scholarly journals Role of Atg5-dependent cell death in the embryonic development of Bax/Bak double-knockout mice

2017 ◽  
Vol 24 (9) ◽  
pp. 1598-1608 ◽  
Author(s):  
Satoko Arakawa ◽  
Masatsune Tsujioka ◽  
Tatsushi Yoshida ◽  
Hajime Tajima-Sakurai ◽  
Yuya Nishida ◽  
...  
Keyword(s):  
Cell Death ◽  
Embryonic Development ◽  
Knockout Mice ◽  
Double Knockout ◽  
Dependent Cell

scholarly journals Mitochondrion-Dependent Cell Death in TDP-43 Proteinopathies

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 376
Author(s):  
Chantal B. Lucini ◽  
Ralf J. Braun
Keyword(s):  
Cell Death ◽  
Oxygen Species ◽  
In Vivo Models ◽  
Dependent Cell ◽  
Cell Death Mechanisms ◽  
Sting Pathway ◽  
Mitochondrial Membrane Permeabilization

In the last decade, pieces of evidence for TDP-43-mediated mitochondrial dysfunction in neurodegenerative diseases have accumulated. In patient samples, in vitro and in vivo models have shown mitochondrial accumulation of TDP-43, concomitantly with hallmarks of mitochondrial destabilization, such as increased production of reactive oxygen species (ROS), reduced level of oxidative phosphorylation (OXPHOS), and mitochondrial membrane permeabilization. Incidences of TDP-43-dependent cell death, which depends on mitochondrial DNA (mtDNA) content, is increased upon ageing. However, the molecular pathways behind mitochondrion-dependent cell death in TDP-43 proteinopathies remained unclear. In this review, we discuss the role of TDP-43 in mitochondria, as well as in mitochondrion-dependent cell death. This review includes the recent discovery of the TDP-43-dependent activation of the innate immunity cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway. Unravelling cell death mechanisms upon TDP-43 accumulation in mitochondria may open up new opportunities in TDP-43 proteinopathy research.

Role of LFA-1/ICAM-1-dependent cell adhesion in CD40-mediated inhibition of anti-IgM antibody-induced B-cell death

1995 ◽  
Vol 96 (6) ◽  
pp. 1136-1144 ◽  
Author(s):  
M MAYUMI ◽  
S SUMIMOTO ◽  
Y OHSHIMA ◽  
K KATAMURA ◽  
T HEIKE ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
B Cell ◽  
Igm Antibody ◽  
Dependent Cell

scholarly journals Ferroptosis in plants: triggers, proposed mechanisms, and the role of iron in modulating cell death

2020 ◽  
Author(s):  
Ayelén Mariana Distéfano ◽  
Gabriel Alejandro López ◽  
Nicolás Setzes ◽  
Fernanda Marchetti ◽  
Maximiliano Cainzos ◽  
...  
Keyword(s):  
Cell Death ◽  
Metabolic Pathways ◽  
Oxygen Species ◽  
Cell Death Pathway ◽  
Plant Life ◽  
Regulated Cell Death ◽  
Dependent Cell ◽  
Plant Life Cycle ◽  
High Degree

Abstract Regulated cell death plays key roles during essential processes throughout the plant life cycle. It takes part in specific developmental programs and maintains homeostasis of the organism in response to unfavorable environments. Ferroptosis is a recently discovered iron-dependent cell death pathway characterized by the accumulation of lipid reactive oxygen species. In plants, ferroptosis shares all the main hallmarks described in other systems. Those specific features include biochemical and morphological signatures that seem to be conserved among species. However, plant cells have specific metabolic pathways and a high degree of metabolic compartmentalization. Together with their particular morphology, these features add more complexity to the plant ferroptosis pathway. In this review, we summarize the most recent advances in elucidating the roles of ferroptosis in plants, focusing on specific triggers, the main players, and underlying pathways.

scholarly journals Polyamine homeostasis in arginase knockout mice

2007 ◽  
Vol 293 (4) ◽  
pp. C1296-C1301 ◽  
Author(s):  
Joshua L. Deignan ◽  
Justin C. Livesay ◽  
Lisa M. Shantz ◽  
Anthony E. Pegg ◽  
William E. O'Brien ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Polyamine Metabolism ◽  
Mrna Levels ◽  
Ornithine Aminotransferase ◽  
Double Knockout ◽  
Mammalian Tissues ◽  
Knockout Animals ◽  
Regulatory Functions ◽  
Arginase I

The role of ornithine decarboxylase (ODC) in polyamine metabolism has long been established, but the exact source of ornithine has always been unclear. The arginase enzymes are capable of producing ornithine for the production of polyamines and may hold important regulatory functions in the maintenance of this pathway. Utilizing our unique set of arginase single and double knockout mice, we analyzed polyamine levels in the livers, brains, kidneys, and small intestines of the mice at 2 wk of age, the latest timepoint at which all of them are still alive, to determine whether tissue polyamine levels were altered in response to a disruption of arginase I (AI) and II (AII) enzymatic activity. Whereas putrescine was minimally increased in the liver and kidneys from the AII knockout mice, spermidine and spermine were maintained. ODC activity was not greatly altered in the knockout animals and did not correlate with the fluctuations in putrescine. mRNA levels of ornithine aminotransferase (OAT), antizyme 1 (AZ1), and spermidine/spermine- N1-acetyltransferase (SSAT) were also measured and only minor alterations were seen, most notably an increase in OAT expression seen in the liver of AI knockout and double knockout mice. It appears that putrescine catabolism may be affected in the liver when AI is disrupted and ornithine levels are highly reduced. These results suggest that endogenous arginase-derived ornithine may not directly contribute to polyamine homeostasis in mice. Alternate sources such as diet may provide sufficient polyamines for maintenance in mammalian tissues.

scholarly journals Dendritic spine morphology and memory formation depend on postsynaptic Caskin proteins

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Norbert Bencsik ◽  
Szilvia Pusztai ◽  
Sándor Borbély ◽  
Anna Fekete ◽  
Metta Dülk ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Knockout Mice ◽  
Hippocampal Neurons ◽  
Pain Perception ◽  
Hippocampal Slices ◽  
Scaffold Proteins ◽  
Double Knockout ◽  
Learning Abilities ◽  
Spine Morphology

AbstractCASK-interactive proteins, Caskin1 and Caskin2, are multidomain neuronal scaffold proteins. Recent data from Caskin1 knockout animals indicated only a mild role of Caskin1 in anxiety and pain perception. In this work, we show that deletion of both Caskins leads to severe deficits in novelty recognition and spatial memory. Ultrastructural analyses revealed a reduction in synaptic profiles and dendritic spine areas of CA1 hippocampal pyramidal neurons of double knockout mice. Loss of Caskin proteins impaired LTP induction in hippocampal slices, while miniature EPSCs in dissociated hippocampal cultures appeared to be unaffected. In cultured Caskin knockout hippocampal neurons, overexpressed Caskin1 was enriched in dendritic spine heads and increased the amount of mushroom-shaped dendritic spines. Chemically induced LTP (cLTP) mediated enlargement of spine heads was augmented in the knockout mice and was not influenced by Caskin1. Immunocytochemistry and immunoprecipitation confirmed that Shank2, a master scaffold of the postsynaptic density, and Caskin1 co-localized within the same complex. Phosphorylation of AMPA receptors was specifically altered by Caskin deficiency and was not elevated by cLTP treatment further. Taken together, our results prove a previously unnoticed postsynaptic role of Caskin scaffold proteins and indicate that Caskins influence learning abilities via regulating spine morphology and AMPA receptor localisation.

scholarly journals Protective Role of Interleukin-1 in Mycobacterial Infection in IL-1 α/β Double-Knockout Mice

2000 ◽  
Vol 80 (5) ◽  
pp. 759-767 ◽  
Author(s):  
Hiroyuki Yamada ◽  
Satoru Mizumo ◽  
Reiko Horai ◽  
Yoichiro Iwakura ◽  
Isamu Sugawara
Keyword(s):  
Knockout Mice ◽  
Interleukin 1 ◽  
Mycobacterial Infection ◽  
Protective Role ◽  
Double Knockout
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