Search Results
Search for other papers by Karim Gariani in
Google Scholar
PubMed
Diabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland
Search for other papers by François R Jornayvaz in
Google Scholar
PubMed
acids will induce the development of several deleterious phenomena such as mitochondrial dysfunction, endoplasmic reticulum stress, oxidative stress and production of reactive oxygen species ( 32 ). In addition, the alteration of intestinal microbiome
Search for other papers by Shenghe Luo in
Google Scholar
PubMed
Department of Cardiology, Yanbian University Hospital, Yanji, China
Search for other papers by Yunhui Zuo in
Google Scholar
PubMed
Search for other papers by Xiaotian Cui in
Google Scholar
PubMed
Search for other papers by Meiping Zhang in
Google Scholar
PubMed
Search for other papers by Honghua Jin in
Google Scholar
PubMed
Search for other papers by Lan Hong in
Google Scholar
PubMed
-like peptide-1 attenuates endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes during hypoxia/reoxygenation through the GLP-1R/PI3K/Akt pathways . Naunyn-Schmiedeberg’s Archives of Pharmacology 2019 392 715 – 722 . ( https://doi.org/10.1007/s
Search for other papers by Jun-Xin Yan in
Google Scholar
PubMed
Search for other papers by Bin-Jing Pan in
Google Scholar
PubMed
Search for other papers by Ping-Ping Zhao in
Google Scholar
PubMed
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China
Search for other papers by Li-Ting Wang in
Google Scholar
PubMed
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China
Search for other papers by Jing-Fang Liu in
Google Scholar
PubMed
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China
Search for other papers by Song-Bo Fu in
Google Scholar
PubMed
ferritin levels and FPG was shown in T2DM with NAFLD. Zou et al. reported that a higher FPG level was a risk factor for NAFLD ( 37 ). First, the higher FPG induces hepatocyte toxicity through oxidative stress and endoplasmic reticulum stress, leading to
Search for other papers by Lin Ji in
Google Scholar
PubMed
Search for other papers by Huan-Tong Wu in
Google Scholar
PubMed
Search for other papers by Xiao-Yan Qin in
Google Scholar
PubMed
Search for other papers by Rongfeng Lan in
Google Scholar
PubMed
activity ( 9 ). Although a full-length transcript is produced and the mutant CPE protein is expressed in these mice, this enzyme activity is deficient, unstable and is rapidly degraded in the endoplasmic reticulum before it can be secreted ( 10 , 11 ). As
Institute of Pediatrics, Nanjing Medical University, Nanjing, China
Search for other papers by Lianghui You in
Google Scholar
PubMed
Institute of Pediatrics, Nanjing Medical University, Nanjing, China
Search for other papers by Yan Wang in
Google Scholar
PubMed
Search for other papers by Yao Gao in
Google Scholar
PubMed
Search for other papers by Xingyun Wang in
Google Scholar
PubMed
Search for other papers by Xianwei Cui in
Google Scholar
PubMed
Search for other papers by Yanyan Zhang in
Google Scholar
PubMed
Search for other papers by Lingxia Pang in
Google Scholar
PubMed
Institute of Pediatrics, Nanjing Medical University, Nanjing, China
Search for other papers by Chenbo Ji in
Google Scholar
PubMed
Search for other papers by Xirong Guo in
Google Scholar
PubMed
Institute of Pediatrics, Nanjing Medical University, Nanjing, China
Search for other papers by Xia Chi in
Google Scholar
PubMed
sites of psiCHECK-2 plasmid (Promega). The target sequence of miR-23b-5p within the endoplasmic reticulum to nucleus signaling 1 ( Ern1 ) 3′UTR-1 was mutated from GGAACCA to CCTTGGA and 3′UTR-2 AGGAACC to ACCTTGG. 3T3-L1 cells (10 4 per well) were
epiWELL, LLC, Ithaca, New York, USA
Search for other papers by Magnolia Ariza-Nieto in
Google Scholar
PubMed
Search for other papers by Joshua B Alley in
Google Scholar
PubMed
Search for other papers by Sanjay Samy in
Google Scholar
PubMed
Search for other papers by Laura Fitzgerald in
Google Scholar
PubMed
Search for other papers by Francoise Vermeylen in
Google Scholar
PubMed
Search for other papers by Michael L Shuler in
Google Scholar
PubMed
Search for other papers by José O Alemán in
Google Scholar
PubMed
-0127 17475934 4 Qiang L Wang H Farmer SR. Adiponectin secretion is regulated by SIRT1 and the endoplasmic reticulum oxidoreductase Ero1-L alpha . Molecular and Cellular Biology 2007 27 4698 – 4707 . ( https://doi.org/10.1128/MCB.02279-06 ) 10.1128/MCB
Search for other papers by Gareth Leng in
Google Scholar
PubMed
rough endoplasmic reticulum that permeates the dendrites ( 31 , 38 , 39 ) – and some, like α-MSH, stimulate dendritic release even while inhibiting spiking activity ( 40 ). This is not to say that spike activity never releases dendritic oxytocin – some
Search for other papers by Lesley A Hill in
Google Scholar
PubMed
Search for other papers by Zeynep Sumer-Bayraktar in
Google Scholar
PubMed
Search for other papers by John G Lewis in
Google Scholar
PubMed
Search for other papers by Eva Morava in
Google Scholar
PubMed
Search for other papers by Morten Thaysen-Andersen in
Google Scholar
PubMed
Search for other papers by Geoffrey L Hammond in
Google Scholar
PubMed
that the type of N -glycan at N238 in human CBG influences its steroid-binding properties suggests that this oligosaccharide interacts with amino acid residues as the nascent glycoprotein is modified in the endoplasmic reticulum and Golgi during
Search for other papers by Madalena von Hafe in
Google Scholar
PubMed
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar São João, Porto, Portugal
Search for other papers by João Sergio Neves in
Google Scholar
PubMed
Search for other papers by Catarina Vale in
Google Scholar
PubMed
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar São João, Porto, Portugal
Search for other papers by Marta Borges-Canha in
Google Scholar
PubMed
Search for other papers by Adelino Leite-Moreira in
Google Scholar
PubMed
; MMP-2, matrix metalloproteinase-2; NO, nitric oxide; SERCA2, sarcoplasmic/endoplasmic reticulum calcium ATPase 2. Another subtype of TH dysfunction called nonthyroidal illness syndrome (NTIS) – also known as euthyroid sick syndrome or low-T3
Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
Endocrine, Cardiovascular & Metabolic Research, Department of Anatomy, Multidisciplinary Unit for Biomedical Research (UMIB), Instituto de Ciências Biomédicas Abel Salazar, University of Porto (ICBAS/UP), Porto, Portugal
Search for other papers by Sofia S Pereira in
Google Scholar
PubMed
Search for other papers by Mariana P Monteiro in
Google Scholar
PubMed
Search for other papers by Sonir R Antonini in
Google Scholar
PubMed
Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
Department of Endocrinology, Hospital S. João, Porto, Portugal
Search for other papers by Duarte Pignatelli in
Google Scholar
PubMed
). Intrinsic apoptosis pathway signaling alterations The intrinsic apoptosis pathway is triggered by intracellular stimuli that include DNA damage, absence of growth factors, oxidative stress and endoplasmic reticulum stress ( 13 ). These stimuli lead to