Affinage

MAP1LC3B

Microtubule-associated protein 1 light chain 3 beta · UniProt Q9GZQ8

Length
125 aa
Mass
14.7 kDa
Annotated
2026-06-10
33 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAP1LC3B is a ubiquitin-like protein central to autophagosome biogenesis that is matured through a conjugation cascade: human Atg4B cleaves its C-terminal Met-121 to expose Gly-120, which is then activated by the E1-like Atg7 and transferred via the E2-like Atg3 for conjugation to phospholipid (PE), generating the membrane-associated lipidated form essential for autophagy (PMID:15355958). Gly-120 is strictly required for both cleavage and lipidation (PMID:15355958), and the protein associates with autophagosomal membranes (PMID:12740394). Its abundance is controlled at multiple levels: ATF4 (downstream of the PERK arm of the UPR) drives transcription that replenishes MAP1LC3B consumed during hypoxic autophagy (PMID:20038797), CHOP/DDIT3 directly binds the MAP1LC3B promoter to upregulate transcription (PMID:24589849), the cochaperone BAG3 selectively controls its translation (PMID:26654586), and protein stability is restrained by LIR-dependent ubiquitination via pVHL (PMID:30902965) and monoubiquitination via HDAC6, which impairs autophagy and promotes cardiac hypertrophy (PMID:40212005). The protein engages substrate-recruiting partners through LIR motifs, including SQSTM1, whose mitochondria-targeted LIR domain is sufficient to force mitophagy (PMID:35574946), and PGRMC1, required for autophagic clearance of ubiquitinated proteins and damaged organelles (PMID:24113030). Beyond canonical degradative autophagy, MAP1LC3B acts upstream of procaspase-8 cleavage in ER stress-induced apoptosis (PMID:31987044), functions as an RNA-binding protein mediating rapid maternal mRNA decay during the maternal-to-zygotic transition (PMID:41231099), and can be covalently conjugated to proteins (ATG8ylation) via Atg7/Atg3 independently of the ATG12-ATG5-ATG16L1 complex [PMID:bio_10.1101_2024.07.03.601942]. Genetic loss in mice causes defects in dendritic-cell autophagy with exaggerated IL-17a-dependent lung pathology during RSV infection (PMID:25669150) and sensitizes lung epithelium to bleomycin-induced fibrosis (PMID:31431059).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2003 Medium

    Established that MAP1LC3B is post-translationally modified and membrane-associated, distinguishing it biochemically from its paralogs and placing it on autophagosomal membranes.

    Evidence Cell fractionation, immunofluorescence, and biochemical modification mapping of three LC3 isoforms

    PMID:12740394

    Open questions at the time
    • Initial claim of Lys-122 modification without C-terminal cleavage was refined by later reconstitution work
    • Enzymes mediating the modification not identified
  2. 2004 High

    Defined the core conjugation mechanism: Atg4B cleavage at Gly-120 licenses Atg7/Atg3-dependent lipidation to PE, answering how LC3B becomes membrane-competent.

    Evidence In vitro cleavage with recombinant Atg4B, G120A mutagenesis, RNAi, fractionation, and enzyme-substrate intermediate IP

    PMID:15355958

    Open questions at the time
    • Does not address upstream membrane-targeting specificity
    • Regulation of the cascade in vivo not resolved
  3. 2009 Medium

    Showed that LC3B protein pools are transcriptionally replenished via PERK/ATF4 signaling during hypoxic autophagy, linking the UPR to autophagy capacity.

    Evidence Reporter assays, western blotting, PERK-deficient cells, and tumor xenografts

    PMID:20038797

    Open questions at the time
    • Direct ATF4 binding to the MAP1LC3B promoter not demonstrated
    • Relative contribution of transcription vs. conjugation to autophagy output unquantified
  4. 2014 Medium

    Identified CHOP/DDIT3 as a direct transcriptional activator binding the MAP1LC3B promoter, distinguishing it from the ATF4 arm which acts on ATG12.

    Evidence Luciferase reporter, ChIP/promoter binding, qPCR, and western blotting in HCV-infected Huh7 cells

    PMID:24589849

    Open questions at the time
    • Cooperativity between CHOP and ATF4 inputs not dissected
    • Context-dependence beyond HCV infection unknown
  5. 2016 Medium

    Revealed a translational control layer in which BAG3 selectively sets basal LC3B protein levels without affecting transcription or lipidation.

    Evidence RNAi, RT-qPCR, western blotting, and polysome profiling in HeLa and HEK293 cells

    PMID:26654586

    Open questions at the time
    • Molecular mechanism by which BAG3 engages LC3B mRNA not defined
    • Specificity for LC3B among ATG mRNAs not fully mapped
  6. 2013 Medium

    Connected LC3B to substrate clearance through PGRMC1, which physically associates with it and is required for autophagic degradation of ubiquitinated proteins and damaged organelles.

    Evidence Co-IP, RNAi, small-molecule inhibition, and autophagy substrate readouts

    PMID:24113030

    Open questions at the time
    • Direct vs. indirect nature of the LC3-PGRMC1 association unresolved
    • No reciprocal validation or structural basis
  7. 2019 Medium

    Established LIR-dependent ubiquitination of LC3B by pVHL as a negative regulator of LC3B-mediated autophagy.

    Evidence Co-IP, ubiquitination assay, and L101A mutagenesis in RCC cell lines

    PMID:30902965

    Open questions at the time
    • Ubiquitin chain topology and fate of ubiquitinated LC3B unspecified
    • In vivo relevance not tested
  8. 2025 Medium

    Identified HDAC6-mediated monoubiquitination as a second ubiquitin-dependent route lowering LC3B levels, with pathological cardiac hypertrophy as the in vivo consequence.

    Evidence Co-IP, ubiquitination assay, HDAC6 overexpression/inhibition, and ISO-induced cardiac hypertrophy mouse model

    PMID:40212005

    Open questions at the time
    • Whether HDAC6 acts as the ligase or a scaffold not clarified
    • Relationship to pVHL-mediated ubiquitination not addressed
  9. 2015 Medium

    Demonstrated in vivo that LC3B is required for dendritic-cell autophagy that restrains IL-17a-dependent lung immunopathology during RSV infection.

    Evidence LC3b knockout mice, bone marrow chimeras, RSV infection, and cytokine measurements

    PMID:25669150

    Open questions at the time
    • Which autophagy substrates suppress inflammation unidentified
    • Mechanism linking LC3B loss to cytokine output undefined
  10. 2019 Medium

    Showed LC3B is protective against bleomycin lung injury and identified cathepsin A as a binding partner whose accumulation drives epithelial apoptosis.

    Evidence LC3B knockout mice, bleomycin model, knockdown/overexpression in MLE12 cells, Co-IP, and EM

    PMID:31431059

    Open questions at the time
    • Whether cathepsin A is an autophagic degradation substrate of LC3B not established
    • Direct vs. indirect binding not resolved
  11. 2020 Medium

    Defined a non-autophagic role for LC3B acting upstream of procaspase-8 cleavage in ER stress-induced apoptosis, regulated by ATF4 and CHOP.

    Evidence RNAi, caspase activity assays, PI staining, and RT-PCR in LNCaP and HCT116 cells

    PMID:31987044

    Open questions at the time
    • Molecular link between LC3B and procaspase-8 activation not mapped
    • Whether lipidation is required for this function unknown
  12. 2022 Medium

    Demonstrated that the LC3B-binding LIR domain of SQSTM1, when targeted to mitochondria, is sufficient to force mitophagy, establishing LIR-LC3B engagement as a deployable cargo-targeting module.

    Evidence Mitochondria-targeted SQSTM1 LIR expression, flow cytometry, microscopy, and mtDNA quantification in HeLa cells and mouse embryos

    PMID:35574946

    Open questions at the time
    • Requirement for endogenous receptor selectivity bypassed by forced system
    • Generalizability to other organelles not tested
  13. 2024 Medium

    Showed that m6A methylation of Map1lc3b mRNA by METTL3/ALKBH5 suppresses autophagy, adding an epitranscriptomic regulatory layer.

    Evidence MeRIP-seq, RNA-seq integration, writer/eraser manipulation, and BPA exposure models

    PMID:39662354

    Open questions at the time
    • Which reader proteins act on methylated Map1lc3b mRNA unidentified
    • Effect on translation vs. stability not separated
  14. 2024 Medium

    Established protein ATG8ylation of LC3B as a conjugation activity requiring Atg7/Atg3 but independent of the ATG12-ATG5-ATG16L1 complex, with ATG7 itself as a conjugation target.

    Evidence CRISPR ATG5/ATG7/ATG3 knockouts, deconjugation-resistant mutant, western blotting, and IP (preprint)

    PMID:bio_10.1101_2024.07.03.601942

    Open questions at the time
    • Functional consequence of protein ATG8ylation not defined
    • Peer review pending; broader substrate range unknown
  15. 2025 Medium

    Identified LC3B as an RNA-binding protein driving rapid maternal mRNA decay during the maternal-to-zygotic transition, a function distinct from membrane autophagy.

    Evidence RIP-seq, RNA-seq, CUT&Tag, LC3B knockdown, and developmental assays in early embryos

    PMID:41231099

    Open questions at the time
    • Structural basis of LC3B RNA binding undefined
    • Whether decay requires lipidation or the conjugation machinery unknown
  16. 2025 Low

    Proposed that LC3B undergoes CASM at the Golgi to support Golgi repair in TRIM46-deficient cells, extending non-degradative ATG8ylation to organelle maintenance.

    Evidence TRIM46 knockout cells, CASM gene knockdown, colocalization, and Golgi fragmentation assays (preprint)

    PMID:bio_10.1101_2025.09.04.674289

    Open questions at the time
    • No biochemical reconstitution; colocalization-based
    • Single lab, preprint not peer-reviewed
    • Direct role of LC3B vs. GABARAP at the Golgi not separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How LC3B's diverse non-canonical activities (RNA-binding mRNA decay, CASM, apoptotic signaling) mechanistically relate to its conjugation chemistry and whether they share or bypass the lipidation cascade remains unresolved.
  • No structural model unifying membrane and RNA-binding functions
  • Substrate determinants for protein ATG8ylation undefined
  • Crosstalk among transcriptional, translational, and ubiquitin-based regulation not integrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0031386 protein tag activity 2 GO:0060090 molecular adaptor activity 2 GO:0003723 RNA binding 1
Localization
GO:0005794 Golgi apparatus 1
Pathway
R-HSA-9612973 Autophagy 4 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-8953854 Metabolism of RNA 1
Partners
ATG3ATG4BATG7BAG3HDAC6PGRMC1SQSTM1VHL

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 MAP1LC3B undergoes a distinct post-translational modification compared to MAP1LC3A and MAP1LC3C: it does not undergo C-terminal cleavage after the conserved Gly-120 residue, and instead is modified at Lys-122. All three isoforms associate with autophagosomal membranes as shown by subcellular fractionation and immunofluorescence. Cell fractionation, immunofluorescence, biochemical characterization of post-translational modifications The Journal of biological chemistry Medium 12740394
2004 The C-terminal Met-121 of MAP1LC3B is cleaved by human Atg4B to expose Gly-120, which is essential for subsequent ubiquitylation-like reactions: formation of Atg7-MAP1LC3B (E1-like) and Atg3-MAP1LC3B (E2-like) intermediates, and conjugation to phospholipid (PE). Gly-120 is required for both C-terminal cleavage and lipidation. RNA interference of MAP1LC3B mRNA decreased both endogenous MAP1LC3B-PL and total MAP1LC3B protein. In vitro cleavage assay with recombinant Atg4B, site-directed mutagenesis (G120A mutant), RNAi knockdown, cell fractionation, immunoprecipitation of enzyme-substrate intermediates The Journal of biological chemistry High 15355958
2009 Hypoxia increases transcription of MAP1LC3B through the transcription factor ATF4, which is regulated by the PERK arm of the UPR. This transcriptional induction replenishes MAP1LC3B protein consumed during extensive autophagy. Cells deficient in PERK signaling fail to induce MAP1LC3B transcription and become depleted of MAP1LC3B protein during hypoxia. Transcriptional reporter assays, western blotting, PERK-deficient cell lines, human tumor xenografts with immunostaining The Journal of clinical investigation Medium 20038797
2014 HCV core protein activates autophagy through UPR pathways: DDIT3/CHOP directly binds to the -253 to -99 base region of the MAP1LC3B promoter to upregulate its transcription. The EIF2AK3/ATF4 pathway upregulates ATG12 but not MAP1LC3B. Luciferase reporter assay, chromatin immunoprecipitation/promoter binding assay, western blotting, qPCR in Huh7 cells Autophagy Medium 24589849
2013 PGRMC1/S2R (progesterone receptor membrane component 1) physically associates with MAP1LC3 and UVRAG. PGRMC1 is required for autophagy-dependent degradation of ubiquitinated proteins and damaged organelles; its inhibition by RNAi or small molecules causes accumulation of autophagy substrates and aberrant mitochondria. Co-immunoprecipitation, RNAi knockdown, small-molecule inhibition, western blotting for autophagy substrates Autophagy Medium 24113030
2016 The cochaperone BAG3 controls the basal amount of MAP1LC3B protein by regulating translation of its mRNA, not its transcription. BAG3 knockdown reduced total LC3B protein without affecting LC3B mRNA levels or LC3B lipidation induced by starvation or proteasome inhibition. This effect appeared specific to LC3B among ATG proteins tested. RNAi knockdown, western blotting, RT-qPCR, polysome profiling/translational analysis in HeLa and HEK293 cells Autophagy Medium 26654586
2019 pVHL (Von Hippel-Lindau protein) interacts with MAP1LC3B via an LIR motif in its beta domain and ubiquitinates MAP1LC3B, thereby inhibiting LC3B-mediated autophagy. The L101A VHL mutant fails to interact with MAP1LC3B and fails to induce its ubiquitination. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis (L101A), western blotting in VHL-deficient and VHL-expressing RCC cell lines Cell death & disease Medium 30902965
2015 MAP1LC3B deficiency in mice leads to failure to upregulate autophagosome formation in dendritic cells upon RSV infection, resulting in IL-1β and IL-6 secretion and enhanced IL-17a-dependent lung pathology. Both hematopoietic and structural cell LC3B deficiency contribute to this phenotype, as shown by bone marrow chimeras. LC3b knockout mice, bone marrow chimeras, RSV infection model, cytokine measurements, in vitro DC assays Mucosal immunology Medium 25669150
2019 LC3B knockout mice show susceptibility to bleomycin-induced lung injury and fibrosis. LC3B knockdown sensitizes lung epithelial cells to bleomycin-induced apoptosis while its overexpression is protective. Cathepsin A was identified as a novel LC3B-binding partner; its overexpression drives lung epithelial cell apoptosis and it accumulates in aged LC3B-/- mice and IPF patient lungs. LC3B knockout mice, bleomycin lung fibrosis model, RNAi knockdown and overexpression in MLE12 cells, co-immunoprecipitation (cathepsin A binding), electron microscopy, proteasomal activity assay FASEB journal Medium 31431059
2020 MAP1LC3B has a non-autophagic function upstream of procaspase-8 cleavage that contributes to ER stress-induced apoptosis triggered by thapsigargin. ATF4 and CHOP independently regulate MAP1LC3B protein upregulation in this context, and this function is required for optimal cytotoxicity in prostate and colon cancer cells. RNAi knockdown, western blotting, caspase activity assays, propidium iodide staining for cell death, real-time RT-PCR in LNCaP and HCT116 cells Cell communication and signaling : CCS Medium 31987044
2025 HDAC6 physically interacts with MAP1LC3B and mediates its monoubiquitination, reducing MAP1LC3B protein levels and impairing autophagy. This promotes pathological cardiac hypertrophy. HDAC6 inhibition restores MAP1LC3B expression and autophagy, attenuating ISO-induced cardiac hypertrophy in mice. Co-immunoprecipitation, ubiquitination assay, HDAC6 overexpression and inhibition, ISO-induced cardiac hypertrophy mouse model, western blotting The Journal of pathology Medium 40212005
2022 Ectopic expression of SQSTM1 and its MAP1LC3B-binding domain (LIR domain) targeted to the mitochondrial outer membrane directly induces mitophagy (forced mitophagy), capable of degrading approximately half of mitochondria and their DNA in HeLa cells and mouse embryos without apparent effects on mitochondrial membrane potential, ROS, mitosis, or embryo development. Ectopic expression of mitochondria-targeted SQSTM1 LIR domain, flow cytometry, fluorescence microscopy, mitochondrial DNA quantification in HeLa cells and mouse embryos Autophagy Medium 35574946
2024 m6A RNA methylation of Map1lc3b mRNA, mediated by METTL3 (writer) and ALKBH5 (eraser), suppresses autophagic processes in Leydig cells exposed to BPA. Integrated transcriptomic and MeRIP-seq analysis identified Map1lc3b mRNA as a specific target of upregulated m6A modification induced by BPA. MeRIP-seq, RNA-seq integration, METTL3/ALKBH5 manipulation, in vivo and in vitro BPA exposure models, western blotting Journal of hazardous materials Medium 39662354
2025 MAP1LC3B functions as an RNA-binding protein in early embryos and mediates maternal mRNA decay during the maternal-to-zygotic transition (MZT). LC3B-mediated mRNA decay operates with faster kinetics than the classical BTG4-CCR4-NOT pathway. Knockdown of LC3B or autophagy inhibition delays maternal mRNA clearance, impairs zygotic genome activation, and causes developmental arrest. Maternal Suv39h2 mRNA was identified as a key LC3B target. RIP-seq, RNA-seq, CUT&Tag in early embryos, LC3B knockdown, autophagy inhibition, developmental assays Autophagy Medium 41231099
2023 IMP1 (IGF2BP1) colocalization with MAP1LC3B transcripts at homeostasis is reduced under stress. IMP1 deletion or mutation of IMP1 phosphorylation sites enhances MAP1LC3B expression at the protein level, promoting autophagy and intestinal stem cell regeneration. Single-molecule FISH, immunofluorescence, IMP1 knockout and phosphorylation-site mutant studies, organoid formation assay, in vivo irradiation regeneration model Cellular and molecular gastroenterology and hepatology Medium 38081361
2024 Protein ATG8ylation of MAP1LC3B (covalent conjugation to cellular proteins rather than lipids) requires E1-like ATG7 and E2-like ATG3, in common with lipid ATG8ylation, but is independent of the E3-like ATG12-ATG5-ATG16L1 complex (ATG5 knockout cells can still form ATG8ylated protein conjugates). ATG7 itself is identified as a target of MAP1LC3B ATG8ylation. CRISPR/Cas9 knockout cell lines (ATG5, ATG7, ATG3), deconjugation-resistant MAP1LC3B mutant (Q116P G120), western blotting, immunoprecipitation bioRxivpreprint Medium bio_10.1101_2024.07.03.601942
2025 MAP1LC3B undergoes CASM (conjugation of ATG8 to single membranes) at the Golgi apparatus in TRIM46-deficient cells. This non-degradative Golgi Atg8ylation mechanistically resembles CASM. Genetic inhibition of CASM in TRIM46-deficient cells exacerbates Golgi morphology defects, and knockdown of CASM genes impairs Golgi reformation after drug-induced fragmentation, demonstrating that CASM contributes to Golgi repair. TRIM46 knockout cells, CASM gene knockdown, immunofluorescence colocalization (LC3B/GABARAP with TGOLN2), drug-induced Golgi fragmentation assay, TFEB activation assays bioRxivpreprint Low bio_10.1101_2025.09.04.674289

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 The unfolded protein response protects human tumor cells during hypoxia through regulation of the autophagy genes MAP1LC3B and ATG5. The Journal of clinical investigation 682 20038797
2003 Post-translational modifications of three members of the human MAP1LC3 family and detection of a novel type of modification for MAP1LC3B. The Journal of biological chemistry 247 12740394
2004 Human light chain 3/MAP1LC3B is cleaved at its carboxyl-terminal Met121 to expose Gly120 for lipidation and targeting to autophagosomal membranes. The Journal of biological chemistry 219 15355958
2014 Hepatitis C virus core protein activates autophagy through EIF2AK3 and ATF6 UPR pathway-mediated MAP1LC3B and ATG12 expression. Autophagy 130 24589849
2020 Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components. Cell communication and signaling : CCS 101 31987044
2015 Deficiency of autophagy protein Map1-LC3b mediates IL-17-dependent lung pathology during respiratory viral infection via ER stress-associated IL-1. Mucosal immunology 74 25669150
2013 Progesterone receptor membrane component 1/Sigma-2 receptor associates with MAP1LC3B and promotes autophagy. Autophagy 64 24113030
2016 BAG3 regulates total MAP1LC3B protein levels through a translational but not transcriptional mechanism. Autophagy 29 26654586
2019 Ubiquitination of MAP1LC3B by pVHL is associated with autophagy and cell death in renal cell carcinoma. Cell death & disease 28 30902965
2015 Monitoring Autophagic Flux by Using Lysosomal Inhibitors and Western Blotting of Endogenous MAP1LC3B. Cold Spring Harbor protocols 28 26240408
2024 Mir221- and Mir222-enriched adsc-exosomes mitigate PM exposure-exacerbated cardiac ischemia-reperfusion injury through the modulation of the BNIP3-MAP1LC3B-BBC3/PUMA pathway. Autophagy 27 39245438
2015 MAP1LC3B overexpression protects against Hermansky-Pudlak syndrome type-1-induced defective autophagy in vitro. American journal of physiology. Lung cellular and molecular physiology 25 26719147
2009 Immunohistochemical expression of MAP1LC3A and MAP1LC3B protein in breast carcinoma tissues. Journal of clinical laboratory analysis 23 19623642
2018 A Rare Variant (rs933717) at FBXO31-MAP1LC3B in Chinese Is Associated With Systemic Lupus Erythematosus. Arthritis & rheumatology (Hoboken, N.J.) 21 29044928
2018 CRISPR/Cas9 Mediated GFP Knock-in at the MAP1LC3B Locus in 293FT Cells Is Better for Bona Fide Monitoring Cellular Autophagy. Biotechnology journal 20 29673078
2019 Susceptibility of microtubule-associated protein 1 light chain 3β (MAP1LC3B/LC3B) knockout mice to lung injury and fibrosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17 31431059
2021 Monitoring basal autophagy in the retina utilizing CAG-mRFP-EGFP-MAP1LC3B reporter mouse: technical and biological considerations. Autophagy 15 34674604
2021 miR-451-3p alleviates myocardial ischemia/reperfusion injury by inhibiting MAP1LC3B-mediated autophagy. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 13 34633468
2021 Ovarian Toxicity Induced by Aluminum Chloride: Alteration of Cyp19a1, Pcna, Puma, and Map1lc3b genes Expression. Toxicology 11 34958889
2022 Genome-Wide Identification and Functional Characterization Reveals the Pivotal Roles of BnaA8.ATG8F in Salt Stress Tolerance and Nitrogen Limitation Adaptation in Allotetraploid Rapeseed. International journal of molecular sciences 10 36232619
2018 Basal level of autophagy and MAP1LC3B-II as potential biomarkers for DHA-induced cytotoxicity in colorectal cancer cells. The FEBS journal 10 29723445
2024 m6A RNA methylation modulates autophagy by targeting Map1lc3b in bisphenol A induced Leydig cell dysfunction. Journal of hazardous materials 9 39662354
2015 Monitoring the Localization of MAP1LC3B by Indirect Immunofluorescence. Cold Spring Harbor protocols 8 26240409
2023 IGF2BP1/IMP1 Deletion Enhances a Facultative Stem Cell State via Regulation of MAP1LC3B. Cellular and molecular gastroenterology and hepatology 6 38081361
2023 ATG8f Interacts with Chilli Veinal Mottle Virus 6K2 Protein to Limit Virus Infection. Viruses 6 38140565
2020 Monitoring the autophagy-endolysosomal system using monomeric Keima-fused MAP1LC3B. PloS one 6 32511278
2025 Histone deacetylase 6 inhibition attenuates pathological cardiac hypertrophy by promoting autophagy through MAP1LC3B ubiquitination. The Journal of pathology 5 40212005
2022 SQSTM1 and its MAP1LC3B-binding domain induce forced mitophagy to degrade mitochondrial carryover during mitochondrial replacement therapy. Autophagy 4 35574946
2021 Combined Evaluation of MAP1LC3B and SQSTM1 for Biological and Clinical Significance in Ductal Carcinoma of Breast Cancer. Biomedicines 3 34829743
2025 HNRNPH1 promotes autophagy to inhibit the development of lung adenocarcinoma via the HSP90AB1/MAP1LC3B axis. Respiratory research 2 40468317
2025 Autophagy regulates the maternal-to-zygotic transition through MAP1LC3B-mediated maternal mRNA decay. Autophagy 1 41231099
2022 Association of CFH and MAP1LC3B gene polymorphisms with age-related macular degeneration in a high-altitude population. International journal of ophthalmology 1 36404982
2026 Urinary mRNA profiling of autophagy-related genes ATG5, ATG7, MAP1LC3B, and mTOR in non-muscle invasive bladder cancer (NMIBC). Cancer treatment and research communications 0 42044567

Missed literature

Know a paper Affinage missed for MAP1LC3B? Flag it for the maintainers and the community.

No submissions yet.