Search for the Molecular Mechanism of Mercury Toxicity. Study of the Mercury(II)−Surfactant Complex Formation in Langmuir Monolayers

2009 ◽  
Vol 113 (13) ◽  
pp. 4275-4283 ◽  
Author(s):  
Marcin Broniatowski ◽  
Patrycja Dynarowicz-Łatka
Keyword(s):  
Complex Formation ◽  
Molecular Mechanism ◽  
Langmuir Monolayers ◽  
Toxicity Study ◽  
Mercury Toxicity ◽  
Surfactant Complex

scholarly journals Sema3A Facilitates a Retrograde Death Signal via CRMP4-Dynein Complex Formation in ALS Motor Axons

2019 ◽  
Author(s):  
Roy Maimon ◽  
Lior Ankol ◽  
Romana Weissova ◽  
Elizabeth Tank ◽  
Tal Gradus Pery ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Complex Formation ◽  
Neuromuscular Junction ◽  
Neurodegenerative Disease ◽  
Effective Treatment ◽  
Molecular Mechanism ◽  
Motor Neurons ◽  
Axon Degeneration ◽  
Destabilizing Factors ◽  
Lateral Sclerosis

AbstractAmyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease with selective dysfunction; it causes the death of motor neurons (MNs). In spite of some progress, currently no effective treatment is available for ALS. Before such treatment can be developed, a more thorough understanding of ALS pathogenesis is required. Recently, we demonstrated that ALS-mutated muscles contribute to ALS pathology via secretion of destabilizing factors such as Sema3A; these factors trigger axon degeneration and Neuromuscular Junction (NMJ) disruption. Here, we focus on the molecular mechanism by which muscle contribute to MNs loss in ALS. We identified CRMP4 as part of a retrograde death signal generated in response to muscle-secreted Sema3A, in ALS-diseased MNs. Exposing distal axons to Sema3A induces CRMP4-dynein complex formation and MN loss in both mouse (SOD1G93A) and human-derived (C9orf72) ALS models. Introducing peptides that interfere with CRMP4-dynein interaction in MN axons profoundly reduces Sema3A-dependent MN loss. Thus, we discovered a novel retrograde death signal mechanism underlying MN loss in ALS.SummaryMaimon et al. identify a novel retrograde death mechanism that contribute to MN loss in ALS, in which CRMP4-Dynein complex is form and retrogradely move along the axon.

scholarly journals Characterization of the Molecular Mechanism Underlying Gibberellin Perception Complex Formation in Rice

2010 ◽  
Vol 22 (8) ◽  
pp. 2680-2696 ◽  
Author(s):  
Ko Hirano ◽  
Kenji Asano ◽  
Hiroyuki Tsuji ◽  
Mayuko Kawamura ◽  
Hitoshi Mori ◽  
...  
Keyword(s):  
Complex Formation ◽  
Molecular Mechanism

scholarly journals MiR-144 regulates adipogenesis by mediating formation of C/EBPα-FoxO1 protein complex

2021 ◽  
Author(s):  
Weimin Lin ◽  
Xianyu Wen ◽  
Xuexin Li ◽  
Lei Chen ◽  
Wei Wei ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Complex Formation ◽  
Molecular Mechanism ◽  
Protein Complex ◽  
Crucial Role ◽  
Type Ii Diabetes ◽  
Basic Unit ◽  
Type Ii ◽  
Treatment Of Obesity ◽  
Competitive Endogenous Rna

Excessive adipogenesis caused obesity, which was a serious risk of health and led to a series of diseases, including type II diabetes (T2D) for example. Adipocyte as the basic unit of adipose tissue has emerged as one of significant target of the treatment of obesity-related metabolic syndromes by revealed its adipogenic molecular mechanism. MicroRNAs (miRNAs) have been demonstrated involving adipogenesis, and played a crucial role in the competitive endogenous RNA (ceRNA) effect. Besides that, C/EBPα as a crucial adipogenic regulator still lacked epigenetic explanation during pre-adipocyte adipogenesis. In this study, we first verified FoxO1 was one of the ceRNA of C/EBPα. They co-regulated adipogenesis through formed a protein complex that directly bound to its promoter to activate AdipoQ, and AdipoQ (Adiponectin) was a negative adipocytokines that suppressed adipogenesis, which played an important role in retaining adipogensis balance. Moreover, an adipose tissue specific enriched miRNA, miR-144 was the key regulator of the ceRNA effect between C/EBPα and FoxO1, which mediated the C/EBPα-FoxO1 complex formation, thus altered AdipoQ, furthermore regulated pre-adipocyte adipogenesis. This research will provide a new supplementary idea of the C/EBPα epigenetic role in pre-adipocyte adipogenesis.

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