scholarly journals Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xiaojiao Wang ◽  
Dan Luo ◽  
Sisi Wu

Atherosclerosis is a chronic lipid-driven inflammatory disease that results in the formation of lipid-rich and immune cell-rich plaques in the arterial wall, which has high morbidity and mortality in the world. The mechanism of atherosclerosis is still unclear now. Potential hypotheses involved in atherosclerosis are chronic inflammation theory, lipid percolation theory, mononuclear-macrophage theory, endothelial cell (EC) injury theory, and smooth muscle cell (SMC) mutation theory. Changes of phospholipids, glucose, critical proteins, etc. on mitochondria-associated endoplasmic reticulum membrane (MAM) can cause the progress of atherosclerosis. This review describes the structural and functional interaction between mitochondria and endoplasmic reticulum (ER) and explains the role of critical molecules in the structure of MAM during atherosclerosis.

1993 ◽  
Vol 4 (9) ◽  
pp. 931-939 ◽  
Author(s):  
D Feldheim ◽  
K Yoshimura ◽  
A Admon ◽  
R Schekman

SEC66 encodes the 31.5-kDa glycoprotein of the Sec63p complex, an integral endoplasmic reticulum membrane protein complex required for translocation of presecretory proteins in Saccharomyces cerevisiae. DNA sequence analysis of SEC66 predicts a 23-kDa protein with no obvious NH2-terminal signal sequence but with one domain of sufficient length and hydrophobicity to span a lipid bilayer. Antibodies directed against a recombinant form of Sec66p were used to confirm the membrane location of Sec66p and that Sec66p is a glycoprotein of 31.5 kDa. A null mutation in SEC66 renders yeast cells temperature sensitive for growth. sec66 cells accumulate some secretory precursors at a permissive temperature and a variety of precursors at the restrictive temperature. sec66 cells show defects in Sec63p complex formation. Because sec66 cells affect the translocation of some, but not all secretory precursor polypeptides, the role of Sec66p may be to interact with the signal peptide of presecretory proteins.


2021 ◽  
Vol 03 (06) ◽  
pp. 199-211
Author(s):  
Ahmed Hamid FALIH ◽  
Rajaa Saadi LAFTA

The pursuit of technology has actively contributed to building advanced societies that have facilitated many human needs, shortened distances, and connected the world with important steady steps in all sciences, especially arts and engineering, including the interior design arts that have developed in the last decade to a point that is almost the top of technical treatments and their effective role at the level of The artificial intelligence that granted the specialist (the interior designer) a new status that is reflected in the transcendence and sophistication, and in it the characteristics of functional interaction and its aesthetic relations appear, so the current study is a cognitive key in identifying the mother of the features of modern technology and the role of artificial intelligence in the production of new designs that fit the needs of the institutional and social individual.


2000 ◽  
Vol 20 (18) ◽  
pp. 6923-6934 ◽  
Author(s):  
Mehdi Kabani ◽  
Jean-Marie Beckerich ◽  
Claude Gaillardin

ABSTRACT We previously characterized the SLS1 gene in the yeastYarrowia lipolytica and showed that it interacts physically with YlKar2p to promote translocation across the endoplasmic-reticulum membrane (A. Boisramé, M. Kabani, J. M. Beckerich, E. Hartmann, and C. Gaillardin, J. Biol. Chem. 273:30903–30908, 1998). A Y. lipolytica Kar2p mutant was isolated that restored interaction with an Sls1p mutant, suggesting that the interaction with Sls1p could be nucleotide and/or conformation dependent. This result was used as a working hypothesis for more accurate investigations in Saccharomyces cerevisiae. We show by two-hybrid an in vitro assays that the S. cerevisiae homologue of Sls1p interacts with ScKar2p. Using dominant lethal mutants of ScKar2p, we were able to show that ScSls1p preferentially interacts with the ADP-bound conformation of the molecular chaperone. Synthetic lethality was observed between ΔScsls1 and translocation-deficientkar2 or sec63-1 mutants, providing in vivo evidence for a role of ScSls1p in protein translocation. Synthetic lethality was also observed with ER-associated degradation and folding-deficient kar2 mutants, strongly suggesting that Sls1p functions are not restricted to the translocation process. We show that Sls1p stimulates in a dose-dependent manner the binding ofScKar2p on the lumenal J domain of Sec63p fused to glutathione S-transferase. Moreover, Sls1p is shown to promote the Sec63p-mediated activation of Kar2p's ATPase activity. Our data strongly suggest that Sls1p could be the first GrpE-like protein described in the endoplasmic reticulum.


Author(s):  
Abdullahi Alausa ◽  
Rofiat Adeyemi ◽  
Barakat Olaleke ◽  
Aminat Ismail ◽  
Faith Sunday Oyelere

COVID-19 infection, a ravaging disease attributed to a SARS-CoV-like illness, has brought the world to its knee, causing a pandemic, with human-human transmission as a major source of the spread of this ailment. Alarmingly, this infection based on clinical manifestations is diagnosed as virus-induced pneumonia, with over 5 million cases with a mortality rate of about 7% (based on the recently published global report). However, most deaths have been associated with patients with underlying immune dysfunction or a compromised immunesystem. As no specific therapeutics and vaccines have been reported, the strengthening of the immune system through nutritional intake and exercise is essential. Also, previous studies have documented the immune-activating capabilities of Vitamin A and D, along with supplementary induction, yielding positive results in combating previous viral challenges. Typically, the gradual upsurge of T-lymphocytes and immune cell activities has been implemented by moderate exercise activities. This review examines the role of nutrition and exercise in immune system enhancement and proposes the possible mechanism of nutrition and exercise in combating COVID-19 infection.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Hiroshi Arakawa ◽  
Karin Araya ◽  
Yusuke Masuo ◽  
Tomohiko Wakayama ◽  
Yukio Kato

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Mei Xue ◽  
Ting Fang ◽  
Hongxi Sun ◽  
Ying Cheng ◽  
Ting Li ◽  
...  

AbstractThe altered homeostasis of mitochondria-associated endoplasmic reticulum (ER) membranes (MAM) was closely associated with the pathological process of nervous system diseases and insulin resistance. Here, the exact implication of phosphofurin acidic cluster sorting protein 2 (PCAS-2), an anchor protein in the MAM interface, in diabetic kidney disease was investigated. In the kidneys of type 1 and type 2 diabetes mice and HG-induced HK-2 cells, a notable disruption of ER-mitochondria interactions, accompanied by a decreased PACS-2 expression in all subcellular fractions. Furthermore, PACS-2 knockout mice with diabetes displayed accelerated development of proteinuria, deterioration of kidney function, and aggravated disruption of MAM area, ER stress, mitochondrial dysfunction, renal apoptosis, and fibrosis. However, overexpression of PACS-2 effectively protected diabetic kidneys and HG-treated HK-2 cells from renal tubular impairments. Importantly, experimental uncoupling of ER-mitochondria contacts reversed the protective effects of PACS-2 restoration on HK-2 cells under HG conditions. In summary, our data indicate a pivotal role of PACS-2 in the development of diabetic renal tubular injury via the stabilization of MAM.


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