Na+,K+-ATPase Was Found to Be the Membrane Component Responsible for the Hydrophobic Behavior of the Brain Membrane Tubulin

1998 ◽  
Vol 253 (3) ◽  
pp. 824-827 ◽  
Author(s):  
Alejandra del C. Alonso ◽  
Mariana Nuñez-Fernandez ◽  
Dante M. Beltramo ◽  
César H. Casale ◽  
Héctor S. Barra
Keyword(s):  
Membrane Component ◽  
Brain Membrane ◽  
Hydrophobic Behavior ◽  
The Brain ◽  
Membrane Tubulin

Na+,K+-ATPase Was Found to Be the Membrane Component Responsible for the Hydrophobic Behavior of the Brain Membrane Tubulin

1999 ◽  
Vol 257 (2) ◽  
pp. 642 ◽  
Author(s):  
Alejandra del C. Alonso ◽  
Mariana Nuñez-Fernandez ◽  
Dante M. Beltramo ◽  
César H. Casale ◽  
Héctor S. Barra
Keyword(s):  
Membrane Component ◽  
Brain Membrane ◽  
Hydrophobic Behavior ◽  
The Brain ◽  
Membrane Tubulin

scholarly journals Influenza A Virus Mediated Downregulation of Progesterone Receptor Membrane Component-1 Inhibits RIG-I-dependent Antiviral Response in Central Nervous System

2020 ◽  
Author(s):  
Kun Huang ◽  
Yufei Zhang ◽  
Wenxiao Gong ◽  
Yong Yang ◽  
Lili Jiang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Progesterone Receptor ◽  
Influenza A Virus ◽  
Influenza A ◽  
Rna Seq ◽  
Membrane Component ◽  
Receptor Membrane ◽  
The Central Nervous System ◽  
The Brain

Abstract Background: The influenza A virus (IAV) enters the central nervous system (CNS) via multiple routes and causes neurological symptoms. In this process, it develops multiple strategies to escape the host anti-viral immune system, and infects the central nervous system (CNS). Progesterone receptor membrane component-1 (PGRMC1) is highly expressed in the CNS, where it exerts a neurotrophic effect. However, how PGRMC1 affects IAV remains unclear.Methods: In this study, we aimed to investigate the role of PGRMC1 in regulating antiviral defense response in brain tissue. Toward this, we used both mouse model of IAV infection and the human neuroblastoma cell line SK-N-SH and human brain glioma cell line U251 . High-throughput RNA sequencing (RNA-seq) was used to obtain an unbiased profile of the cellular response to IAV H5N6 infection in mice brain. Results: Here, RNA-seq revealed 240 differentially expressed genes in the IAV-infected brains. Among the significantly down-regulated genes, we focused on the gene encoding progesterone receptor membrane component-1 (PGRMC1) and observed that IAV H5N6 infection clearly inhibited PGRMC1 in both neuroblastoma and glioma cells. Furthermore, treatment with AG205, a PGRMC1-specific inhibitor, or PGRMC1 knockout promoted H5N6 multiplication in vitro, while overexpression of PGRMC1 resulted in opposite effects. Furthermore, AG205 treatment or PGRMC1 knockout significantly inhibited RIG-I-mediated IFN-β signaling pathway and reduced the levels of several antiviral proteins (Mx1 and ISG15). In addition, PGRMC1-mediated regulation of IFN signaling relied on inhibition of the expression and ubiquitination of RIG-I.Conclusion: Conclusively, our results show for the first time that IAV H5N6 down-regulates PGRMC1 expression to contribute to virus proliferation by inhibiting RIG-I-mediated IFN-β production in the brain. These findings may offer new insights regarding the interplay between IAV and host factors that may impact IAV pathogenicity in the brain.

scholarly journals Lipoamidase is a multiple hydrolase

1990 ◽  
Vol 271 (1) ◽  
pp. 45-49 ◽  
Author(s):  
J Oizumi ◽  
K Hayakawa
Keyword(s):  
Molecular Structure ◽  
Methyl Ester ◽  
Substrate Specificity ◽  
Molecular Mass ◽  
Brain Membrane ◽  
Structural Requirements ◽  
Electric Eel ◽  
Single Polypeptide ◽  
The Brain

The substrate specificity of lipoamidase, purified from the pig brain membrane with lipoyl 4-aminobenzoate (LPAB) as a substrate, was extensively studied. This single polypeptide was found to hydrolyse the bonding between amide, ester and peptide compounds. However, stringent structural requirements were found in the substrates, e.g. LPAB was hydrolysed, whereas biotinyl 4-aminobenzoate was not, as stated in our previous paper [Oizmui & Hayakawa (1990) Biochem. J. 266, 427-434]. The enzyme specifically recognized the whole molecular structure of the substrate, whereas it loosely recognized the bond structure of the substrate; e.g. the dipeptide Asp-Phe was not hydrolysed, whereas the methyl ester of Asp-Phe (aspartame) was. The exopeptidase activity was demonstrated by lipoamidase; however, longer peptides than the hexamer seemed not to be substrates. Lipoyl esters, which were electrically neutral, exhibited higher specificity with longer acyl groups. Molecular mass and molecular hydrophobicity (hydropathy) seemed to determine the substrate specificity. Lipoyl-lysine, acetylcholine and oligopeptides were hydrolysed at similar Km values; however, acetylcholine was hydrolysed at a velocity 100 times higher. Although many similar specificities were found between electric eel acetylcholinesterase and lipoamidase, distinctly different specificity was demonstrated with lipoyl compounds. The role of lipoamidase, which resides on the brain membrane and possesses higher specificity for hydrophobic molecules, remains to be elucidated.

scholarly journals Mast Cells, Astrocytes, Arachidonic Acid: Do They Play a Role in Depression?

2020 ◽  
Vol 10 (10) ◽  
pp. 3455 ◽  
Author(s):  
Giovanna Traina ◽  
Massimo Cocchi
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Mast Cells ◽  
Gut Microbiota ◽  
Depression And Anxiety ◽  
Brain Membrane ◽  
Fatty Acids Profile ◽  
The One ◽  
The Brain ◽  
Depressive Condition

Evidence support that brain membrane fatty acids play a crucial role in psychopathologies such as depression and anxiety disorders. Although the pathogenesis of depression is not still defined, drugs commonly used to reduce arachidonic turnover in the brain can control mood disorders, such as depression. Both astrocytes and mast cells release arachidonic acid during silent inflammation. Here, we hypothesize that arachidonic acid freed from lipid droplets of mast cells, as well as the one released from activated astrocytes, could contribute to characterize a depressive condition, and the fatty acids profile of mast cells, astrocytes and microglia could also vary, reflecting the pathophysiological depressive state of the subject. Finally, there is evidence that gut microbiota is deeply implicated in mood and behavioral disorders. Human gut microbiota can control nervous system diseases through neuroimmune pathways.

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