia, the resident innate immune cells in retina, are implicated as principal components of the immunological insult to retinal neural cells. The involvement of microglia in retinal inflammation is complex and here we propose for the first time that necroptosis in microglia triggers neuroinflammation and exacerbates retinal neural damage and degeneration. We found microglia experienced receptor-interacting protein kinase 1 (RIP1)- and RIP3-dependent necroptosis not only in the retinal degenerative rd1 mice, but also in the acute retinal neural injury mice...
September 8, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28862703/fine-tuning-and-autoregulation-of-the-intestinal-determinant-and-tumor-suppressor-homeobox-gene-cdx2-by-alternative-splicing
#9
Camille Balbinot, Marie Vanier, Olivier Armant, Asmaa Nair, Julien Penichon, Christine Soret, Elisabeth Martin, Thoueiba Saandi, Jean-Marie Reimund, Jacqueline Deschamps, Felix Beck, Claire Domon-Dell, Isabelle Gross, Isabelle Duluc, Jean-Noël Freund
On the basis of phylogenetic analyses, we uncovered a variant of the CDX2 homeobox gene, a major regulator of the development and homeostasis of the gut epithelium, also involved in cancer. This variant, miniCDX2, is generated by alternative splicing coupled to alternative translation initiation, and contains the DNA-binding homeodomain but is devoid of transactivation domain. It is predominantly expressed in crypt cells, whereas the CDX2 protein is present in crypt cells but also in differentiated villous cells...
September 1, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28862702/the-emerging-role-of-rnas-in-dna-damage-repair
#10
Ben R Hawley, Wei-Ting Lu, Ania Wilczynska, Martin Bushell
This corrects the article DOI: 10.1038/cdd.2017.16.
September 1, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28862701/deletion-of-nedd4-2-results-in-progressive-kidney-disease-in-mice
#11
Tanya L Henshall, Jantina A Manning, Omri S Alfassy, Pranay Goel, Natasha A Boase, Hiroshi Kawabe, Sharad Kumar
NEDD4-2 (NEDD4L), a ubiquitin protein ligase of the Nedd4 family, is a key regulator of cell surface expression and activity of the amiloride-sensitive epithelial Na(+) channel (ENaC). While hypomorphic alleles of Nedd4-2 in mice show salt-sensitive hypertension, complete knockout results in pulmonary distress and perinatal lethality due to increased cell surface levels of ENaC. We now show that Nedd4-2 deficiency in mice also results in an unexpected progressive kidney injury phenotype associated with elevated ENaC and Na(+)Cl(-) cotransporter expression, increased Na(+) reabsorption, hypertension and markedly reduced levels of aldosterone...
September 1, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28841214/tudor-domain-protein-phf20l1-reads-lysine-methylated-retinoblastoma-tumour-suppressor-protein
#12
Simon M Carr, Shonagh Munro, Cari A Sagum, Oleg Fedorov, Mark T Bedford, Nicholas B La Thangue
The retinoblastoma tumour suppressor protein (pRb) classically functions to regulate early cell cycle progression where it acts to enforce a number of checkpoints in response to cellular stress and DNA damage. Methylation at lysine (K) 810, which occurs within a critical CDK phosphorylation site and antagonises a CDK-dependent phosphorylation event at the neighbouring S807 residue, acts to hold pRb in the hypo-phosphorylated growth-suppressing state. This is mediated in part by the recruitment of the reader protein 53BP1 to di-methylated K810, which allows pRb activity to be effectively integrated with the DNA damage response...
August 25, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28841213/complete-in-vitro-oogenesis-retrospects-and-prospects
#13
REVIEW
Jun-Jie Wang, Wei Ge, Jing-Cai Liu, Francesca Gioia Klinger, Paul W Dyce, Massimo De Felici, Wei Shen
Precise control of mammalian oogenesis has been a traditional focus of reproductive and developmental biology research. Recently, new reports have introduced the possibility of obtaining functional gametes derived in vitro from stem cells. The potential to produce functional gametes from stem cells has exciting applications for regenerative medicine though still remains challenging. In mammalian females ovulation and fertilization is a privilege reserved for a small number of oocytes. In reality the vast majority of oocytes formed from primordial germ cells (PGCs) will undergo apoptosis, or other forms of cell death...
August 25, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800132/sphingolipid-accumulation-causes-mitochondrial-dysregulation-and-cell-death
#14
Jeffrey Knupp, Fernando Martinez-Montañés, Francoise Van Den Bergh, Stephanie Cottier, Roger Schneiter, Daniel Beard, Amy Chang
Sphingolipids are structural components of cell membranes that have signaling roles to regulate many activities, including mitochondrial function and cell death. Sphingolipid metabolism is integrated with numerous metabolic networks, and dysregulated sphingolipid metabolism is associated with disease. Here, we describe a monogenic yeast model for sphingolipid accumulation. A csg2Δ mutant cannot readily metabolize and accumulates the complex sphingolipid inositol phosphorylceramide (IPC). In these cells, aberrant activation of Ras GTPase is IPC-dependent, and accompanied by increased mitochondrial reactive oxygen species (ROS) and reduced mitochondrial mass...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800131/atg2a-b-deficiency-switches-cytoprotective-autophagy-to-non-canonical-caspase-8-activation-and-apoptosis
#15
Zhenyuan Tang, Yoshinori Takahashi, Chong Chen, Ying Liu, Haiyan He, Nikolaos Tsotakos, Jacob M Serfass, Melat T Gebru, Han Chen, Megan M Young, Hong-Gang Wang
Autophagosomal membranes are emerging as platforms for various cell survival and death signaling networks beyond autophagy. While autophagy-dependent cell death has been reported in response to a variety of stimuli, the underlying molecular mechanisms remain far from clear. Here, we demonstrate that inhibition of autophagosome completion by Atg2A/B deletion accumulates immature autophagosomal membranes that promote non-canonical caspase-8 activation in response to nutrient starvation via an intracellular death-inducing signaling complex (iDISC)...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800130/mir-130a-upregulates-mtor-pathway-by-targeting-tsc1-and-is-transactivated-by-nf-%C3%AE%C2%BAb-in-high-grade-serous-ovarian-carcinoma
#16
Yuqiong Wang, Xiyu Zhang, Wei Tang, Zhenghong Lin, Limei Xu, Ruifen Dong, Yinuo Li, Jieyin Li, Zaixin Zhang, Xiangzhi Li, Ling Zhao, Jian-Jun Wei, Changshun Shao, Beihua Kong, Zhaojian Liu
Activation of mammalian target of rapamycin (mTOR) signaling pathway is associated with poor prognosis of epithelial ovarian cancer. The TSC1-TSC2 complex is a critical negative regulator of mTOR signaling. Here, we demonstrated that TSC1 was frequently downregulated in high-grade serous ovarian carcinoma (HGSOC) and low TSC1 expression level is associated with advanced tumor stage. We next identified miR-130a to be a negative regulator of TSC1 by targeting its 3'UTR. miR-130a was overexpressed in HGSOC and could drive proliferation and invasion/metastasis of ovarian cancer cells...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800129/the-combination-of-reduced-mcl-1-and-standard-chemotherapeutics-is-tolerable-in-mice
#17
Kerstin Brinkmann, Stephanie Grabow, Craig D Hyland, Charis E Teh, Warren S Alexander, Marco J Herold, Andreas Strasser
A common therapeutic strategy to combat human cancer is the use of combinations of drugs, each targeting different cellular processes or vulnerabilities. Recent studies suggest that addition of an MCL-1 inhibitor to such anticancer drug treatments could be an attractive therapeutic strategy. Thus, it is of great interest to understand whether combinations of conventional anticancer drugs with an MCL-1 inhibitor will be tolerable and efficacious. In order to mimic the combination of MCL-1 inhibition with other cancer therapeutics, we treated Mcl-1(+/-) heterozygous mice, which have a ~50% reduction in MCL-1 protein in their cells, with a broad range of chemotherapeutic drugs...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800128/adult-cardiac-stem-cells-are-multipotent-and-robustly-myogenic-c-kit-expression-is-necessary-but-not-sufficient-for-their-identification
#18
Carla Vicinanza, Iolanda Aquila, Mariangela Scalise, Francesca Cristiano, Fabiola Marino, Eleonora Cianflone, Teresa Mancuso, Pina Marotta, Walter Sacco, Fiona C Lewis, Liam Couch, Victoria Shone, Giulia Gritti, Annalaura Torella, Andrew J Smith, Cesare Mn Terracciano, Domenico Britti, Pierangelo Veltri, Ciro Indolfi, Bernardo Nadal-Ginard, Georgina M Ellison-Hughes, Daniele Torella
Multipotent adult resident cardiac stem cells (CSCs) were first identified by the expression of c-kit, the stem cell factor receptor. However, in the adult myocardium c-kit alone cannot distinguish CSCs from other c-kit-expressing (c-kit(pos)) cells. The adult heart indeed contains a heterogeneous mixture of c-kit(pos) cells, mainly composed of mast and endothelial/progenitor cells. This heterogeneity of cardiac c-kit(pos) cells has generated confusion and controversy about the existence and role of CSCs in the adult heart...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28800127/mnt-modulates-myc-driven-lymphomagenesis
#19
Kirsteen J Campbell, Cassandra J Vandenberg, Natasha S Anstee, Peter J Hurlin, Suzanne Cory
The transcriptional represser Mnt is a functional antagonist of the proto-oncoprotein Myc. Both Mnt and Myc utilise Max as an obligate partner for DNA binding, and Myc/Max and Mnt/Max complexes compete for occupancy at E-box DNA sequences in promoter regions. We have previously shown in transgenic mouse models that the phenotype and kinetics of onset of haemopoietic tumours varies with the level of Myc expression. We reasoned that a decrease in the level of Mnt would increase the functional level of Myc and accelerate Myc-driven tumorigenesis...
August 11, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28777375/inhibition-of-bcl-xl-prevents-pro-death-actions-of-%C3%AE-n-bcl-xl-at-the-mitochondrial-inner-membrane-during-glutamate-excitotoxicity
#20
Han-A Park, Pawel Licznerski, Nelli Mnatsakanyan, Yulong Niu, Silvio Sacchetti, Jing Wu, Brian M Polster, Kambiz N Alavian, Elizabeth A Jonas
ABT-737 is a pharmacological inhibitor of the anti-apoptotic activity of B-cell lymphoma-extra large (Bcl-xL) protein; it promotes apoptosis of cancer cells by occupying the BH3-binding pocket. We have shown previously that ABT-737 lowers cell metabolic efficiency by inhibiting ATP synthase activity. However, we also found that ABT-737 protects rodent brain from ischemic injury in vivo by inhibiting formation of the pro-apoptotic, cleaved form of Bcl-xL, ΔN-Bcl-xL. We now report that a high concentration of ABT-737 (1 μM), or a more selective Bcl-xL inhibitor WEHI-539 (5 μM) enhances glutamate-induced neurotoxicity while a low concentration of ABT-737 (10 nM) or WEHI-539 (10 nM) is neuroprotective...
August 4, 2017: Cell Death and Differentiation
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