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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/29786076/c-myc-inhibits-myoblast-differentiation-and-promotes-myoblast-proliferation-and-muscle-fibre-hypertrophy-by-regulating-the-expression-of-its-target-genes-mirnas-and-lincrnas
#1
Wen Luo, Jiahui Chen, Limin Li, Xueyi Ren, Tian Cheng, Shiyi Lu, Raman Akinyanju Lawal, Qinghua Nie, Xiquan Zhang, Olivier Hanotte
The transcription factor c-Myc is an important regulator of cellular proliferation, differentiation and embryogenesis. While c-Myc can inhibit myoblast differentiation, the underlying mechanisms remain poorly understood. Here, we found that c-Myc does not only inhibits myoblast differentiation but also promotes myoblast proliferation and muscle fibre hypertrophy. By performing chromatin immunoprecipitation and high-throughput sequencing (ChIP-seq), we identified the genome-wide binding profile of c-Myc in skeletal muscle cells...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786075/tp53-gain-of-function-mutation-promotes-inflammation-in-glioblastoma
#2
Seok Won Ham, Hee-Young Jeon, Xiong Jin, Eun-Jung Kim, Jun-Kyum Kim, Yong Jae Shin, Yeri Lee, Se Hoon Kim, Seon Yong Lee, Sunyoung Seo, Min Gi Park, Hye-Mi Kim, Do-Hyun Nam, Hyunggee Kim
Glioblastoma (GBM), the most severe and common brain tumor in adults, is characterized by multiple somatic mutations and aberrant activation of inflammatory responses. Immune cell infiltration and subsequent inflammation cause tumor growth and resistance to therapy. Somatic loss-of-function mutations in the gene encoding tumor suppressor protein p53 (TP53) are frequently observed in various cancers. However, numerous studies suggest that TP53 regulates malignant phenotypes by gain-of-function (GOF) mutations...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786074/constitutive-interferon-signaling-maintains-critical-threshold-of-mlkl-expression-to-license-necroptosis
#3
Joseph Sarhan, Beiyun C Liu, Hayley I Muendlein, Chi G Weindel, Irina Smirnova, Amy Y Tang, Vladimir Ilyukha, Maxim Sorokin, Anton Buzdin, Katherine A Fitzgerald, Alexander Poltorak
Interferons (IFNs) are critical determinants in immune-competence and autoimmunity, and are endogenously regulated by a low-level constitutive feedback loop. However, little is known about the functions and origins of constitutive IFN. Recently, lipopolysaccharide (LPS)-induced IFN was implicated as a driver of necroptosis, a necrotic form of cell death downstream of receptor-interacting protein (RIP) kinase activation and executed by mixed lineage kinase like-domain (MLKL) protein. We found that the pre-established IFN status of the cell, instead of LPS-induced IFN, is critical for the early initiation of necroptosis in macrophages...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786073/integrin-%C3%AE-6%C3%AE-4-src-akt-signaling-induces-cellular-senescence-by-counteracting-apoptosis-in-irradiated-tumor-cells-and-tissues
#4
Seung Hee Jung, Minyoung Lee, Hyun A Park, Hyung Chul Lee, Donghee Kang, Hyun Jung Hwang, Chanho Park, Dong-Min Yu, Yu Ri Jung, Mi-Na Hong, Yong-Nyun Kim, Heon Joo Park, Young-Gyu Ko, Jae-Seon Lee
Cellular senescence refers to an irreversible growth arrest that is triggered by various intrinsic and extrinsic stresses. Many recent studies have demonstrated that cellular senescence plays a crucial role in the regression of tumors exposed to ionizing radiation (IR), but the underlying mechanism remains unknown. Here we show that the activation of integrin β4 is essential for IR-induced cellular senescence. IR treatment results in the phosphorylation of integrin β4 at tyrosine residue 1510, leading to activation of the integrin α6β4-Src-AKT signaling pathway...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786072/mptp-driven-nlrp3-inflammasome-activation-in-microglia-plays-a-central-role-in-dopaminergic-neurodegeneration
#5
Eunju Lee, Inhwa Hwang, Sangjun Park, Sujeong Hong, Boreum Hwang, Yoeseph Cho, Junghyun Son, Je-Wook Yu
Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN) and the reduction of dopamine levels in the striatum. Although details of the molecular mechanisms underlying dopaminergic neuronal death in PD remain unclear, neuroinflammation is also considered a potent mediator in the pathogenesis and progression of PD. In the present study, we present evidences that microglial NLRP3 inflammasome activation is critical for dopaminergic neuronal loss and the subsequent motor deficits in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786071/dopamine-d2-receptor-restricts-astrocytic-nlrp3-inflammasome-activation-via-enhancing-the-interaction-of-%C3%AE-arrestin2-and-nlrp3
#6
Jialei Zhu, Zhaoli Hu, Xiaojuan Han, Dongshuo Wang, Qingling Jiang, Jianhua Ding, Ming Xiao, Cong Wang, Ming Lu, Gang Hu
Astrocytes are involved in the neuroinflammation of neurodegenerative diseases, such as Parkinson's disease (PD). Among the numerous inflammatory cytokines, interleukin-1β (IL-1β) produced by astrocytic Nod-like receptor protein (NLRP) inflammasome is crucial in the pathogenesis of PD. β-arrestin2-mediated dopamine D2 receptor (Drd2) signal transduction has been regarded as a potential anti-inflammatory target. Our previous study revealed that astrocytic Drd2 suppresses neuroinflammation in the central nervous system...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786070/selective-elimination-of-senescent-cells-by-mitochondrial-targeting-is-regulated-by-ant2
#7
Sona Hubackova, Eliska Davidova, Katerina Rohlenova, Jan Stursa, Lukas Werner, Ladislav Andera, LanFeng Dong, Mikkel G Terp, Zdenek Hodny, Henrik J Ditzel, Jakub Rohlena, Jiri Neuzil
Cellular senescence is a form of cell cycle arrest that limits the proliferative potential of cells, including tumour cells. However, inability of immune cells to subsequently eliminate senescent cells from the organism may lead to tissue damage, inflammation, enhanced carcinogenesis and development of age-related diseases. We found that the anticancer agent mitochondria-targeted tamoxifen (MitoTam), unlike conventional anticancer agents, kills cancer cells without inducing senescence in vitro and in vivo. Surprisingly, it also selectively eliminates both malignant and non-cancerous senescent cells...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786069/ve-cadherin-promotes-vasculogenic-mimicry-by-modulating-kaiso-dependent-gene-expression
#8
Daniel Delgado-Bellido, Mónica Fernández-Cortés, María Isabel Rodríguez, Santiago Serrano-Sáenz, Arkaitz Carracedo, Angel Garcia-Diaz, F Javier Oliver
Aberrant extra-vascular expression of VE-cadherin (VEC) has been observed in metastasis associated with vasculogenic mimicry (VM); however, the ultimate reason why non-endothelial VEC favors the acquisition of this phenotype is not established. In this study, we show that human malignant melanoma cells have a constitutively high expression of phoshoVEC (pVEC) at Y658; pVEC is a target of focal adhesion kinase (FAK) and forms a complex with p120-catenin and the transcriptional repressor kaiso in the nucleus...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29786068/mitochondrial-pip3-binding-protein-fundc2-supports-platelet-survival-via-akt-signaling-pathway
#9
Qi Ma, Chongzhuo Zhu, Weilin Zhang, Na Ta, Rong Zhang, Lei Liu, Du Feng, Heping Cheng, Junling Liu, Quan Chen
Platelets undergo apoptosis in response to a variety of stimuli in the circulation. Mitochondria in platelets are essential for their apoptosis. Specifically, pro-survival protein BCL-xL on mitochondria is the key regulator of platelet lifespan. Here we identify an outer mitochondrial membrane protein FUNDC2 for platelet survival. FUNDC2 knockout mice carrying excessively apoptotic platelets exhibit thrombocytopenia in response to hypoxia. Mechanistically, FUNDC2 binds the lipid PIP3 via its unique, highly conserved N-terminal motif...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29769640/hypoxia-induced-microrna-191-contributes-to-hepatic-ischemia-reperfusion-injury-through-the-zonab-cyclin-d1-axis
#10
Wenming Pan, Lin Wang, Xiao-Fei Zhang, Hongji Zhang, Jinxiang Zhang, Guoliang Wang, Peng Xu, Yunwei Zhang, Ping Hu, Xiao-Dong Zhang, Run-Lei Du, Hui Wang
Hepatic ischemia/reperfusion injury (IRI) is a common cause of morbidity and mortality in liver transplantation settings and involves severe cell death and inflammatory responses. MicroRNA-191 has recently been reported to be abnormally expressed in hepatocellular carcinoma and other liver diseases in the regulation of important cellular processes. However, little is known about its function and molecular mechanism in IRI. Here, we demonstrate that miR-191 is significantly upregulated in a cultured cell line during hypoxia/reperfusion (H/R) and in liver tissue during IRI in mice...
May 16, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29769639/a-novel-cell-penetrating-peptide-protects-against-neuron-apoptosis-after-cerebral-ischemia-by-inhibiting-the-nuclear-translocation-of-annexin-a1
#11
Xing Li, Lu Zheng, Qian Xia, Lu Liu, Meng Mao, Huijuan Zhou, Yin Zhao, Jing Shi
Nuclear translocation of annexin A1 (ANXA1) has recently been reported to participate in neuronal apoptosis after cerebral ischemia. Prevention of the nuclear translocation of ANXA1 should therefore inhibit neuronal apoptosis and protect against cerebral stroke. Here, we found that, in the repeat III domain of ANXA1, the amino-acid residues from R228 to F237 function as a unique nuclear translocation signal (NTS) and are required for nuclear translocation of ANXA1. Intriguingly, we synthesized a cell-penetrating peptide derived by conjugating the trans-activator of transcription (Tat) domain to the NTS sequence...
May 16, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29765111/new-insights-into-apoptosome-structure-and-function
#12
REVIEW
Loretta Dorstyn, Christopher W Akey, Sharad Kumar
The apoptosome is a platform that activates apical procaspases in response to intrinsic cell death signals. Biochemical and structural studies in the past two decades have extended our understanding of apoptosome composition and structure, while illuminating the requirements for initiator procaspase activation. A number of studies have now provided high-resolution structures for apoptosomes from C. elegans (CED-4), D. melanogaster (Dark), and H. sapiens (Apaf-1), which define critical protein interfaces, including intra and interdomain interactions...
May 15, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29748601/trabid-inhibits-hepatocellular-carcinoma-growth-and-metastasis-by-cleaving-rnf8-induced-k63-ubiquitination-of-twist1
#13
Yuekun Zhu, Chao Qu, Xuehui Hong, Yanyan Jia, Meihu Lin, Yunmei Luo, Fengqin Lin, Xiaolong Xie, Xiaoqi Xie, Juan Huang, Qin Wu, Xingfeng Qiu, Daxun Piao, Yanwei Xing, Tian Yu, Yuanfu Lu, Qiang Huang, Changyin Yu, Junfei Jin, Zhiyong Zhang
TRAF-binding domain (Trabid), one of deubiquitination enzymes, was recently reported to activate Wnt/ β-catenin signaling pathway. However, the role of Trabid in tumors including hepatocellular carcinoma (HCC) and the underlying mechanisms controlling its activity remain poorly understood. Here, we report that Trabid is significantly downregulated in HCC tumor samples and cell lines compared with normal controls and that its expression level is negatively correlated with HCC pathological grading, recurrence, and metastasis...
May 10, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29748600/caspase-selective-reagents-for-diagnosing-apoptotic-mechanisms
#14
Marcin Poreba, Katarzyna Groborz, Mario Navarro, Scott J Snipas, Marcin Drag, Guy S Salvesen
Apical caspases initiate and effector caspases execute apoptosis. Reagents that can distinguish between caspases, particularly apical caspases-8, 9, and 10 are scarce and generally nonspecific. Based upon a previously described large-scale screen of peptide-based caspase substrates termed HyCoSuL, we sought to develop reagents to distinguish between apical caspases in order to reveal their function in apoptotic cell death paradigms. To this end, we selected tetrapeptide-based sequences that deliver optimal substrate selectivity and converted them to inhibitors equipped with a detectable tag (activity-based probes-ABPs)...
May 10, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29743560/caspases-in-metabolic-disease-and-their-therapeutic-potential
#15
Claire H Wilson, Sharad Kumar
Caspases, a family of cysteine-dependent aspartate-specific proteases, are central to the maintenance of cellular and organismal homoeostasis by functioning as key mediators of the inflammatory response and/or apoptosis. Both metabolic inflammation and apoptosis play a central role in the pathogenesis of metabolic disease such as obesity and the progression of nonalcoholic steatohepatisis (NASH) to more severe liver disease. Obesity and nonalcoholic fatty liver disease (NAFLD) are the leading global health challenges associated with the development of numerous comorbidities including insulin resistance, type-2 diabetes and early mortality...
May 9, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29743559/antigen-specific-primed-cytotoxic-t-cells-eliminate-tumour-cells-in-vivo-and-prevent-tumour-development-regardless-of-the-presence-of-anti-apoptotic-mutations-conferring-drug-resistance
#16
Paula Jaime-Sánchez, Elena Catalán, Iratxe Uranga-Murillo, Nacho Aguiló, Llipsy Santiago, Pilar M Lanuza, Diego de Miguel, Maykel A Arias, Julián Pardo
Cytotoxic CD8+ T (Tc) cells are the main executors of transformed and cancer cells during cancer immunotherapy. The latest clinical results evidence a high efficacy of novel immunotherapy agents that modulate Tc cell activity against bad prognosis cancers. However, it has not been determined yet whether the efficacy of these treatments can be affected by selection of tumoural cells with mutations in the cell death machinery, known to promote drug resistance and cancer recurrence. Here, using a model of prophylactic tumour vaccination based on the LCMV-gp33 antigen and the mouse EL4 T lymphoma, we analysed the molecular mechanism employed by Tc cells to eliminate cancer cells in vivo and the impact of mutations in the apoptotic machinery on tumour development...
May 9, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29725115/micu3-is-a-tissue-specific-enhancer-of-mitochondrial-calcium-uptake
#17
Maria Patron, Veronica Granatiero, Javier Espino, Rosario Rizzuto, Diego De Stefani
The versatility and universality of Ca2+ as intracellular messenger is guaranteed by the compartmentalization of changes in [Ca2+ ]. In this context, mitochondrial Ca2+ plays a central role, by regulating both specific organelle functions and global cellular events. This versatility is also guaranteed by a cell type-specific Ca2+ signaling toolkit controlling specific cellular functions. Accordingly, mitochondrial Ca2+ uptake is mediated by a multimolecular structure, the MCU complex, which differs among various tissues...
May 3, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29674627/ciap1-regulates-the-egfr-snai2-axis-in-triple-negative-breast-cancer-cells
#18
Maria Teresa Majorini, Giacomo Manenti, Miguel Mano, Loris De Cecco, Annalisa Conti, Patrizia Pinciroli, Enrico Fontanella, Elda Tagliabue, Claudia Chiodoni, Mario Paolo Colombo, Domenico Delia, Daniele Lecis
Inhibitor of apoptosis (IAP) proteins constitute a family of conserved molecules that regulate both apoptosis and receptor signaling. They are often deregulated in cancer cells and represent potential targets for therapy. In our work, we investigated the effect of IAP inhibition in vivo to identify novel downstream genes expressed in an IAP-dependent manner that could contribute to cancer aggressiveness. To this end, immunocompromised mice engrafted subcutaneously with the triple-negative breast cancer MDA-MB231 cell line were treated with SM83, a Smac mimetic that acts as a pan-IAP inhibitor, and tumor nodules were profiled for gene expression...
April 19, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29666477/single-cell-analysis-of-pyroptosis-dynamics-reveals-conserved-gsdmd-mediated-subcellular-events-that-precede-plasma-membrane-rupture
#19
Nathalia M de Vasconcelos, Nina Van Opdenbosch, Hanne Van Gorp, Eef Parthoens, Mohamed Lamkanfi
Pyroptosis is rapidly emerging as a mechanism of anti-microbial host defense, and of extracellular release of the inflammasome-dependent cytokines interleukin (IL)-1β and IL-18, which contributes to autoinflammatory pathology. Caspases 1, 4, 5 and 11 trigger this regulated form of necrosis by cleaving the pyroptosis effector gasdermin D (GSDMD), causing its pore-forming amino-terminal domain to oligomerize and perforate the plasma membrane. However, the subcellular events that precede pyroptotic cell lysis are ill defined...
April 17, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29666476/hif1a-inactivation-rescues-photoreceptor-degeneration-induced-by-a-chronic-hypoxia-like-stress
#20
Maya Barben, Divya Ail, Federica Storti, Katrin Klee, Christian Schori, Marijana Samardzija, Stylianos Michalakis, Martin Biel, Isabelle Meneau, Frank Blaser, Daniel Barthelmes, Christian Grimm
Reduced choroidal blood flow and tissue changes in the ageing human eye impair oxygen delivery to photoreceptors and the retinal pigment epithelium. As a consequence, mild but chronic hypoxia may develop and disturb cell metabolism, function and ultimately survival, potentially contributing to retinal pathologies such as age-related macular degeneration (AMD). Here, we show that several hypoxia-inducible genes were expressed at higher levels in the aged human retina suggesting increased activity of hypoxia-inducible transcription factors (HIFs) during the physiological ageing process...
April 17, 2018: Cell Death and Differentiation
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