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Cell Death & Disease

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https://www.readbyqxmd.com/read/28079897/tsc1-expression-by-dendritic-cells-is-required-to-preserve-t-cell-homeostasis-and-response
#1
Yuechen Luo, Wenwen Li, Gang Yu, Juan Yu, Ling Han, Ting Xue, Zhina Sun, Song Chen, Chunming Fang, Chunxiao Zhao, Qing Niu, Fei Yang, Zhongchao Han, Tao Cheng, Yun Zeng, Fang Liao, Guogang Xu, Xiaoming Feng
Dendritic cells (DCs) are pivotal to the induction of adaptive T-cell immune responses. Recent evidence highlights a critical role of tuberous sclerosis complex 1 (Tsc1), a primarily upstream negative regulator of mammalian target of rapamycin (mTOR), in DC development, but whether and how Tsc1 directly regulate mature DC function in vivo remains elusive. Here we show that selective disruption of Tsc1 in DCs results in a lymphoproliferative disorder with the spontaneous activation of T cells. Tsc1 deficiency results in the activation of mTORC1-PPARγ pathway, which leads to the upregulation of neuropilin-1 (Nrp1) expression on DCs to stimulate naive T-cell proliferation...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079896/impaired-embryonic-development-in-glucose-6-phosphate-dehydrogenase-deficient-caenorhabditis-elegans-due-to-abnormal-redox-homeostasis-induced-activation-of-calcium-independent-phospholipase-and-alteration-of-glycerophospholipid-metabolism
#2
Tzu-Ling Chen, Hung-Chi Yang, Cheng-Yu Hung, Meng-Hsin Ou, Yi-Yun Pan, Mei-Ling Cheng, Arnold Stern, Szecheng J Lo, Daniel Tsun-Yee Chiu
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly pervasive inherited disease in many parts of the world. The complete lack of G6PD activity in a mouse model causes embryonic lethality. The G6PD-deficient Caenorhabditis elegans model also shows embryonic death as indicated by a severe hatching defect. Although increased oxidative stress has been implicated in both cases as the underlying cause, the exact mechanism has not been clearly delineated. In this study with C. elegans, membrane-associated defects, including enhanced permeability, defective polarity and cytokinesis, were found in G6PD-deficient embryos...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079895/tnf-induced-chronic-inflammation-does-not-affect-tumorigenesis-driven-by-p53-loss
#3
Derek Lacey, Andreas Strasser, Philippe Bouillet
No abstract text is available yet for this article.
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079894/mir-26-enhances-chemosensitivity-and-promotes-apoptosis-of-hepatocellular-carcinoma-cells-through-inhibiting-autophagy
#4
Fangfang Jin, Yanbo Wang, Mingzhen Li, Yanan Zhu, Hongwei Liang, Chen Wang, Feng Wang, Chen-Yu Zhang, Ke Zen, Limin Li
Hepatocellular carcinoma (HCC) generally possesses a high resistance to chemotherapy. Given that autophagy is an important factor promoting tumor chemoresistance and HCC express low level of miR-26, we aim to investigate the functional role of miR-26 in autophagy-mediated chemoresistance of HCC. We found that chemotherapeutic drug doxorubicin (Dox) induced autophagy but decreased the level of miR-26a/b in HCC cells. Activating autophagy using rapamycin can directly downregulate the level of miR-26a/b in HCC cells...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079893/mitochondrial-respiratory-dysfunction-disturbs-neuronal-and-cardiac-lineage-commitment-of-human-ipscs
#5
Mutsumi Yokota, Hideyuki Hatakeyama, Yasuha Ono, Miyuki Kanazawa, Yu-Ichi Goto
Mitochondrial diseases are genetically heterogeneous and present a broad clinical spectrum among patients; in most cases, genetic determinants of mitochondrial diseases are heteroplasmic mitochondrial DNA (mtDNA) mutations. However, it is uncertain whether and how heteroplasmic mtDNA mutations affect particular cellular fate-determination processes, which are closely associated with the cell-type-specific pathophysiology of mitochondrial diseases. In this study, we established two isogenic induced pluripotent stem cell (iPSC) lines each carrying different proportions of a heteroplasmic m...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079892/hif-2%C3%AE-and-oct4-have-synergistic-effects-on-survival-and-myocardial-repair-of-very-small-embryonic-like-mesenchymal-stem-cells-in-infarcted-hearts
#6
Shaoheng Zhang, Lan Zhao, Jiahong Wang, Nannan Chen, Jian Yan, Xin Pan
Poor cell survival and limited functional benefits have restricted mesenchymal stem cell (MSC) efficacy for treating myocardial infarction (MI), suggesting that a better understanding of stem cell biology is needed. The transcription factor HIF-2α is an essential regulator of the transcriptional response to hypoxia, which can interact with embryonic stem cells (ESCs) transcription factor Oct4 and modulate its signaling. Here, we obtained very small embryonic-like mesenchymal stem cells (vselMSCs) from MI patients, which possessed the very small embryonic-like stem cells' (VSELs) morphology as well as ESCs' pluripotency...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079891/crb3-regulates-contact-inhibition-by-activating-the-hippo-pathway-in-mammary-epithelial-cells
#7
Xiaona Mao, Pingping Li, Yaochun Wang, Zheyong Liang, Jie Liu, Juan Li, Yina Jiang, Gang Bao, Lei Li, Bofeng Zhu, Yu Ren, Xinhan Zhao, Jianmin Zhang, Yu Liu, Jin Yang, Peijun Liu
The loss of contact inhibition is a hallmark of cancer cells. The Hippo pathway has recently been shown to be an important regulator of contact inhibition, and the cell apical polarity determinant protein CRB3 has been suggested to be involved in Hippo signalling. However, whether CRB3 regulates contact inhibition in mammary cells remains unclear, and the underlying mechanisms have not been elucidated. As shown in the present study, CRB3 decreases cell proliferation, promotes apoptosis, and enhances the formation of tight and adherens junctions...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079890/structural-insight-into-an-evolutionarily-ancient-programmed-cell-death-regulator-the-crystal-structure-of-marine-sponge-bhp2-bound-to-lb-bak-2
#8
Sofia Caria, Mark G Hinds, Marc Kvansakul
Sponges of the porifera family harbor some of the evolutionary most ancient orthologs of the B-cell lymphoma-2 (Bcl-2) family, a protein family critical to regulation of apoptosis. The genome of the sponge Geodia cydonium contains the putative pro-survival Bcl-2 homolog BHP2, which protects sponge tissue as well as mammalian Hek-293 and NIH-3T3 cells against diverse apoptotic stimuli. The Lake Baikal demosponge Lubomirskia baicalensis has been shown to encode both putative pro-survival Bcl-2 (LB-Bcl-2) and pro-apoptotic Bcl-2 members (LB-Bak-2), which have been implied in axis formation (branches) in L...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079889/deletion-of-the-bh3-only-protein-noxa-alters-electrographic-seizures-but-does-not-protect-against-hippocampal-damage-after-status-epilepticus-in-mice
#9
Naoki Ichikawa, Mariana Alves, Shona Pfeiffer, Elena Langa, Yasmina E Hernández-Santana, Hidenori Suzuki, Jochen Hm Prehn, Tobias Engel, David C Henshall
Several members of the Bcl-2 gene family are dysregulated in human temporal lobe epilepsy and animal studies show that genetic deletion of some of these proteins influence electrographic seizure responses to chemoconvulsants and associated brain damage. The BH3-only proteins form a subgroup comprising direct activators of Bax-Bak that are potently proapoptotic and a number of weaker proapoptotic BH3-only proteins that act as sensitizers by neutralization of antiapoptotic Bcl-2 family members. Noxa was originally characterized as a weaker proapoptotic, 'sensitizer' BH3-only protein, although recent evidence suggests it too may be potently proapoptotic...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079888/antiphospholipid-antibodies-enhance-rat-neonatal-cardiomyocyte-apoptosis-in-an-in-vitro-hypoxia-reoxygenation-injury-model-via-p38-mapk
#10
Lauren T Bourke, Thomas McDonnell, James McCormick, Charis Pericleous, Vera M Ripoll, Ian Giles, Anisur Rahman, Anastasis Stephanou, Yiannis Ioannou
A significant amount of myocardial damage during a myocardial infarction (MI) occurs during the reperfusion stage, termed ischaemia/reperfusion (I/R) injury, and accounts for up to 50% of total infarcted tissue post-MI. During the reperfusion phase, a complex interplay of multiple pathways and mechanisms is activated, which ultimately leads to cell death, primarily through apoptosis. There is some evidence from a lupus mouse model that lupus IgG, specifically the antiphospholipid (aPL) antibody subset, is pathogenic in mesenteric I/R injury...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079887/drp-1-is-required-for-bh3-mimetic-mediated-mitochondrial-fragmentation-and-apoptosis
#11
Mateus Milani, Dominic P Byrne, Georgia Greaves, Michael Butterworth, Gerald M Cohen, Patrick A Eyers, Shankar Varadarajan
The concept of using BH3 mimetics as anticancer agents has been substantiated by the efficacy of selective drugs, such as Navitoclax and Venetoclax, in treating BCL-2-dependent haematological malignancies. However, most solid tumours depend on MCL-1 for survival, which is highly amplified in multiple cancers and a major factor determining chemoresistance. Most MCL-1 inhibitors that have been generated so far, while demonstrating early promise in vitro, fail to exhibit specificity and potency in a cellular context...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079886/hiv-1-nef-is-released-in-extracellular-vesicles-derived-from-astrocytes-evidence-for-nef-mediated-neurotoxicity
#12
A Sami Saribas, Stephanie Cicalese, Taha Mohseni Ahooyi, Kamel Khalili, Shohreh Amini, Ilker Kudret Sariyer
Human immunodeficiency virus-associated neurological disorders (HANDs) affect the majority of AIDS patients and are a significant problem among HIV-1-infected individuals who live longer because of combined anti-retroviral therapies. HIV-1 utilizes a number of viral proteins and subsequent cytokine inductions to unleash its toxicity on neurons. Among HIV-1 viral proteins, Nef is a small protein expressed abundantly in astrocytes of HIV-1-infected brains and has been suggested to have a role in the pathogenesis of HAND...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079885/mirna182-regulates-percentage-of-myeloid-and-erythroid-cells-in-chronic-myeloid-leukemia
#13
Deepak Arya, Sasikala P Sachithanandan, Cecil Ross, Dasaradhi Palakodeti, Shang Li, Sudhir Krishna
The deregulation of lineage control programs is often associated with the progression of haematological malignancies. The molecular regulators of lineage choices in the context of tyrosine kinase inhibitor (TKI) resistance remain poorly understood in chronic myeloid leukemia (CML). To find a potential molecular regulator contributing to lineage distribution and TKI resistance, we undertook an RNA-sequencing approach for identifying microRNAs (miRNAs). Following an unbiased screen, elevated miRNA182-5p levels were detected in Bcr-Abl-inhibited K562 cells (CML blast crisis cell line) and in a panel of CML patients...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079884/lack-of-collagen-xv-is-protective-after-ischemic-stroke-in-mice
#14
Hiramani Dhungana, Mikko T Huuskonen, Taina Pihlajaniemi, Ritva Heljasvaara, Denis Vivien, Katja M Kanninen, Tarja Malm, Jari Koistinaho, Sighild Lemarchant
Collagens are key structural components of basement membranes, providing a scaffold for other components or adhering cells. Collagens and collagen-derived active fragments contribute to biological activities such as cell growth, differentiation and migration. Here, we report that collagen XV knock-out (ColXV KO) mice are resistant to experimental ischemic stroke. Interestingly, the infarcts of ColXV KO mice were as small as those of wild-type (WT) mice thrombolysed with recombinant tissue plasminogen activator (rtPA), the actual treatment for ischemic stroke...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079883/cysteamine-re-establishes-the-clearance-of-pseudomonas-aeruginosa-by-macrophages-bearing-the-cystic-fibrosis-relevant-f508del-cftr-mutation
#15
Eleonora Ferrari, Romina Monzani, Valeria R Villella, Speranza Esposito, Francesca Saluzzo, Federica Rossin, Manuela D'Eletto, Antonella Tosco, Fabiola De Gregorio, Valentina Izzo, Maria C Maiuri, Guido Kroemer, Valeria Raia, Luigi Maiuri
Cystic fibrosis (CF), the most common lethal monogenic disease in Caucasians, is characterized by recurrent bacterial infections and colonization, mainly by Pseudomonas aeruginosa, resulting in unresolved airway inflammation. CF is caused by mutations in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein, which functions as a chloride channel in epithelial cells, macrophages, and other cell types. Impaired bacterial handling by macrophages is a feature of CF airways, although it is still debated how defective CFTR impairs bacterial killing...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079882/stability-of-the-cancer-target-ddias-is-regulated-by-the-chip-hsp70-pathway-in-lung-cancer-cells
#16
Kyoung-Jae Won, Joo-Young Im, Bo-Kyung Kim, Hyun Seung Ban, Young-Jin Jung, Kyeong Eun Jung, Misun Won
DNA damage-induced apoptosis suppressor (DDIAS) rescues lung cancer cells from apoptosis in response to DNA damage. DDIAS is transcriptionally activated by NFATc1 and EGF-mediated ERK5/MEF2B, leading to cisplatin resistance and cell invasion. Therefore, DDIAS is suggested as a therapeutic target for lung cancer. Here, we report that DDIAS stability is regulated by E3 U-box ubiquitin ligase carboxyl terminus of HSP70-interacting protein (CHIP)-mediated proteasomal degradation. We first isolated CHIP as an interacting partner of DDIAS by yeast two-hybrid screening...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28079881/translational-upregulation-of-aurora-a-by-hnrnp-q1-contributes-to-cell-proliferation-and-tumorigenesis-in-colorectal-cancer
#17
Chien-Hsien Lai, Yu-Chuan Huang, Jenq-Chang Lee, Joseph Ta-Chien Tseng, Kung-Chao Chang, Yen-Ju Chen, Nai-Jhu Ding, Pao-Hsuan Huang, Wen-Chang Chang, Bo-Wen Lin, Ruo-Yu Chen, Yu-Chu Wang, Yi-Chien Lai, Liang-Yi Hung
By using RNA-immunoprecipitation assay following next-generation sequencing, a group of cell cycle-related genes targeted by hnRNP Q1 were identified, including Aurora-A kinase. Overexpressed hnRNP Q1 can upregulate Aurora-A protein, but not alter the mRNA level, through enhancing the translational efficiency of Aurora-A mRNA, either in a cap-dependent or -independent manner, by interacting with the 5'-UTR of Aurora-A mRNA through its RNA-binding domains (RBDs) 2 and 3. By ribosomal profiling assay further confirmed the translational regulation of Aurora-A mRNA by hnRNP Q1...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28055019/rep1-inhibits-foxo3-mediated-apoptosis-to-promote-cancer-cell-survival
#18
Kwon-Ho Song, Seon Rang Woo, Joon-Yong Chung, Hyo-Jung Lee, Se Jin Oh, Soon-Oh Hong, Jaegal Shim, Yong Nyun Kim, Seung Bae Rho, Seung-Mo Hong, Hanbyoul Cho, Masahiko Hibi, Dong-Jun Bae, Sang-Yeob Kim, Min Gyu Kim, Tae Woo Kim, Young-Ki Bae
Rab escort protein 1 (REP1) is a component of Rab geranyl-geranyl transferase 2 complex. Mutations in REP1 cause a disease called choroideremia (CHM), which is an X-linked eye disease. Although it is postulated that REP1 has functions in cell survival or death of various tissues in addition to the eye, how REP1 functions in normal and cancer cells remains to be elucidated. Here, we demonstrated that REP1 is required for the survival of intestinal cells in addition to eyes or a variety of cells in zebrafish, and also has important roles in tumorigenesis...
January 5, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28055018/sumoylation-deficient-prdx6-gains-protective-function-by-amplifying-enzymatic-activity-and-stability-and-escapes-oxidative-stress-induced-aberrant-sumoylation
#19
Bhavana Chhunchha, Eri Kubo, Nigar Fatma, Dhirendra P Singh
Aberrant Sumoylation of protein(s) in response to oxidative stress or during aging is known to be involved in etiopathogenesis of many diseases. Upon oxidative stress, Peroxiredoxin (Prdx) 6 is aberrantly Sumoylated by Sumo1, resulting in loss of functions and cell death. We identified lysines (K) 122 and 142 as the major Sumo1 conjugation sites in Prdx6. Intriguingly, the mutant Prdx6 K122/142 R (arginine) gained protective efficacy, increasing in abundance and promoting glutathione (GSH) peroxidase and acidic calcium-independent phospholipase A2 (aiPLA2) activities...
January 5, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28055017/rny-yrna-derived-small-rnas-regulate-cell-death-and-inflammation-in-monocytes-macrophages
#20
Zoheir Hizir, Silvia Bottini, Valerie Grandjean, Michele Trabucchi, Emanuela Repetto
The recent discovery of new classes of small RNAs has opened unknown territories to explore new regulations of physiopathological events. We have recently demonstrated that RNY (or Y RNA)-derived small RNAs (referred to as s-RNYs) are an independent class of clinical biomarkers to detect coronary artery lesions and are associated with atherosclerosis burden. Here, we have studied the role of s-RNYs in human and mouse monocytes/macrophages and have shown that in lipid-laden monocytes/macrophages s-RNY expression is timely correlated to the activation of both NF-κB and caspase 3-dependent cell death pathways...
January 5, 2017: Cell Death & Disease
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