scholarly journals Nonsense suppressor therapies rescue peroxisome lipid metabolism and assembly in cells from patients with specific PEX gene mutations

2011 ◽  
Vol 112 (5) ◽  
pp. 1250-1258 ◽  
Author(s):  
Patricia K. Dranchak ◽  
Erminia Di Pietro ◽  
Ann Snowden ◽  
Nathan Oesch ◽  
Nancy E. Braverman ◽  
...  
Physiology ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 244-249
Author(s):  
DV Gallacher

A common effect of neurotransmitters and hormones that stimulate the metabolism of inositol lipids is the ability to increase the permeability of membranes to Ca2+. This effect occurs at surface membranes by the influx of Ca2+ from extracellular to intracellular fluid and at internal membranes by release of Ca2+ sequestered in intracellular organelles. Recent evidence suggests that it is the inositol polyphosphate products of lipid metabolism that regulate Ca2+ fluxes across both internal and cell surface membranes.


1998 ◽  
Vol 253 (2) ◽  
pp. 430-436 ◽  
Author(s):  
Florian Guthmann ◽  
Carsten Hohoff ◽  
Henry Fechner ◽  
Peter Humbert ◽  
Torsten Borchers ◽  
...  

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2073 ◽  
Author(s):  
Marcos Palacio Rojas ◽  
Carem Prieto ◽  
Valmore Bermúdez ◽  
Carlos Garicano ◽  
Trina Núñez Nava ◽  
...  

The direct link between lipid metabolism alterations and the increase of cardiovascular risk are well documented. Dyslipidemias, including isolated high LDL-c or mixed dyslipidemia, such as those seen in diabetes (hypertriglyceridemia, high LDL-c or low HDL-c), correlate with a significant risk of cardiovascular and cerebrovascular disease worldwide.  This review analyzes the current knowledge concerning the genetic basis of lipid metabolism alterations, emphasizing lipoprotein lipase gene mutations and the HindIII polymorphism, which are associated with decreased levels of triglycerides and LDL-c, as well as higher levels of HDL-c. These patterns would be associated with decreased global morbidity and mortality, providing protection against cardiovascular and cerebrovascular diseases.


2019 ◽  
Vol 20 (3) ◽  
pp. 644 ◽  
Author(s):  
Anika Dutta ◽  
Neelam Sharma-Walia

Lipids play a fundamental role in maintaining normal function in healthy cells. Their functions include signaling, storing energy, and acting as the central structural component of cell membranes. Alteration of lipid metabolism is a prominent feature of cancer, as cancer cells must modify their metabolism to fulfill the demands of their accelerated proliferation rate. This aberrant lipid metabolism can affect cellular processes such as cell growth, survival, and migration. Besides the gene mutations, environmental factors, and inheritance, several infectious pathogens are also linked with human cancers worldwide. Tumor viruses are top on the list of infectious pathogens to cause human cancers. These viruses insert their own DNA (or RNA) into that of the host cell and affect host cellular processes such as cell growth, survival, and migration. Several of these cancer-causing viruses are reported to be reprogramming host cell lipid metabolism. The reliance of cancer cells and viruses on lipid metabolism suggests enzymes that can be used as therapeutic targets to exploit the addiction of infected diseased cells on lipids and abrogate tumor growth. This review focuses on normal lipid metabolism, lipid metabolic pathways and their reprogramming in human cancers and viral infection linked cancers and the potential anticancer drugs that target specific lipid metabolic enzymes. Here, we discuss statins and fibrates as drugs to intervene in disordered lipid pathways in cancer cells. Further insight into the dysregulated pathways in lipid metabolism can help create more effective anticancer therapies.


Author(s):  
Robert E. Anderson ◽  
Robert B. Cumming ◽  
Marva Walton ◽  
Fred Snyder

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1415
Author(s):  
Vittoria Cenni ◽  
Stefano Squarzoni ◽  
Manuela Loi ◽  
Elisabetta Mattioli ◽  
Giovanna Lattanzi ◽  
...  

Reactive Oxygen Species (ROS) are reactive molecules required for the maintenance of physiological functions. Oxidative stress arises when ROS production exceeds the cellular ability to eliminate such molecules. In this study, we showed that oxidative stress induces post-translational modification of the inner nuclear membrane protein emerin. In particular, emerin is phosphorylated at the early stages of the oxidative stress response, while protein phosphorylation is abolished upon recovery from stress. A finely tuned balance between emerin phosphorylation and O-GlcNAcylation seems to govern this dynamic and modulates emerin–BAF interaction and BAF nucleoplasmic localization during the oxidative stress response. Interestingly, emerin post-translational modifications, similar to those observed during the stress response, are detected in cells bearing LMNA gene mutations and are characterized by a free radical generating environment. On the other hand, under oxidative stress conditions, a delay in DNA damage repair and cell cycle progression is found in cells from Emery–Dreifuss Muscular Dystrophy type 1, which do not express emerin. These results suggest a role of the emerin–BAF protein platform in the DNA damage response aimed at counteracting the detrimental effects of elevated levels of ROS.


RSC Advances ◽  
2020 ◽  
Vol 10 (36) ◽  
pp. 21248-21258
Author(s):  
Youdong Li ◽  
Jinwei Li ◽  
Peirang Cao ◽  
Yuanfa Liu

Sinapine reduces lipid accumulation in cells and the liver by regulating lipid metabolism.


1971 ◽  
Vol 10 (3) ◽  
pp. 251-265 ◽  
Author(s):  
K. McIntosh ◽  
S. Payne ◽  
W. C. Russell
Keyword(s):  

1982 ◽  
Vol 94 (4) ◽  
pp. 1410-1412
Author(s):  
V. V. Tertov ◽  
A. N. Orekhov ◽  
V. A. Kosykh ◽  
V. S. Repin

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