Affinage

MAP1S

Microtubule-associated protein 1S · UniProt Q66K74

Length
1059 aa
Mass
112.2 kDa
Annotated
2026-06-10
28 papers in source corpus 24 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAP1S is a microtubule-associated protein that couples the microtubule cytoskeleton to autophagy, mitochondrial quality control, and mitotic fidelity (PMID:15899810, PMID:21262964, PMID:17234756). It binds and accumulates on stabilized microtubules through a basic C-terminal microtubule-binding domain, while a distinct C-terminal sequence drives perinuclear mitochondrial aggregation and genome destruction upon overexpression (PMID:15899810); its N-terminus is required for anchoring to microtubule-organizing centers, and loss of MAP1S disrupts spindle architecture, tubulin nucleation, microtubule dynamics, and cytokinesis, producing premature sister-chromatid separation, lagging chromosomes, and multipolar spindles (PMID:17234756, PMID:25300793). In autophagy, MAP1S directly binds LC3 and recruits it to stable microtubules, and through its interaction with the mitochondria-associated protein LRPPRC it links autophagosomal biogenesis to clearance of defective mitochondria and other dysfunctional organelles (PMID:21262964). MAP1S thereby drives autophagic degradation of diverse substrates—p62-associated aggresomes, lipid droplets, fibronectin, mutant huntingtin aggregates, and MyD88—and its loss in mice causes accumulation of these cargoes, genome instability, liver and renal fibrosis, oxidative stress, and reduced lifespan (PMID:22037873, PMID:26701856, PMID:26750654, PMID:27236336, PMID:26540094, PMID:26565030). MAP1S protein stability is controlled by HDAC4, which destabilizes it via deacetylation; the polyamine spermidine depletes cytosolic HDAC4 to stabilize MAP1S and enhance autophagy, an effect genetically dependent on MAP1S (PMID:26540094, PMID:28386016). MAP1S also activates NRF2 by competing with KEAP1 for NRF2 binding through an ETGE motif and by accelerating p62-dependent autophagic degradation of KEAP1 (PMID:30873635). Its microtubule binding is further tuned by post-translational inputs, including CDKL5 phosphorylation at S786/S812 that governs dynein-mediated transport and tubulin tyrosination in neurons, and alpha-tubulin arginylation at E77 by ATE1 [PMID:bio_10.1101_2024.08.28.610038, PMID:39852692]. MAP1S interacts with RASSF1A to influence microtubule hyperstabilization and chemosensitivity (PMID:15753381, PMID:33442234).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2003 Low

    Established the existence of MAP1S as a MAP1A/MAP1B-homologous protein and a candidate cytoskeletal adaptor, answering what gene/protein this locus encodes.

    Evidence Yeast two-hybrid against VCY2, Northern blot, in situ hybridization

    PMID:14627543

    Open questions at the time
    • VCY2 interaction never functionally validated in mammalian cells
    • no demonstrated cytoskeletal function at this stage
  2. 2005 High

    Defined MAP1S as a genuine microtubule-binding protein with separable functional domains, resolving how it engages microtubules versus triggering organelle/genome destruction.

    Evidence In vitro microtubule binding with purified tubulin, deletion mutagenesis, immunofluorescence in mammalian cells

    PMID:15899810

    Open questions at the time
    • physiological trigger of MAGD phenotype unclear
    • domain boundaries not validated structurally
  3. 2005 Medium

    Connected MAP1S to RASSF1A-dependent microtubule hyperstabilization and to mitochondria/DNA through LRPPRC binding and intrinsic dsDNA binding, framing MAP1S as a hub linking cytoskeleton to mitochondria and genome.

    Evidence Coexpression colocalization assays; Co-IP with LRPPRC, DNA affinity chromatography, in vitro DNA binding

    PMID:15753381 PMID:15907802

    Open questions at the time
    • functional consequence of DNA binding not established (no DNase activity)
    • single-lab interaction data without reciprocal structural mapping
  4. 2007 High

    Demonstrated a required mitotic role for MAP1S, answering whether the protein is functionally needed at the spindle and MTOC rather than merely binding microtubules when overexpressed.

    Evidence siRNA knockdown, time-lapse microscopy, nocodazole washout, immunofluorescence

    PMID:17234756

    Open questions at the time
    • molecular mechanism of MTOC anchoring by the N-terminus undefined
    • link to tubulin nucleation machinery not resolved
  5. 2011 High

    Identified MAP1S as a positive regulator of autophagy via direct LC3 binding and LRPPRC/Parkin-linked mitophagy, establishing the autophagy axis that became its central characterized function.

    Evidence Co-IP, MAP1S knockout mice, immunofluorescence, nutritive-stress assays; in vivo DEN hepatocarcinoma model

    PMID:21262964 PMID:22037873

    Open questions at the time
    • how LC3 recruitment to microtubules couples to autophagosome maturation not mechanistically detailed
    • relationship between mitotic and autophagic roles unresolved
  6. 2014 Medium

    Extended MAP1S beyond mitosis and cancer into microtubule dynamics control, transcriptional induction during differentiation, and innate-immune/TLR signaling, broadening its functional scope.

    Evidence MT plus-end tracking and monopolar cytokinesis assays; PU.1 ChIP at the MAP1S promoter; TLR5/flagellin signaling and MyD88 autophagy assays with knockdown

    PMID:24466264 PMID:25043887 PMID:25300793

    Open questions at the time
    • mechanism linking MAP1S to global MT acetylation not defined
    • TLR/MyD88 pathway placement relies on knockdown epistasis in single labs
  7. 2015 High

    Identified HDAC4 as a regulator of MAP1S stability and MyD88 as a direct autophagic substrate, answering how MAP1S levels are controlled and how it executes selective cargo clearance.

    Evidence Co-IP defining HDAC4-binding domain, HBD overexpression rescue, autophagy flux and aggregate assays; Co-IP with MyD88, MAP1S KO macrophage phagocytosis and LC3 colocalization

    PMID:26540094 PMID:26565030

    Open questions at the time
    • how deacetylation destabilizes MAP1S mechanistically unclear
    • MyD88 interaction characterized in single lab
  8. 2016 High

    Established specific autophagic substrates (lipid droplets, fibronectin) whose accumulation drives organ fibrosis and shortened lifespan, linking MAP1S autophagy directly to disease-relevant pathology.

    Evidence MAP1S KD/overexpression and KO/LC3-transgenic mice, autophagy flux, substrate quantification, lifespan analysis

    PMID:26701856 PMID:26750654 PMID:27236336

    Open questions at the time
    • selectivity mechanism distinguishing these cargoes from others not defined
    • lysosomal degradation step mechanistically uncharacterized
  9. 2017 High

    Placed MAP1S downstream of the polyamine spermidine via HDAC4-dependent stabilization, providing a pharmacological lever on MAP1S-mediated autophagy and lifespan.

    Evidence Co-IP, MAP1S KO mice, spermidine treatment with genetic epistasis, autophagy flux assays

    PMID:28386016

    Open questions at the time
    • how spermidine depletes cytosolic HDAC4 not resolved
    • translational relevance beyond mouse liver unestablished
  10. 2019 High

    Resolved a dual mechanism by which MAP1S activates NRF2 — ETGE-mediated competition with KEAP1 and p62-dependent autophagic KEAP1 degradation — connecting MAP1S to antioxidant defense.

    Evidence Co-IP, competitive binding assays, autophagy assays, Nrf2/p62/double KO mice in CCl4 fibrosis model

    PMID:30873635

    Open questions at the time
    • relative contribution of the two parallel mechanisms not quantified
    • ETGE-KEAP1 interface not structurally mapped
  11. 2021 Medium

    Linked RASSF1A regulation of MAP1S to KEAP1-NRF2 inactivation and cisplatin chemosensitivity, tying the early RASSF1A interaction into the autophagy/NRF2 framework.

    Evidence Co-IP, overexpression/knockdown, autophagy assays, xenograft model

    PMID:33442234

    Open questions at the time
    • mechanism of RASSF1A regulation of MAP1S not defined
    • pathway placement partly inferred from prior studies
  12. 2024 Medium

    Identified a MAP1S/HDAC6/Smad axis whereby MAP1S-driven autophagic HDAC6 degradation increases MT acetylation and Smad nuclear translocation, implicating MAP1S in TGF-β signaling and HBV-driven HCC.

    Evidence MAP1S knockdown in vitro and in vivo, nuclear fractionation, Co-IP, tumor growth assays

    PMID:39374711

    Open questions at the time
    • HDAC6 as a direct autophagy substrate not biochemically confirmed
    • single-lab pathway epistasis
  13. 2025 Medium

    Defined post-translational control of MAP1S microtubule binding by CDKL5 phosphorylation, SRPK phosphorylation/CAPN10 proteolytic maturation, and alpha-tubulin E77 arginylation, explaining how MAP1S microtubule affinity and dynein-dependent transport are regulated developmentally.

    Evidence Phosphomutant knock-in mice with live imaging and TTL rescue (preprint); phosphoproteomics, in vitro kinase and processing assays (preprint); Ate1 KO cells, tubulinE77A, Map1s siRNA rescue, co-sedimentation

    PMID:39852692 PMID:bio_10.1101_2024.08.28.610038 PMID:bio_10.1101_2025.09.19.677315

    Open questions at the time
    • two of three studies are unreviewed preprints
    • integration of phosphorylation, proteolysis, and arginylation inputs not unified
    • structural basis of regulated MT binding unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MAP1S coordinates its distinct roles—mitotic spindle/MTOC function, selective autophagic cargo recognition, and NRF2/TGF-β signaling—into a single regulatory logic remains unresolved.
  • no high-resolution structure of MAP1S or its domain complexes
  • selectivity determinants for autophagic substrates undefined
  • no direct evidence linking the genome-instability/mitotic role to the autophagy role mechanistically

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 2 GO:0003677 DNA binding 1
Localization
GO:0005856 cytoskeleton 3 GO:0005739 mitochondrion 2 GO:0005815 microtubule organizing center 1 GO:0005829 cytosol 1
Pathway
R-HSA-9612973 Autophagy 4 R-HSA-1640170 Cell Cycle 2 R-HSA-168256 Immune System 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
CDKL5HDAC4KEAP1LC3LRPPRCMYD88NRF2RASSF1A

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 MAP1S (VCY2IP-1) was identified as a direct binding partner of VCY2 using yeast two-hybrid, showing homology to MAP1A/MAP1B and mapping to chromosome 19p13.11. The interaction suggests MAP1S links VCY2 to the cytoskeletal network. Yeast two-hybrid, Northern blot, in situ hybridization Biology of reproduction Low 14627543
2005 C19ORF5/MAP1S (also called MAP1S) specifically accumulates on paclitaxel-stabilized microtubules and interacts directly with paclitaxel-stabilized microtubules in vitro. A C-terminal 393-residue domain (C19ORF5C) mediates microtubule binding through a highly basic region of <100 residues. Accumulation of MAP1S on stabilized microtubules progressively induces perinuclear mitochondrial aggregation and genome destruction (MAGD), mediated by a distinct 25-residue sequence (F967-A991) separate from the microtubule-binding domain. Deletion mutagenesis defined these two functional domains. Recombinant protein overexpression in mammalian cells, in vitro microtubule binding assay, deletion mutagenesis, immunofluorescence Cancer research High 15899810
2005 C19ORF5/MAP1S interacts with RASSF1A and RASSF1C, and coexpression reveals that the unique N-terminal sequence of RASSF1C prevents it from hyperstabilizing microtubules, conferring specificity on RASSF1A for microtubule hyperstabilization and MAP1S accumulation on microtubules. Both RASSF1 isoforms share identical microtubule-association sequence domains. Coexpression in mammalian cells, colocalization, functional microtubule assays Cancer research Medium 15753381
2005 The C-terminus of MAP1S (C19ORF5C) interacts with the mitochondria-associated DNA-binding protein LRPPRC in liver cells. MAP1S itself binds double-stranded DNA through its microtubule-binding domain, with affinity sufficient for DNA affinity chromatography, but exhibits no intrinsic DNase activity. Co-immunoprecipitation, DNA affinity chromatography, deletion mutagenesis, in vitro DNA binding assay Biochemical and biophysical research communications Medium 15907802
2007 siRNA-mediated knockdown of MAP1S (C19ORF5) causes mitotic abnormalities including failure to form a stable metaphase plate, premature sister chromatid separation, lagging chromosomes, and multipolar spindles. MAP1S localizes to spindle microtubules and to microtubule-organizing centers during regrowth after nocodazole washout. Knockdown disrupts the MTOC and alters alpha- and gamma-tubulin localization and sites of nucleation. The N-terminus of MAP1S is essential for MTOC anchoring. siRNA knockdown, time-lapse video microscopy, immunofluorescence, nocodazole washout assay Cancer research High 17234756
2010 MAP1S binds prestin (SLC26A5) via the prestin STAS domain and the region connecting the heavy and light chain of MAP1S, identified by yeast two-hybrid and confirmed by reciprocal immunoprecipitation and FRET. Co-expression of prestin with MAP1S results in a 2.7-fold increase in voltage-evoked charge density and a 2.8-fold increase in prestin surface expression in transfected cells. Yeast two-hybrid, reciprocal co-immunoprecipitation, FRET, electrophysiology, surface expression quantification The Journal of biological chemistry High 20418376
2011 MAP1S isoforms interact with the autophagosome-associated protein LC3 and recruit it to stable microtubules in an isoform-dependent manner. MAP1S also interacts with the mitochondria-associated protein LRPPRC, which interacts with the mitophagy initiator Parkin. MAP1S knockout mice exhibit reduced Bcl-2/xL and P27 protein levels, accumulation of defective mitochondria, and severe defects in response to nutritive stress, indicating roles in autophagosomal biogenesis and clearance. Co-immunoprecipitation, MAP1S knockout mice, immunofluorescence, cellular stress assays The Journal of biological chemistry High 21262964
2011 Elevation of MAP1S levels in mouse liver in response to diethylnitrosamine-induced or genome instability-driven metabolic stress enhances autophagy to remove p62-associated aggresomes and dysfunctional organelles, thereby reducing DNA double-strand breaks, genome instability, and suppressing hepatocarcinogenesis. MAP1S KO and overexpression mouse models, diethylnitrosamine-induced hepatocarcinoma model, genome stability assays, autophagy flux measurements Cancer research High 22037873
2012 MAP1S (MAP8) interacts with nemitin, a novel LisH/WD40 repeat protein enriched in the nervous system. Co-expression of nemitin with MAP1S results in nemitin redistributing from a diffuse cytosolic pattern to decorating microtubules uniformly, indicating MAP1S mediates nemitin's association with microtubules. Co-expression in non-neuronal cells, immunofluorescence, co-IP PloS one Medium 22523538
2014 MAP1S knockdown alters microtubule dynamics throughout the cell cycle, resulting in faster-growing but short-lived microtubules and a global loss of microtubule acetylation. MAP1S guides MT-dependent initiation of cytokinesis as shown in monopolar cytokinesis assays. siRNA knockdown, quantitative MT plus-end tracking, monopolar cytokinesis assay, immunofluorescence Journal of cell science High 25300793
2014 PU.1 transcription factor binds the MAP1S promoter and induces MAP1S expression during neutrophil/APL differentiation. Inhibiting MAP1S in this context results in aberrant neutrophil differentiation and impaired autophagy. ChIP assay (PU.1 binding to MAP1S promoter), siRNA knockdown, differentiation assays, autophagy assays Leukemia research Medium 25043887
2014 MAP1S regulates TLR5/flagellin signaling in breast cancer cells by enhancing NF-κB activity and cytokine secretion. MAP1S knockdown abolishes flagellin-mediated tumor growth suppression and migration inhibition. MAP1S also mediates degradation of MyD88 via autophagy upon TLR activation. siRNA knockdown, tumor growth assays, cytokine measurements, NF-κB reporter assays PloS one Medium 24466264
2015 MAP1S interacts with HDAC4 via a defined HDAC4-binding domain (HBD) on MAP1S. HDAC4 destabilizes MAP1S by increasing its deacetylation, suppresses autophagy flux, and promotes accumulation of mutant huntingtin aggregates. Suppression of HDAC4 or overexpression of the MAP1S HBD stabilizes MAP1S, activates autophagy flux, and clears mHTT aggregates. Co-immunoprecipitation, siRNA knockdown, overexpression of HBD domain, autophagy flux assays, aggregate quantification Aging High 26540094
2015 MAP1S interacts directly with MyD88 upon TLR activation and affects the TLR signaling pathway. MAP1S-deficient macrophages are impaired in bacterial phagocytosis. Upon TLR activation, MyD88 participates in autophagy processing in a MAP1S-dependent manner by co-localizing with LC3. Co-immunoprecipitation, MAP1S KO macrophages, phagocytosis assays, co-localization with LC3 The Journal of biological chemistry Medium 26565030
2016 MAP1S promotes autophagic clearance of lipid droplets (coated by ADFP) in renal cells. Suppression of MAP1S impairs autophagic clearance, while overexpression activates autophagy flux and reduces lipid droplets and associated DNA double-strand breaks. MAP1S KD/overexpression, autophagy flux assays, lipid droplet quantification, DNA damage assays Oncotarget Medium 26701856
2016 MAP1S-mediated autophagy is required for lysosomal degradation of fibronectin. In MAP1S-deficient mice, LC3-driven synthesis of fibronectin accumulates because MAP1S depletion impairs lysosomal degradation, causing liver fibrosis, oxidative stress, and lifespan reduction. MAP1S KO mice, LC3 transgenic mice, Western blot, autophagy flux assays, fibronectin quantification, lifespan analysis Aging cell High 26750654 27236336
2017 MAP1S interacts with LC3 and positively regulates autophagy flux. MAP1S stability is regulated by HDAC4, which destabilizes it. Spermidine depletes cytosolic HDAC4, thereby stabilizing MAP1S and enhancing autophagy. MAP1S-deficient mice show reduced lifespan and develop liver fibrosis and HCC; spermidine's lifespan extension and liver protection are dependent on MAP1S-mediated autophagy. Co-immunoprecipitation, MAP1S KO mice, spermidine treatment, genetic epistasis (MAP1S KO abolishes spermidine effects), autophagy flux assays Cancer research High 28386016
2019 MAP1S activates NRF2 signaling through two parallel mechanisms: (1) MAP1S competes with KEAP1 for NRF2 binding via an ETGE motif present on MAP1S, stabilizing NRF2; (2) MAP1S accelerates p62-dependent autophagic degradation of KEAP1. Both mechanisms result in NRF2 stabilization. Spermidine-mediated liver protection requires both NRF2 and p62-dependent autophagy pathways. Co-immunoprecipitation, competitive binding assays, autophagy assays, Nrf2 KO / p62 KO / double KO mouse models with CCl4-induced liver fibrosis Hepatology High 30873635
2021 RASSF1A interacts with MAP1S (confirmed by Co-IP) and regulates MAP1S to inactivate the Keap1-Nrf2 pathway, thereby activating autophagy and enhancing chemosensitivity to cisplatin in NSCLC cells. Co-immunoprecipitation, overexpression/knockdown, autophagy assays (LC3 puncta, Western blot), xenograft model Drug design, development and therapy Medium 33442234
2024 MAP1S promotes degradation of HDAC6 via autophagy, leading to increased microtubule acetylation and nuclear translocation of the Smad complex, thereby enhancing downstream TGF-β signaling. HBV X protein upregulates MAP1S to establish a MAP1S/Smad/TGF-β1 feedback loop promoting HCC proliferation and migration. MAP1S knockdown in vitro and in vivo, Western blot, nuclear fractionation, Co-IP, tumor growth assays International journal of biological macromolecules Medium 39374711
2025 CDKL5 phosphorylates MAP1S at S786 and S812, regulating MAP1S binding to microtubules. MAP1S phosphomutant (S786/812A) mice show severely reduced dynein binding to microtubules, impaired dynein motility in neurons, reduced delivery of AMPA receptors in dendrites, reduced tubulin tyrosination, decreased spine density and synapses, and behavioral deficits. Expression of tubulin tyrosine kinase TTL rescues dynein motility defects, placing MAP1S phosphorylation upstream of tubulin tyrosination and dynein-mediated transport. MAP1S phosphomutant knock-in mice, microtubule co-sedimentation assay, time-lapse live imaging in neurons, dendritic cargo tracking, TTL rescue experiment, behavioral phenotyping bioRxivpreprint Medium bio_10.1101_2024.08.28.610038
2025 SRPK directly phosphorylates MAP1S at multiple sites in a C-terminal region involved in proteolytic maturation and microtubule binding. SRPK-dependent MAP1S phosphorylation modulates the affinity of the MAP1S microtubule-binding domain for microtubules and MAP1S proteolytic processing by the Calpain-10 (CAPN10) protease. MAP1S proteolytic processing occurs progressively during neurodevelopment via a specific CAPN10 expression switch, corresponding with MAP1S acquisition of microtubule binding activity. Global phosphoproteomic screening, in vitro kinase assay, microtubule binding assays, proteolytic processing assays, developmental expression analysis bioRxivpreprint Medium bio_10.1101_2025.09.19.677315
2025 Alpha-tubulin is arginylated at E77 by ATE1, and loss of this arginylation (Ate1-/- cells or tubulinE77A overexpression) increases the fraction of MAP1S associated with microtubules. MAP1S knockdown rescues the reduced microtubule growth rate and increased stability seen in Ate1-/- cells to wild-type levels, demonstrating that E77 arginylation directly regulates MAP1S microtubule binding and thereby controls microtubule dynamics. Ate1 KO cells, alpha-tubulinE77A overexpression, Map1s siRNA knockdown, microtubule co-sedimentation, live-cell MT dynamics imaging The Journal of cell biology High 39852692

Source papers

Stage 0 corpus · 28 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Spermidine Prolongs Lifespan and Prevents Liver Fibrosis and Hepatocellular Carcinoma by Activating MAP1S-Mediated Autophagy. Cancer research 153 28386016
2011 Microtubule-associated protein 1S (MAP1S) bridges autophagic components with microtubules and mitochondria to affect autophagosomal biogenesis and degradation. The Journal of biological chemistry 93 21262964
2019 Spermidine Confers Liver Protection by Enhancing NRF2 Signaling Through a MAP1S-Mediated Noncanonical Mechanism. Hepatology (Baltimore, Md.) 63 30873635
2011 Autophagy enhanced by microtubule- and mitochondrion-associated MAP1S suppresses genome instability and hepatocarcinogenesis. Cancer research 53 22037873
2005 Specificity of the methylation-suppressed A isoform of candidate tumor suppressor RASSF1 for microtubule hyperstabilization is determined by cell death inducer C19ORF5. Cancer research 51 15753381
2005 Distinct structural domains within C19ORF5 support association with stabilized microtubules and mitochondrial aggregation and genome destruction. Cancer research 50 15899810
2016 Fast clearance of lipid droplets through MAP1S-activated autophagy suppresses clear cell renal cell carcinomas and promotes patient survival. Oncotarget 45 26701856
2007 Depletion of the Ras association domain family 1, isoform A-associated novel microtubule-associated protein, C19ORF5/MAP1S, causes mitotic abnormalities. Cancer research 42 17234756
2012 MAP1S enhances autophagy to suppress tumorigenesis. Autophagy 37 22301994
2003 Identification and characterization of human VCY2-interacting protein: VCY2IP-1, a microtubule-associated protein-like protein. Biology of reproduction 35 14627543
2015 Blocking the association of HDAC4 with MAP1S accelerates autophagy clearance of mutant Huntingtin. Aging 27 26540094
2014 MAP1S controls breast cancer cell TLR5 signaling pathway and promotes TLR5 signaling-based tumor suppression. PloS one 27 24466264
2016 Defects in MAP1S-mediated autophagy turnover of fibronectin cause renal fibrosis. Aging 26 27236336
2016 Defects in MAP1S-mediated autophagy cause reduction in mouse lifespans especially when fibronectin is overexpressed. Aging cell 23 26750654
2005 Putative tumor suppressor RASSF1 interactive protein and cell death inducer C19ORF5 is a DNA binding protein. Biochemical and biophysical research communications 23 15907802
2010 Prestin surface expression and activity are augmented by interaction with MAP1S, a microtubule-associated protein. The Journal of biological chemistry 21 20418376
2015 MAP1S Protein Regulates the Phagocytosis of Bacteria and Toll-like Receptor (TLR) Signaling. The Journal of biological chemistry 18 26565030
2014 MAP1S controls microtubule stability throughout the cell cycle in human cells. Journal of cell science 17 25300793
2023 Spermidine suppresses the activation of hepatic stellate cells to cure liver fibrosis through autophagy activator MAP1S. Liver international : official journal of the International Association for the Study of the Liver 16 36892418
2019 Overexpression of microRNA-216a inhibits autophagy by targeting regulated MAP1S in colorectal cancer. OncoTargets and therapy 16 31354295
2014 Induction of the autophagy-associated gene MAP1S via PU.1 supports APL differentiation. Leukemia research 16 25043887
2012 Nemitin, a novel Map8/Map1s interacting protein with Wd40 repeats. PloS one 14 22523538
2021 RASSF1A Enhances Chemosensitivity of NSCLC Cells Through Activating Autophagy by Regulating MAP1S to Inactivate Keap1-Nrf2 Pathway. Drug design, development and therapy 10 33442234
2015 Transforming Growth Factor TGFβ Increases Levels of Microtubule-Associated Protein MAP1S and Autophagy Flux in Pancreatic Ductal Adenocarcinomas. PloS one 10 26571030
2020 Production and characterization of a monoclonal antibody against the sialidase of Gardnerella vaginalis using a synthetic peptide in a MAP8 format. Applied microbiology and biotechnology 7 32462244
2024 HBx-induced upregulation of MAP1S drives hepatocellular carcinoma proliferation and migration via MAP1S/Smad/TGF-β1 loop. International journal of biological macromolecules 4 39374711
2025 Arginylation of ⍺-tubulin at E77 regulates microtubule dynamics via MAP1S. The Journal of cell biology 3 39852692
2026 A mechanistic study revealing that SLCO1B3 promotes gastric cancer development and metastasis through MAP1S expression downregulation. BMC cancer 0 41906106

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