TIGAR exacerbates obesity by triggering LRRK2-mediated defects in macroautophagy and chaperone-mediated autophagy in adipocytes
Autophagy. 2024 Apr 30:1-21. doi: 10.1080/15548627.2024.2338576. Online ahead of print.ABSTRACTObesity is one of the most common metabolic diseases around the world, which is distinguished by the abnormal buildup of triglycerides within adipose cells. Recent research has revealed that autophagy regulates lipid mobilization to maintain energy balance. TIGAR (Trp53 induced glycolysis regulatory phosphatase) has been identified as a glycolysis inhibitor, whether it plays a role in the metabolism of lipids is unknown. Here, we found that TIGAR transgenic (TIGAR+/+) mice exhibited increased fat mass and trended to obesity pheno...
Source: Autophagy - April 30, 2024 Category: Cytology Authors: Tian Zhang Ke-Gang Linghu Jia Tan Mingming Wang Diao Chen Yan Shen Junchao Wu Mingjun Shi Yuxia Zhou Lei Tang Lirong Liu Zheng-Hong Qin Bing Guo Source Type: research
TIGAR exacerbates obesity by triggering LRRK2-mediated defects in macroautophagy and chaperone-mediated autophagy in adipocytes
Autophagy. 2024 Apr 30:1-21. doi: 10.1080/15548627.2024.2338576. Online ahead of print.ABSTRACTObesity is one of the most common metabolic diseases around the world, which is distinguished by the abnormal buildup of triglycerides within adipose cells. Recent research has revealed that autophagy regulates lipid mobilization to maintain energy balance. TIGAR (Trp53 induced glycolysis regulatory phosphatase) has been identified as a glycolysis inhibitor, whether it plays a role in the metabolism of lipids is unknown. Here, we found that TIGAR transgenic (TIGAR+/+) mice exhibited increased fat mass and trended to obesity pheno...
Source: Autophagy - April 30, 2024 Category: Cytology Authors: Tian Zhang Ke-Gang Linghu Jia Tan Mingming Wang Diao Chen Yan Shen Junchao Wu Mingjun Shi Yuxia Zhou Lei Tang Lirong Liu Zheng-Hong Qin Bing Guo Source Type: research
The Wolfram-like variant WFS1 < sup > E864K < /sup > destabilizes MAM and compromises autophagy and mitophagy in human and mice
Autophagy. 2024 Apr 23:1-12. doi: 10.1080/15548627.2024.2341588. Online ahead of print.ABSTRACTDominant variants in WFS1 (wolframin ER transmembrane glycoprotein), the gene coding for a mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) resident protein, have been associated with Wolfram-like syndrome (WLS). In vitro and in vivo, WFS1 loss results in reduced ER to mitochondria calcium (Ca2+) transfer, mitochondrial dysfunction, and enhanced macroautophagy/autophagy and mitophagy. However, in the WLS pathological context, whether the mutant protein triggers the same cellular processes is unknown. Here, we sho...
Source: Autophagy - April 23, 2024 Category: Cytology Authors: Simone Patergnani M éghane S Bataillard Alberto Danese Stacy Alves Chantal Cazevieille Ren é Valéro Lisbeth Tranebj ærg Tangui Maurice Paolo Pinton Benjamin Delprat Elodie M Richard Source Type: research
The Wolfram-like variant WFS1 < sup > E864K < /sup > destabilizes MAM and compromises autophagy and mitophagy in human and mice
Autophagy. 2024 Apr 23:1-12. doi: 10.1080/15548627.2024.2341588. Online ahead of print.ABSTRACTDominant variants in WFS1 (wolframin ER transmembrane glycoprotein), the gene coding for a mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) resident protein, have been associated with Wolfram-like syndrome (WLS). In vitro and in vivo, WFS1 loss results in reduced ER to mitochondria calcium (Ca2+) transfer, mitochondrial dysfunction, and enhanced macroautophagy/autophagy and mitophagy. However, in the WLS pathological context, whether the mutant protein triggers the same cellular processes is unknown. Here, we sho...
Source: Autophagy - April 23, 2024 Category: Cytology Authors: Simone Patergnani M éghane S Bataillard Alberto Danese Stacy Alves Chantal Cazevieille Ren é Valéro Lisbeth Tranebj ærg Tangui Maurice Paolo Pinton Benjamin Delprat Elodie M Richard Source Type: research
The Wolfram-like variant WFS1 < sup > E864K < /sup > destabilizes MAM and compromises autophagy and mitophagy in human and mice
Autophagy. 2024 Apr 23:1-12. doi: 10.1080/15548627.2024.2341588. Online ahead of print.ABSTRACTDominant variants in WFS1 (wolframin ER transmembrane glycoprotein), the gene coding for a mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) resident protein, have been associated with Wolfram-like syndrome (WLS). In vitro and in vivo, WFS1 loss results in reduced ER to mitochondria calcium (Ca2+) transfer, mitochondrial dysfunction, and enhanced macroautophagy/autophagy and mitophagy. However, in the WLS pathological context, whether the mutant protein triggers the same cellular processes is unknown. Here, we sho...
Source: Autophagy - April 23, 2024 Category: Cytology Authors: Simone Patergnani M éghane S Bataillard Alberto Danese Stacy Alves Chantal Cazevieille Ren é Valéro Lisbeth Tranebj ærg Tangui Maurice Paolo Pinton Benjamin Delprat Elodie M Richard Source Type: research
The Wolfram-like variant WFS1 < sup > E864K < /sup > destabilizes MAM and compromises autophagy and mitophagy in human and mice
Autophagy. 2024 Apr 23:1-12. doi: 10.1080/15548627.2024.2341588. Online ahead of print.ABSTRACTDominant variants in WFS1 (wolframin ER transmembrane glycoprotein), the gene coding for a mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) resident protein, have been associated with Wolfram-like syndrome (WLS). In vitro and in vivo, WFS1 loss results in reduced ER to mitochondria calcium (Ca2+) transfer, mitochondrial dysfunction, and enhanced macroautophagy/autophagy and mitophagy. However, in the WLS pathological context, whether the mutant protein triggers the same cellular processes is unknown. Here, we sho...
Source: Autophagy - April 23, 2024 Category: Cytology Authors: Simone Patergnani M éghane S Bataillard Alberto Danese Stacy Alves Chantal Cazevieille Ren é Valéro Lisbeth Tranebj ærg Tangui Maurice Paolo Pinton Benjamin Delprat Elodie M Richard Source Type: research
The Wolfram-like variant WFS1 < sup > E864K < /sup > destabilizes MAM and compromises autophagy and mitophagy in human and mice
Autophagy. 2024 Apr 23:1-12. doi: 10.1080/15548627.2024.2341588. Online ahead of print.ABSTRACTDominant variants in WFS1 (wolframin ER transmembrane glycoprotein), the gene coding for a mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) resident protein, have been associated with Wolfram-like syndrome (WLS). In vitro and in vivo, WFS1 loss results in reduced ER to mitochondria calcium (Ca2+) transfer, mitochondrial dysfunction, and enhanced macroautophagy/autophagy and mitophagy. However, in the WLS pathological context, whether the mutant protein triggers the same cellular processes is unknown. Here, we sho...
Source: Autophagy - April 23, 2024 Category: Cytology Authors: Simone Patergnani M éghane S Bataillard Alberto Danese Stacy Alves Chantal Cazevieille Ren é Valéro Lisbeth Tranebj ærg Tangui Maurice Paolo Pinton Benjamin Delprat Elodie M Richard Source Type: research
Autophagy cooperates with PDGFRA to support oncogenic growth signaling
Autophagy. 2024 Apr 18:1-2. doi: 10.1080/15548627.2024.2338572. Online ahead of print.ABSTRACTMacroautophagy (referred to as autophagy hereafter) is a highly conserved catabolic process which sequesters intracellular substrates for lysosomal degradation. Autophagy-related proteins have been shown to be involved in various aspects of tumor development by engaging with multiple cellular substrates. We recently uncovered a novel role for autophagy in regulating the signaling and levels of PDGFRA, a receptor tyrosine kinase amplified in several cancers. We discovered that PDGFRA can be targeted to autophagic degradation by bin...
Source: Autophagy - April 18, 2024 Category: Cytology Authors: Joanne E Simpson Noor Gammoh Source Type: research
Autophagy cooperates with PDGFRA to support oncogenic growth signaling
Autophagy. 2024 Apr 18:1-2. doi: 10.1080/15548627.2024.2338572. Online ahead of print.ABSTRACTMacroautophagy (referred to as autophagy hereafter) is a highly conserved catabolic process which sequesters intracellular substrates for lysosomal degradation. Autophagy-related proteins have been shown to be involved in various aspects of tumor development by engaging with multiple cellular substrates. We recently uncovered a novel role for autophagy in regulating the signaling and levels of PDGFRA, a receptor tyrosine kinase amplified in several cancers. We discovered that PDGFRA can be targeted to autophagic degradation by bin...
Source: Autophagy - April 18, 2024 Category: Cytology Authors: Joanne E Simpson Noor Gammoh Source Type: research
Toxic gain-of-function mechanisms in < em > C9orf72 < /em > ALS-FTD neurons drive autophagy and lysosome dysfunction
Autophagy. 2024 Apr 18:1-3. doi: 10.1080/15548627.2024.2340415. Online ahead of print.ABSTRACTHexanucleotide repeat expansions in the C9orf72 gene are the primary genetic cause for both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative diseases. Significant advances in the elucidation of the disease mechanisms responsible for C9orf72 ALS-FTD have revealed both a toxic gain-of-function and a loss-of-function mechanism as possible underlying disease cause. As the differential contribution of both gain and loss of function in C9orf72 ALS-FTD pathogenesis remains debated, we i...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Jimmy Beckers Philip Van Damme Source Type: research
Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms
Autophagy. 2024 Apr 18:1-17. doi: 10.1080/15548627.2024.2338574. Online ahead of print.ABSTRACTCrohn disease (CD) is an inflammatory bowel disease whose pathogenesis involves inappropriate immune responses toward gut microbiota on genetically predisposed backgrounds. Notably, CD is associated with single-nucleotide polymorphisms affecting several genes involved in macroautophagy/autophagy, the catabolic process that ensures the degradation and recycling of cytosolic components and microorganisms. In a clinical translation perspective, monitoring the autophagic activity of CD patients will require some knowledge on the intr...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Ga ëlle Quiniou Leslie Andromaque R émi Duclaux-Loras Oc éane Dinet Ornella Cervantes Mallorie Verdet Camille Meunier Gilles Boschetti Christophe Viret St éphane Nancey Mathias Faure Aurore Rozi ères Source Type: research
Toxic gain-of-function mechanisms in < em > C9orf72 < /em > ALS-FTD neurons drive autophagy and lysosome dysfunction
Autophagy. 2024 Apr 14. doi: 10.1080/15548627.2024.2340415. Online ahead of print.ABSTRACTHexanucleotide repeat expansions in the C9orf72 gene are the primary genetic cause for both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative diseases. Significant advances in the elucidation of the disease mechanisms responsible for C9orf72 ALS-FTD have revealed both a toxic gain-of-function and a loss-of-function mechanism as possible underlying disease cause. As the differential contribution of both gain and loss of function in C9orf72 ALS-FTD pathogenesis remains debated, we inves...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Jimmy Beckers Philip Van Damme Source Type: research
Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms
Autophagy. 2024 Apr 14. doi: 10.1080/15548627.2024.2338574. Online ahead of print.ABSTRACTCrohn disease (CD) is an inflammatory bowel disease whose pathogenesis involves inappropriate immune responses toward gut microbiota on genetically predisposed backgrounds. Notably, CD is associated with single-nucleotide polymorphisms affecting several genes involved in macroautophagy/autophagy, the catabolic process that ensures the degradation and recycling of cytosolic components and microorganisms. In a clinical translation perspective, monitoring the autophagic activity of CD patients will require some knowledge on the intrinsic...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Ga ëlle Quiniou Leslie Andromaque R émi Duclaux-Loras Oc éane Dinet Ornella Cervantes Mallorie Verdet Camille Meunier Gilles Boschetti Christophe Viret St éphane Nancey Mathias Faure Aurore Rozi ères Source Type: research
Toxic gain-of-function mechanisms in < em > C9orf72 < /em > ALS-FTD neurons drive autophagy and lysosome dysfunction
Autophagy. 2024 Apr 14. doi: 10.1080/15548627.2024.2340415. Online ahead of print.ABSTRACTHexanucleotide repeat expansions in the C9orf72 gene are the primary genetic cause for both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative diseases. Significant advances in the elucidation of the disease mechanisms responsible for C9orf72 ALS-FTD have revealed both a toxic gain-of-function and a loss-of-function mechanism as possible underlying disease cause. As the differential contribution of both gain and loss of function in C9orf72 ALS-FTD pathogenesis remains debated, we inves...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Jimmy Beckers Philip Van Damme Source Type: research
Impaired reprogramming of the autophagy flux in maturing dendritic cells from crohn disease patients with core autophagy gene-related polymorphisms
Autophagy. 2024 Apr 14. doi: 10.1080/15548627.2024.2338574. Online ahead of print.ABSTRACTCrohn disease (CD) is an inflammatory bowel disease whose pathogenesis involves inappropriate immune responses toward gut microbiota on genetically predisposed backgrounds. Notably, CD is associated with single-nucleotide polymorphisms affecting several genes involved in macroautophagy/autophagy, the catabolic process that ensures the degradation and recycling of cytosolic components and microorganisms. In a clinical translation perspective, monitoring the autophagic activity of CD patients will require some knowledge on the intrinsic...
Source: Autophagy - April 14, 2024 Category: Cytology Authors: Ga ëlle Quiniou Leslie Andromaque R émi Duclaux-Loras Oc éane Dinet Ornella Cervantes Mallorie Verdet Camille Meunier Gilles Boschetti Christophe Viret St éphane Nancey Mathias Faure Aurore Rozi ères Source Type: research
