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Cell Death Discovery

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https://www.readbyqxmd.com/read/27275396/loss-of-function-of-ywhah-in-mice-induces-deafness-and-cochlear-outer-hair-cells-degeneration
#1
L Buret, G Rebillard, E Brun, C Angebault, M Pequignot, M Lenoir, M Do-Cruzeiro, E Tournier, K Cornille, A Saleur, N Gueguen, P Reynier, P Amati-Bonneau, A Barakat, C Blanchet, P Chinnery, P Yu-Wai-Man, J Kaplan, A-F Roux, G Van Camp, B Wissinger, O Boespflug-Tanguy, F Giraudet, J-L Puel, G Lenaers, C Hamel, B Delprat, C Delettre
In vertebrates, 14-3-3 proteins form a family of seven highly conserved isoforms with chaperone activity, which bind phosphorylated substrates mostly involved in regulatory and checkpoint pathways. 14-3-3 proteins are the most abundant protein in the brain and are abundantly found in the cerebrospinal fluid in neurodegenerative diseases, suggesting a critical role in neuron physiology and death. Here we show that 14-3-3eta-deficient mice displayed auditory impairment accompanied by cochlear hair cells' degeneration...
March 7, 2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27019748/caspase-2-resides-in-the-mitochondria-and-mediates-apoptosis-directly-from-the-mitochondrial-compartment
#2
M Lopez-Cruzan, R Sharma, M Tiwari, S Karbach, D Holstein, C R Martin, J D Lechleiter, B Herman
Caspase-2 plays an important role in apoptosis induced by several stimuli, including oxidative stress. However, the subcellular localization of caspase-2, particularly its presence in the mitochondria, is unclear. It is also not known if cytosolic caspase-2 translocates to the mitochondria to trigger the intrinsic pathway of apoptosis or if caspase-2 is constitutively present in the mitochondria that then selectively mediates this apoptotic effect. Here, we demonstrate the presence of caspase-2 in purified mitochondrial fractions from in vitro-cultured cells and in liver hepatocytes using immunoblots and confocal microscopy...
February 15, 2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924227/otx2-impedes-self-renewal-of-porcine-ips-cells-through-downregulation-of-nanog-expression
#3
Ning Wang, Yaxian Wang, Youlong Xie, Huayan Wang
The transcription factor Otx2 acts as a negative switch in the regulation of transition from naive to primed pluripotency in mouse pluripotent stem cells. However, the molecular features and function of porcine OTX2 have not been well elucidated in porcine-induced pluripotent stem cells (piPSCs). By studying high-throughput transcriptome sequencing and interfering endogenous OTX2 expression, we demonstrate that OTX2 is able to downgrade the self-renewal of piPSCs. OTX2 is highly expressed in porcine brain, reproductive tissues, and preimplantation embryos, but is undetectable in fibroblasts and most somatic tissues...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924226/questions-and-controversies-the-role-of-necroptosis-in-liver-disease
#4
REVIEW
Lily Dara, Zhang-Xu Liu, Neil Kaplowitz
Acute and chronic liver injury results in hepatocyte death and turnover. If injury becomes chronic, the continuous cell death and turnover leads to chronic inflammation, fibrosis and ultimately cirrhosis and hepatocellular carcinoma. Controlling liver cell death both in acute injury, to rescue the liver from acute liver failure, and in chronic injury, to curb secondary inflammation and fibrosis, is of paramount importance as a therapeutic strategy. Both apoptosis and necrosis occur in the liver, but the occurrence of necroptosis in the liver and its contribution to liver disease is controversial...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924225/conference-survival-guide-the-dos-and-don-ts
#5
EDITORIAL
Tatiana P Soares da Costa
No abstract text is available yet for this article.
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924224/micu1-may-be-a-promising-intervention-target-for-gut-derived-sepsis-induced-by-intra-abdominal-hypertension
#6
Yuxin Leng, Qinggang Ge, Zhiling Zhao, Kun Wang, Gaiqi Yao
Intra-abdominal hypertension (IAH) is a common and serious complication in critically ill patients, for which there is no targeted therapy. IAH-induced dysfunction of intestinal barriers is closely associated with oxidative imbalances, which are considered to provide a pathophysiological basis for subsequent gut-derived sepsis. However, the upstream mechanism that produces oxidative damage during IAH remains unknown. It is not clear whether 'mitochondrial Ca(2+) uptake 1' (MICU1, the key protein regulating the oxidative process) is involved in preventing Ca(2+)m (mitochondrial Ca(2+)) overload...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924223/mitochondrial-permeability-transition-pore-induction-is-linked-to-formation-of-the-complex-of-atpase-c-subunit-polyhydroxybutyrate-and-inorganic-polyphosphate
#7
P A Elustondo, M Nichols, A Negoda, A Thirumaran, E Zakharian, G S Robertson, E V Pavlov
Mitochondrial permeability transition pore (mPTP) opening allows free movement of ions and small molecules leading to mitochondrial membrane depolarization and ATP depletion that triggers cell death. A multi-protein complex of the mitochondrial ATP synthase has an essential role in mPTP. However, the molecular identity of the central 'pore' part of mPTP complex is not known. A highly purified fraction of mammalian mitochondria containing C-subunit of ATPase (C-subunit), calcium, inorganic polyphosphate (polyP) and polyhydroxybutyrate (PHB) forms ion channels with properties that resemble the native mPTP...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27924222/otopathogenic-pseudomonas-aeruginosa-induces-myd88-dependent-auditory-hair-cell-damage
#8
Rahul Mittal, M'hamed Grati, Denise Yan, Xue Z Liu
No abstract text is available yet for this article.
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27867537/aquaporin-3-facilitates-chemoresistance-in-gastric-cancer-cells-to-cisplatin-via-autophagy
#9
Xuqiang Dong, Yao Wang, Yangchun Zhou, Jianfei Wen, Shoulin Wang, Lizong Shen
Cisplatin (cDDP) remains one of the first-line chemotherapeutic agents for gastric cancer (GC) treatment, and resistance to cDDP is the major limitation in its clinical application. Mechanisms of cDDP resistance have been shown to be varied and complicated. Aquaporin 3 (AQP3) has been demonstrated to be overexpressed in GC tissues and is thought to be involved in GC carcinogenesis and progression. However, the role of AQP3 in chemosensitivity of GC to cytotoxic agents remains unknown. In this study, we show that AQP3 overexpression induced resistance to cDDP in AGS cells (P<0...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27833761/e1a-enhances-cellular-sensitivity-to-dna-damage-induced-apoptosis-through-pidd-dependent-caspase-2-activation
#10
Jay R Radke, Zeba K Siddiqui, Iris Figueroa, James L Cook
Expression of the adenoviral protein, E1A, sensitizes mammalian cells to a wide variety of apoptosis-inducing agents through multiple cellular pathways. For example, E1A sensitizes cells to apoptosis induced by TNF-superfamily members by inhibiting NF-kappa B (NF-κB)-dependent gene expression. In contrast, E1A sensitization to nitric oxide, an inducer of the intrinsic apoptotic pathway, is not dependent upon repression of NF-κB-dependent transcription but rather is dependent upon caspase-2 activation. The latter observation suggested that E1A-induced enhancement of caspase-2 activation might be a critical factor in cellular sensitization to other intrinsic apoptosis pathway-inducing agents...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27818790/bub1-and-survivin-proteins-are-not-degraded-after-a-prolonged-mitosis-and-accumulate-in-the-nuclei-of-hct116-cells
#11
Marco A Andonegui-Elguera, Rodrigo E Cáceres-Gutiérrez, Fernando Luna-Maldonado, Alejandro López-Saavedra, José Díaz-Chávez, Fernanda Cisneros-Soberanis, Diddier Prada, Julia Mendoza-Pérez, Luis A Herrera
Spindle poisons activate the spindle assembly checkpoint and prevent mitotic exit until cells die or override the arrest. Several studies have focused on spindle poison-mediated cell death, but less is known about consequences in cells that survive a mitotic arrest. During mitosis, proteins such as CYCLIN B, SECURIN, BUB1 and SURVIVIN are degraded in order to allow mitotic exit, and these proteins are maintained at low levels in the next interphase. In contrast, exit from a prolonged mitosis depends only on degradation of CYCLIN B; it is not known whether the levels of other proteins decrease or remain high...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27785370/arsenic-induced-instrumental-genes-of-apoptotic-signal-amplification-in-death-survival-interplay
#12
Sonali Roy, Bardwi Narzary, Atish Ray, Manobjyoti Bordoloi
Arsenic is a global health concern at present and it is well reported for causing systemic toxicity. It is also well known for generation of free radical and inducing apoptosis in different cell types. Paradoxically arsenic is reported to be a susceptible carcinogen as well. There are several reports demonstrating diverse mechanism of apoptosis in different cell types. However, the universal scenario of instrumental genes and their interaction leading to amplification of apoptotic signal are yet to be completely uncovered, which is predicted here...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27785369/targeting-the-non-neuronal-cholinergic-system-in-macrophages-for-the-management-of-infectious-diseases-and-cancer-challenge-and-promise
#13
REVIEW
Sandra Reichrath, Jörg Reichrath, Amira-Talaat Moussa, Carola Meier, Thomas Tschernig
Macrophages represent key players of the immune system exerting highly effective defense mechanisms against microbial infections and cancer that include phagocytosis and programmed cell removal. Recent findings highlight the relevance of the non-neuronal cholinergic system for the regulation of macrophage function that opens promising new concepts for the treatment of infectious diseases and cancer. This mini review summarizes our present knowledge on this topic and gives an outlook on future developments.
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27777789/foxo1-interacts-with-transcription-factor-eb-and-differentially-regulates-mitochondrial-uncoupling-proteins-via-autophagy-in-adipocytes
#14
Longhua Liu, Zhipeng Tao, Louise D Zheng, Joseph P Brooke, Cayleen M Smith, Dongmin Liu, Yun Chau Long, Zhiyong Cheng
Mitochondrial uncoupling proteins (UCPs) are inducible and play an important role in metabolic and redox homeostasis. Recent studies have suggested that FoxO1 controls mitochondrial biogenesis and morphology, but it remains largely unknown how FoxO1 may regulate mitochondrial UCPs. Here we show that FoxO1 interacted with transcription factor EB (Tfeb), a key regulator of autophagosome and lysosome, and mediated the expression of UCP1, UCP2 and UCP3 differentially via autophagy in adipocytes. UCP1 was down-regulated but UCP2 and UCP3 were upregulated during adipocyte differentiation, which was associated with increased Tfeb and autophagy activity...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27777788/a-novel-ligand-of-calcitonin-receptor-reveals-a-potential-new-sensor-that-modulates-programmed-cell-death
#15
Sgb Furness, D L Hare, A Kourakis, A M Turnley, P J Wookey
We have discovered that the accumulation of an anti-calcitonin receptor (anti-CTR) antibody conjugated to a fluorophore (mAb2C4:AF568) provides a robust signal for cells undergoing apoptotic programmed cell death (PCD). PCD is an absolute requirement for normal development of metazoan organisms. PCD is a hallmark of common diseases such as cardiovascular disease and tissue rejection in graft versus host pathologies, and chemotherapeutics work by increasing PCD. This robust signal or high fluorescent events were verified by confocal microscopy and flow cytometry in several cell lines and a primary culture in which PCD had been induced...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27752365/protein-arginylation-regulates-cellular-stress-response-by-stabilizing-hsp70-and-hsp40-transcripts
#16
Kamalakshi Deka, Archana Singh, Surajit Chakraborty, Rupak Mukhopadhyay, Sougata Saha
ATE1-mediated post-translational addition of arginine to a protein has been shown to regulate activity, interaction, and stability of the protein substrates. Arginylation has been linked to many different stress conditions, namely ER stress, cytosolic misfolded protein stress, and nitrosative stress. However, clear understanding about the effect of arginylation in cellular stress responses is yet to emerge. In this study, we investigated the role of arginylation in heat-stress response. Our findings suggest that Ate1 knock out (KO) cells are more susceptible to heat stress compared with its wild-type counterparts due to the induction of apoptosis in KO cells...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27752364/p53-regulates-disruption-of-neuronal-development-in-the-adult-hippocampus-after-irradiation
#17
Y-Q Li, Zw-C Cheng, Sk-W Liu, I Aubert, C S Wong
Inhibition of hippocampal neurogenesis is implicated in neurocognitive dysfunction after cranial irradiation for brain tumors. How irradiation results in impaired neuronal development remains poorly understood. The Trp53 (p53) gene is known to regulate cellular DNA damage response after irradiation. Whether it has a role in disruption of late neuronal development remains unknown. Here we characterized the effects of p53 on neuronal development in adult mouse hippocampus after irradiation. Different bromodeoxyuridine incorporation paradigms and a transplantation study were used for cell fate mapping...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27752363/how-well-can-morphology-assess-cell-death-modality-a-proteomics-study
#18
Alexey L Chernobrovkin, Roman A Zubarev
While the focus of attempts to classify cell death programs has finally shifted in 2010s from microscopy-based morphological characteristics to biochemical assays, more recent discoveries have put the underlying assumptions of many such assays under severe stress, mostly because of the limited specificity of the assays. On the other hand, proteomics can quantitatively measure the abundances of thousands of proteins in a single experiment. Thus proteomics could develop a modern alternative to both semiquantitative morphology assessment as well as single-molecule biochemical assays...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27752362/simultaneous-induction-of-apoptosis-and-necroptosis-by-tanshinone-iia-in-human-hepatocellular-carcinoma-hepg2-cells
#19
C-Y Lin, T-W Chang, W-H Hsieh, M-C Hung, I-H Lin, S-C Lai, Y-J Tzeng
Tanshinone IIA (Tan IIA), a constituent of the traditional medicinal plant Salvia miltiorrhiza BUNGE, has been reported to possess anticancer activity through induction of apoptosis in many cancer cells. Surprisingly, the present study finds that Tan IIA simultaneously causes apoptosis and necroptosis in human hepatocellular carcinoma HepG2 cells. We further find that apoptosis can be converted to necroptosis by pan-caspase inhibitor Z-VAD-fmk, and the two death modes can be blocked by necroptotic inhibitor necrostatin-1...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27752361/immune-modulating-effects-of-bevacizumab-in-metastatic-non-small-cell-lung-cancer-patients
#20
E C Martino, G Misso, P Pastina, S Costantini, F Vanni, C Gandolfo, C Botta, F Capone, A Lombardi, L Pirtoli, P Tassone, C Ulivieri, P Tagliaferri, M G Cusi, M Caraglia, P Correale
The mPEBev is an anticancer regimen which combines a chemotherapy doublet, based on cisplatin and oral etoposide (mPE), with bevacizumab (mPEBev), a mAb targeting the vasculo-endothelial growth factor (VEGF). In previous studies, this regimen showed powerful anti-angiogenetic effects and significant antitumor activity in metastatic non-small-cell lung cancer (mNSCLC) patients. We also recorded the best benefit in patients exhibiting low-systemic inflammatory profile at baseline. On these bases, we hypothesized that mPEBev antitumor activity could be partially related to bevacizumab-associated immunological effects...
2016: Cell Death Discovery
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