MAP1LC3B2

Last update 08 May 2025

Basic Info

Synonyms

ATG8G, MAP1LC3B2, microtubule associated protein 1 light chain 3 beta 2

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Introduction

Ubiquitin-like modifier involved in formation of autophagosomal vacuoles (autophagosomes). Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. In response to cellular stress and upon mitochondria fission, binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria. While LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation.

100 Clinical Results associated with MAP1LC3B2

100 Translational Medicine associated with MAP1LC3B2

0 Patents (Medical) associated with MAP1LC3B2

258

Literatures (Medical) associated with MAP1LC3B2

28 Mar 2025·Science Advances

Mycobacterium tuberculosis phagosome Ca ²⁺ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages

Article

Author: Chen, Di ; Fearns, Antony ; Gutierrez, Maximiliano G.

The role of canonical autophagy in controlling Mycobacterium tuberculosis (Mtb), referred to as xenophagy, is understood to involve targeting Mtb to autophagosomes, which subsequently fuse with lysosomes for degradation. Here, we found that Ca 2+ leakage after Mtb phagosome damage in human macrophages is the signal that triggers autophagy-related protein 8/microtubule-associated proteins 1A/1B light chain 3 (ATG8/LC3) lipidation. Unexpectedly, ATG8/LC3 lipidation did not target Mtb to lysosomes, excluding the canonical xenophagy. Upon Mtb phagosome damage, the Ca 2+ leakage–dependent ATG8/LC3 lipidation occurred on multiple membranes instead of single or double membranes excluding the noncanonical autophagy pathways. Mechanistically, Ca 2+ leakage from the phagosome triggered the recruitment of the V-ATPase–ATG16L1 complex independently of FIP200, ATG13, and proton gradient disruption. Furthermore, the Ca 2+ leakage–dependent ATG8/LC3 lipidation limited Mtb phagosome damage and restricted Mtb replication. Together, we uncovered Ca 2+ leakage as the key signal that triggers ATG8/LC3 lipidation on multiple membranes to mitigate Mtb phagosome damage.

01 Mar 2025·Cell Transplantation

The Impact of Obesity on Autophagy in Human Adipose-Derived Mesenchymal Stromal Cells

Article

Author: Lu, Bo ; Mondesir, Ronscardy ; Al Saeedi, Mina ; Sohi, Gurparneet Kaur ; Zhu, Xiang-Yang ; Eirin, Alfonso ; Lerman, Lilach O. ; Xing, Li ; Glasstetter, Logan M.

Mesenchymal stromal cells (MSCs) possess therapeutic properties, which can be blunted by obesity. Autophagy, a cellular recycling process, is essential for MSC function. We investigated the mechanisms by which obesity affects the properties of MSCs, with a focus on autophagy. Adipose tissue was obtained from kidney donors [body mass index (BMI) <30 kg/m 2 , non-obese] or individuals undergoing weight loss surgery (BMI ≥30 kg/m 2 , obese) for MSC harvesting ( n = 11 each); samples were randomized to sequencing (seq; n = 5 each) or functional studies ( n = 6 each). MSCs were sequenced to determine their epigenetic (5-hydroxymethylcytosine) and transcriptomic profiles across autophagy-related genes using hydroxymethylated DNA immunoprecipitation sequencing and mRNA-seq, respectively. Genes with shared trends in both datasets underwent Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) validation. During functional studies, 2-h starvation was used to induce autophagy in vitro , enabling detection of changes in the protein expression of microtubule-associated protein 1A/1B-light chain-3 and in autophagic flux. Obesity amplified a starvation-induced reduction in autophagic flux in MSCs while promoting earlier generation of new autophagosomes during autophagy initiation. Integrated analysis of the two sequencing datasets revealed 124 differentially hydroxymethylated genes and 30 differentially expressed mRNAs. Among six overlapping autophagy-related genes, three exhibited same-direction trends. Of these, STX12 and SLC25A4 may be implicated in the impact of obesity on autophagic changes in MSCs. Therefore, human obesity may alter autophagy in adipose tissue–derived MSC, and thereby their metabolism and function.

01 Mar 2025·International Urogynecology Journal

Autophagy Attenuates Oxidative Stress-Induced Collagen Degradation in Vaginal Fibroblasts: Implications for Pelvic Organ Prolapse

Article

Author: Liu, Juan ; Zhou, YouJun ; Tan, Liping ; Liu, Qihuang ; Zhou, Xingnan ; Chen, Yan

INTRODUCTION AND HYPOTHESISThe relationship between autophagy and pelvic organ prolapse (POP) remains unknown. The aim of this novel experimental study, utilizing tissue samples derived from women undergoing gynecological surgery, is to investigate the role of autophagy in mitigating collagen degradation in human vaginal fibroblasts induced by oxidative stress, with particular emphasis on its implications in the pathogenesis of POP. Exploring the role of autophagy in protecting against collagen degradation and cellular senescence in human vaginal fibroblasts under oxidative stress may offer new insights into therapeutic strategies for conditions such as POP.METHODSThis study consists of laboratory-based experimental research that utilizes tissue samples collected from female patients undergoing gynecological surgery to analyze the role of autophagy in collagen degradation induced by oxidative stress. By treating with different concentrations of hydrogen peroxide (H₂O₂) and using rapamycin (RAPA) and 3-methyladenine (3-MA) as autophagy activators and inhibitors respectively, the effects on human vaginal fibroblasts (HVFs) were evaluated. Cell viability was determined using the Cell Counting Kit-8 test. Cellular senescence was determined with senescence-associated-β-galactosidase labeling and western blotting to identify the expression of p21 and p53. Reactive oxygen species (ROS) were determined with 2,7-dichlorofluorescin diacetate. Additionally, western blotting was used to establish collagen I, collagen III, microtubule-associated protein 1A/1B-light chain 3 (LC3), Beclin-1, and p62 and reverse transcription-quantitative polymerase chain reaction was used to determine the mRNA levels of COL3A1, COL1A1, TIMP1, MMP9, LC3, and Beclin-1 to investigate collagen metabolism and autophagic activity.RESULTSThe results showed that high-dose H₂O₂ significantly increased ROS levels, cell senescence, and collagen degradation in HVFs. The combined use of RAPA significantly reduced ROS levels, collagen degradation, and cell senescence, but this protective effect disappeared when 3-MA was added. Nevertheless, co-treatment of HVFs with RAPA, H₂O₂, and 3-MA abolished the positive impact of RAPA via boosting autophagy resistance.CONCLUSIONSAutophagy inhibits collagen degeneration and cellular senescence caused by oxidative stress.

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MAP1LC3B2

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