Cancers, Vol. 15, Pages 5305: Exosomal Long Non-Coding Ribonucleic Acid Ribonuclease Component of Mitochondrial Ribonucleic Acid Processing Endoribonuclease Is Defined as a Potential Non-Invasive Diagnostic Biomarker for Bladder Cancer and Facilitates Tumorigenesis via the miR-206/G6PD Axis
In this study, we employed RNA-sequencing to compare the expression patterns of lncRNAs in urine exosomes from three BLCA patients and three healthy individuals. RMRP displayed the most significant differential expression. Elevated RMRP expression levels were observed in urinary and plasma exosomes from BLCA patients compared with those from healthy individuals. RMRP exhibited significant associations with certain BLCA patient clinicopathological features, including tumor stage, poor prognosis, and tumor grade. Combined diagnosis using RMRP in urine and plasma exosomes demonstrated a superior diagnostic performance with re...
Source: Cancers - November 6, 2023 Category: Cancer & Oncology Authors: Yuting Gao Xuan Wang Huarong Luo Chen Chen Jing Li Ruixin Sun Dong Li Zujun Sun Tags: Article Source Type: research
Potentially pathogenic and pathogenic G6PD variants
In their interesting and comprehensive paper in the February 2, 2023 issue of this journal, Geck et al.1 have illustrated several aspects of genetic variation at the X-linked G6PD locus that is rather unique in terms of its clinical and public health implications. Their analysis supports the recently revised WHO classification: this is gratifying and not surprising, since the WHO revision was ca rried out after long deliberation, based in large part on recently reviewed data2,3 that Geck et al.1 have also analyzed. (Source: The American Journal of Human Genetics)
Source: The American Journal of Human Genetics - November 2, 2023 Category: Genetics & Stem Cells Authors: Lucio Luzzatto, Caterina Nannelli, Rosario Notaro Tags: Letter to the editor Source Type: research
Response to Luzzatto et al.
To the editor: In the last few years, updates to G6PD variant interpretation and drug use guidelines have been published, highlighting the importance and continued interest in connecting G6PD variation with G6PD deficiency, chronic anemia, and risk of adverse drug reactions. However, many challenges remain for G6PD variant interpretation, including those raised by Luzzatto et al.1 (Source: The American Journal of Human Genetics)
Source: The American Journal of Human Genetics - November 2, 2023 Category: Genetics & Stem Cells Authors: Renee C. Geck, Nicholas R. Powell, Maitreya J. Dunham Tags: Letter to the Editor Source Type: research
27-Year-Old Woman With Hypoxemia
A 27-year-old woman presented to the clinic for home pulse oximetry readings persistently below 90% with associated dyspnea for several months. She denied additional complaints. Her medical history was notable for bipolar disorder, type I diabetes, hypertension, obesity, hypothyroidism, gastroesophageal reflux disease, prior cholecystectomy, and episodic jaundice. Medications on presentation were lamotrigine, insulin, hydrochlorothiazide, levothyroxine, and omeprazole. Episodic jaundice had been attributed to glucose-6-phosphate dehydrogenase (G6PD) deficiency diagnosed at 2 years of age when the patient developed acute an...
Source: Mayo Clinic Proceedings - November 1, 2023 Category: Internal Medicine Authors: Holly M. Thomson, Surbhi Shah Tags: Residents ’ clinic Source Type: research
Reply to Letter to the Editor - Glutathione S-Transferase and Moderate Neonatal Hyperbilirubinemia Associated with Glucose-6-Phosphate Dehydrogenase Deficiency
We thank Dr. Al Abdi for his interest in our recent paper (1) and for his comments. While we did emphasize the role of UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms in the pathogenesis of glucose-6-phosphate dehydrogenase (G6PD) deficiency-associated neonatal hyperbilirubinemia, there was no intention of designating these as the only genetic factors contributing to the hyperbilirubinemia. Indeed, G6PD-deficiency-associated neonatal hyperbilirubinemia has been characterized as a complexity of interactions between genes and environment. (Source: The Journal of Pediatrics)
Source: The Journal of Pediatrics - October 31, 2023 Category: Pediatrics Authors: Michael Kaplan, Cathy Hammerman, Steven M. Shapiro Tags: Letters to the Editor Source Type: research
Glutathione S-Transferase and Moderate Neonatal Hyperbilirubinemia Associated with Glucose-6-Phosphate Dehydrogenase Deficiency
The neonate presented in the Grand Rounds article by Kaplan et al had an unfortunate outcome with many sequelae of kernicterus.1 These authors seem to imply that the mutation of UDP-glucuronosyltransferase 1A1 was the only genetic factor that contributed to the moderate neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency in their report.1 I would like to add that the mutation of glutathione S-transferase (GST) may have a role in the development of G6PD deficiency –associated moderate neonatal hyperbilirubinemia and should not be overlooked. (Source: The Journal of Pediatrics)
Source: The Journal of Pediatrics - October 31, 2023 Category: Pediatrics Authors: Sameer Yaseen Al-Abdi Tags: Letters to the Editor Source Type: research
Reply to Letter to the Editor –Glutathione S-transferase and moderate neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase deficiency
We thank Dr. Al Abdi for his interest in our recent paper1 and for his comments. While we did emphasize the role of UDP-glucuronosyltransferase 1A1 polymorphisms in the pathogenesis of glucose-6-phosphate dehydrogenase (G6PD) deficiency-associated neonatal hyperbilirubinemia, there was no intention of designating these as the only genetic factors contributing to the hyperbilirubinemia. Indeed, G6PD-deficiency-associated neonatal hyperbilirubinemia has been characterized as a complexity of interactions between genes and environment. (Source: The Journal of Pediatrics)
Source: The Journal of Pediatrics - October 31, 2023 Category: Pediatrics Authors: Michael Kaplan, Cathy Hammerman, Steven M. Shapiro Tags: Letters to the Editor Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
