Structure and function of DHHC protein S-acyltransferases

2017 ◽  
Vol 45 (4) ◽  
pp. 923-928 ◽  
Author(s):  
Colin D. Gottlieb ◽  
Maurine E. Linder
Keyword(s):  
Mouse Models ◽  
Protein Function ◽  
Molecular Mechanisms ◽  
Protein S ◽  
Structure And Function ◽  
Deficient Mouse ◽  
Enzymatic Function ◽  
Cytoplasmic Face ◽  
Dhhc Protein ◽  
And Function

It has been estimated that 10% of the human genome encodes proteins that are fatty acylated at cysteine residues. The vast majority of these proteins are modified by members of the DHHC protein family, which carry out their enzymatic function on the cytoplasmic face of cell membranes. The biomedical importance of DHHC proteins is underscored by their association with human disease; unique and essential roles for DHHC proteins have been uncovered using DHHC-deficient mouse models. Accordingly, there is great interest in elucidating the molecular mechanisms that underlie DHHC protein function. In this review, we present recent insights into the structure and function of DHHC enzymes.

scholarly journals Desmin is essential for the structure and function of the sinoatrial node: implications for increased arrhythmogenesis

2020 ◽  
Vol 319 (3) ◽  
pp. H557-H570
Author(s):  
Manolis Mavroidis ◽  
Nikolaos C. Athanasiadis ◽  
Pavlos Rigas ◽  
Ioanna Kostavasili ◽  
Ismini Kloukina ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Mouse Models ◽  
Cyclic Nucleotide ◽  
Sinoatrial Node ◽  
Structure And Function ◽  
Deficient Mouse ◽  
Autonomic Nervous System Dysfunction ◽  
Cardiac Autonomic Nervous System ◽  
And Function

The sinoatrial node exhibits high amounts of desmin and desmoplakin in structures we call “lateral intercalated disks,” connecting side-by-side adjacent cardiomyocytes. These structures are diminished in desmin-deficient mouse models. Misregulation of T-type Ca2+ current and hyperpolarization-activated cyclic nucleotide-gated K+ channel 1 was proved along with prolonged interatrial conduction and cardiac autonomic nervous system dysfunction.

scholarly journals Severity of Demyelinating and Axonal Neuropathy Mouse Models Is Modified by Genes Affecting Structure and Function of Peripheral Nodes

Cell Reports ◽  
2017 ◽  
Vol 18 (13) ◽  
pp. 3178-3191 ◽  
Author(s):  
Kathryn H. Morelli ◽  
Kevin L. Seburn ◽  
David G. Schroeder ◽  
Emily L. Spaulding ◽  
Loiuse A. Dionne ◽  
...  
Keyword(s):  
Mouse Models ◽  
Axonal Neuropathy ◽  
Structure And Function ◽  
And Function

scholarly journals Exotoxins of Staphylococcus aureus

2000 ◽  
Vol 13 (1) ◽  
pp. 16-34 ◽  
Author(s):  
Martin M. Dinges ◽  
Paul M. Orwin ◽  
Patrick M. Schlievert
Keyword(s):  
Staphylococcus Aureus ◽  
Toxic Shock Syndrome ◽  
Molecular Basis ◽  
Molecular Mechanisms ◽  
Food Poisoning ◽  
Structure And Function ◽  
Toxic Shock ◽  
The Family ◽  
Toxic Shock Syndrome Toxin ◽  
And Function

SUMMARY This article reviews the literature regarding the structure and function of two types of exotoxins expressed by Staphylococcus aureus, pyrogenic toxin superantigens (PTSAgs) and hemolysins. The molecular basis of PTSAg toxicity is presented in the context of two diseases known to be caused by these exotoxins: toxic shock syndrome and staphylococcal food poisoning. The family of staphylococcal PTSAgs presently includes toxic shock syndrome toxin-1 (TSST-1) and most of the staphylococcal enterotoxins (SEs) (SEA, SEB, SEC, SED, SEE, SEG, and SEH). As the name implies, the PTSAgs are multifunctional proteins that invariably exhibit lethal activity, pyrogenicity, superantigenicity, and the capacity to induce lethal hypersensitivity to endotoxin. Other properties exhibited by one or more staphylococcal PTSAgs include emetic activity (SEs) and penetration across mucosal barriers (TSST-1). A detailed review of the molecular mechanisms underlying the toxicity of the staphylococcal hemolysins is also presented.

scholarly journals Targeting Age-Related Pathways in Heart Failure

2020 ◽  
Vol 126 (4) ◽  
pp. 533-551 ◽  
Author(s):  
Haobo Li ◽  
Margaret H. Hastings ◽  
James Rhee ◽  
Lena E. Trager ◽  
Jason D. Roh ◽  
...  
Keyword(s):  
Heart Failure ◽  
Elderly Population ◽  
Molecular Mechanisms ◽  
The Elderly ◽  
Structure And Function ◽  
Experimental Platform ◽  
Age Related ◽  
Cardiac Structure And Function ◽  
And Function ◽  
Increased Susceptibility

During aging, deterioration in cardiac structure and function leads to increased susceptibility to heart failure. The need for interventions to combat this age-related cardiac decline is becoming increasingly urgent as the elderly population continues to grow. Our understanding of cardiac aging, and aging in general, is limited. However, recent studies of age-related decline and its prevention through interventions like exercise have revealed novel pathological and cardioprotective pathways. In this review, we summarize recent findings concerning the molecular mechanisms of age-related heart failure and highlight exercise as a valuable experimental platform for the discovery of much-needed novel therapeutic targets in this chronic disease.

scholarly journals Quantitative Analysis of Retinal Structure and Function in Two Chromosomally Altered Mouse Models of Down Syndrome

2020 ◽  
Vol 61 (5) ◽  
pp. 25
Author(s):  
Daniella B. Victorino ◽  
Jonah J. Scott-McKean ◽  
Mark W. Johnson ◽  
Alberto C. S. Costa
Keyword(s):  
Down Syndrome ◽  
Quantitative Analysis ◽  
Mouse Models ◽  
Structure And Function ◽  
Retinal Structure ◽  
And Function

scholarly journals General discussion summary

2002 ◽  
Vol 357 (1426) ◽  
pp. 1419-1420 ◽  
Keyword(s):  
Water Splitting ◽  
Molecular Mechanisms ◽  
Structure And Function ◽  
X Ray ◽  
X Ray Crystallography ◽  
And Function ◽  
Splitting Process

This general discussion was chaired by A. W. Rutherford ( Service de Bioénergétique, Saclay, France ) and revolved around two major topics: (i) the implications of X–ray crystallography on the relationships between structure and function; (ii) the molecular mechanisms of the water–splitting process.

scholarly journals Reconstitution of the membrane protein OmpF into biomimetic block copolymer–phospholipid hybrid membranes

2016 ◽  
Vol 7 ◽  
pp. 881-892 ◽  
Author(s):  
Matthias Bieligmeyer ◽  
Franjo Artukovic ◽  
Stephan Nussberger ◽  
Thomas Hirth ◽  
Thomas Schiestel ◽  
...  
Keyword(s):  
Block Copolymers ◽  
Membrane Protein ◽  
Protein Function ◽  
Transmembrane Proteins ◽  
Synthetic Polymer ◽  
Structure And Function ◽  
Membrane Thickness ◽  
Channel Conductance ◽  
Biomimetic Polymer ◽  
And Function

Structure and function of many transmembrane proteins are affected by their environment. In this respect, reconstitution of a membrane protein into a biomimetic polymer membrane can alter its function. To overcome this problem we used membranes formed by poly(1,4-isoprene-block-ethylene oxide) block copolymers blended with 1,2-diphytanoyl-sn-glycero-3-phosphocholine. By reconstituting the outer membrane protein OmpF from Escherichia coli into these membranes, we demonstrate functionality of this protein in biomimetic lipopolymer membranes, independent of the molecular weight of the block copolymers. At low voltages, the channel conductance of OmpF in 1 M KCl was around 2.3 nS. In line with these experiments, integration of OmpF was also revealed by impedance spectroscopy. Our results indicate that blending synthetic polymer membranes with phospholipids allows for the reconstitution of transmembrane proteins under preservation of protein function, independent of the membrane thickness.

scholarly journals Structure and Function of HIV-1 Reverse Transcriptase: Molecular Mechanisms of Polymerization and Inhibition

2009 ◽  
Vol 385 (3) ◽  
pp. 693-713 ◽  
Author(s):  
Stefan G. Sarafianos ◽  
Bruno Marchand ◽  
Kalyan Das ◽  
Daniel M. Himmel ◽  
Michael A. Parniak ◽  
...  
Keyword(s):  
Reverse Transcriptase ◽  
Molecular Mechanisms ◽  
Structure And Function ◽  
And Function ◽  
Hiv 1

scholarly journals Recent progress in research on molecular mechanisms of autophagy in the heart

2015 ◽  
Vol 308 (4) ◽  
pp. H259-H268 ◽  
Author(s):  
Yasuhiro Maejima ◽  
Yun Chen ◽  
Mitsuaki Isobe ◽  
Åsa B. Gustafsson ◽  
Richard N. Kitsis ◽  
...  
Keyword(s):  
Heart Disease ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Degradation Process ◽  
Structure And Function ◽  
Cellular Functions ◽  
Evolutionarily Conserved ◽  
And Function ◽  
Cellular Dysfunction

Dysregulation of autophagy, an evolutionarily conserved process for degradation of long-lived proteins and organelles, has been implicated in the pathogenesis of human disease. Recent research has uncovered pathways that control autophagy in the heart and molecular mechanisms by which alterations in this process affect cardiac structure and function. Although initially thought to be a nonselective degradation process, autophagy, as it has become increasingly clear, can exhibit specificity in the degradation of molecules and organelles, such as mitochondria. Furthermore, it has been shown that autophagy is involved in a wide variety of previously unrecognized cellular functions, such as cell death and metabolism. A growing body of evidence suggests that deviation from appropriate levels of autophagy causes cellular dysfunction and death, which in turn leads to heart disease. Here, we review recent advances in understanding the role of autophagy in heart disease, highlight unsolved issues, and discuss the therapeutic potential of modulating autophagy in heart disease.

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