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Protein import into the endoplasmic reticulum (ER) is the first step in the biogenesis of approximately 10,000 different soluble and membrane proteins of human cells, which amounts to about 30% of the proteome. Most of these proteins fulfill their functions either in the membrane or lumen of the ER plus the nuclear envelope, in one of the organelles of the pathways for endo- and exocytosis (ERGIC, Golgi apparatus, endosome, lysosome, and trafficking vesicles), or at the cell surface as plasma membrane or secreted proteins. An increasing number of membrane proteins destined to lipid droplets, peroxisomes or mitochondria are first targeted to and inserted into the ER membrane prior to their integration into budding lipid droplets or peroxisomes or prior to their delivery to mitochondria via the ER-SURF pathway. ER protein import involves two stages, ER targeting, which guarantees membrane specificity, and the insertion of nascent membrane proteins into or translocation of soluble precursor polypeptides across the ER membrane. In most cases, both processes depend on amino-terminal signal peptides or transmembrane helices, which serve as signal peptide equivalents. However, the targeting reaction can also involve the ER targeting of specific mRNAs or ribosome–nascent chain complexes. Both processes may occur co- or post-translationally and are facilitated by various sophisticated machineries, which reside in the cytosol and the ER membrane, respectively. Except for resident ER and mitochondrial membrane proteins, the mature proteins are delivered to their functional locations by vesicular transport.

chaperones --- contact sites --- endoplasmic reticulum --- ER-SURF --- membrane extraction --- mitochondria --- protein targeting --- bimolecular luminescence complementation --- competition --- split luciferase --- membrane proteins --- protein–protein interactions --- Sec61 complex --- Sec63 --- synthetic peptide complementation --- TRAP complex --- ER protein translocase --- signal peptide --- protein translocation --- nascent peptide chain --- membrane insertion --- molecular modelling --- molecular dynamics simulations --- molecular docking --- signal peptidase --- ER translocon --- signal recognition particle dependent protein targeting --- Sec61 dependent translocation --- co-translational translocation --- inhibitor --- high throughput screening --- Sec61 --- Sec62 --- folding --- insertion --- membrane protein --- translocon --- ribosome --- transmembrane segment --- lipid droplets --- peroxisomes --- PEX3 --- membrane protein insertion --- label-free quantitative mass spectrometry --- differential protein abundance analysis --- Zellweger syndrome --- GET --- protein transport --- SND --- SRP --- EMC --- positive-inside rule --- hydrophobicity --- transmembrane helix --- signal recognition particle --- nascent polypeptide-associated complex --- fidelity --- cyclotriazadisulfonamide --- ER quality control --- DNAJC3 --- preprotein --- Sec61 translocon --- ribosome stalling --- signal sequence --- Sec61 translocase --- NAC --- n/a --- protein-protein interactions

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Even though initially considered as a passive means for storing energy, lipids are now regarded as multifaceted molecules with crucial structural and functional activities. For instance, some of them play essential roles as key components of cell membranes whereas others act as signaling molecules in the regulation of cell homeostasis. In recent years, lipid research has attracted increasing interest because of the involvement of this class of compounds in human health. Indeed, a plethora of pathological conditions are characterized by alterations in lipid metabolism, such as cardiovascular diseases and brain disorders. This Special Issue is a collection of papers from different experts in lipid research, with the aim of providing new insights into the physiopathological involvement of lipids and their impact on human health. This collection also demonstrates the usefulness of interdisciplinary approaches in the development of novel methods to study and manipulate lipid metabolism, which may represent an attractive target for designing effective therapeutic strategies to counteract numerous pathologies.

Medicine --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- n/a

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

Research & information: general --- Biology, life sciences --- Biochemistry --- nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography