Affinage

LMAN2

Vesicular integral-membrane protein VIP36 · UniProt Q12907

Length
356 aa
Mass
40.2 kDa
Annotated
2026-06-10
27 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LMAN2 (VIP36) is a type I transmembrane L-type lectin of the early secretory pathway that recognizes high-mannose N-glycans and recycles glycoprotein cargo between the Golgi and the ER as part of post-ER quality control (PMID:8157011, PMID:10406849, PMID:20477988). Its luminal carbohydrate recognition domain is a 17-stranded antiparallel beta-sandwich that coordinates Ca²⁺ through Asp131, Asn166, and His190 and engages the α1,2-linked D1 trimannose arm of Man7-9GlcNAc2 oligosaccharides through extensive hydrogen bonding by eight residues (PMID:17652092). Binding is D1-arm-specific with a bell-shaped pH optimum near 6.5, a property that favors cargo capture in the acidic cis-Golgi and release at the higher pH of the ER; a single amino acid difference distinguishes this narrow specificity from the broader high-mannose binding of the related lectin ERGIC-53 (PMID:16129679, PMID:18025080, PMID:24498414). Through this glycan-dependent recognition LMAN2 captures clients including alpha1-antitrypsin, the receptor guanylyl cyclase GC-C, and alpha-amylase, and silencing LMAN2 accelerates alpha1-antitrypsin transport, consistent with a retrograde Golgi-to-ER recycling role rather than an anterograde one (PMID:15070860, PMID:20477988, PMID:23269669). The lectin also localizes apically in polarized epithelial cells where its carbohydrate activity is required for apical transport and secretion of high-mannose glycoproteins, and it restricts exosome cargo GPRC5B exit from the Golgi by interfering with GGA1-mediated transport (PMID:11872745, PMID:27765817). Beyond the secretory pathway, LMAN2 reaches the cell surface where it undergoes ADAM-type ectodomain shedding followed by gamma-secretase-mediated intramembrane proteolysis governed by C-terminal transmembrane residues, with surface levels controlling macrophage phagocytosis (PMID:22016386, PMID:38219489). LMAN2 additionally functions as an auxiliary regulator of Kv1.2 potassium channels, producing a depolarizing shift in activation voltage through the intracellular S2-S3 linker (residues F251/T252) and competing with the Slc7a5 transporter for the channel voltage-sensing domain (PMID:39264045, PMID:39659243).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1994 Medium

    Establishing the existence and trafficking itinerary of VIP36 was the first step, framing it as a membrane protein of the Golgi-to-cell-surface route with lectin homology.

    Evidence Biochemical purification from MDCK raft fractions, cDNA cloning, and imaging of transiently expressed protein

    PMID:8157011

    Open questions at the time
    • Overexpression localization may not reflect endogenous steady state
    • No glycan ligand defined
    • No functional cargo identified
  2. 1996 Medium

    Demonstrating Ca²⁺-dependent, sugar-competable binding confirmed VIP36 is a functional lectin rather than merely a lectin-homologous protein.

    Evidence Recombinant luminal domain Ca²⁺ and membrane-binding assays with GalNAc inhibition and glycopeptide affinity chromatography

    PMID:8834812

    Open questions at the time
    • GalNAc-based specificity later revised toward high-mannose glycans
    • Physiological ligand not yet defined
    • No structural basis for binding
  3. 1999 High

    Localizing the endogenous protein to the ERGIC and defining its high-mannose D1-arm specificity established VIP36 as a recycling early-secretory-pathway lectin with a pH-tuned binding profile.

    Evidence Confocal microscopy with brefeldin A and ERGIC-53/coatomer co-localization; SPR and inhibition with defined glycans

    PMID:10406849 PMID:10444376

    Open questions at the time
    • Direction of cargo flow (anterograde vs retrograde) not resolved
    • Endogenous cargo not identified
    • Ca²⁺ dependence reported inconsistently between binding studies
  4. 2002 Medium

    Functional mutagenesis showed lectin activity is required for apical glycoprotein transport, assigning VIP36 a sorting role in polarized cells.

    Evidence Wild-type and lectin-dead VIP36 expression in polarized MDCK cells with apical/basolateral cargo distribution and secretion readouts

    PMID:11872745

    Open questions at the time
    • Mechanism of apical sorting not defined
    • Generality beyond MDCK unclear
    • Conflicts with later retrograde quality-control model
  5. 2003 Medium

    Tissue localization to secretory granules of parotid acinar cells, and glycan-dependent co-precipitation with alpha-amylase, identified a physiological client engaged through high-mannose glycans.

    Evidence Immunoelectron microscopy of rat parotid gland and co-IP with endo H sensitivity

    PMID:12871987 PMID:15070860

    Open questions at the time
    • Functional consequence for amylase secretion not tested
    • Single tissue system
    • Direct vs indirect association not fully separated
  6. 2005 High

    Defining the bell-shaped pH dependence of D1-trimannose binding provided a physical model for cargo capture in the cis-Golgi and release in the ER, framing a quality-control cycle.

    Evidence Frontal affinity chromatography of recombinant CRD against a pyridylaminated oligosaccharide library

    PMID:16129679

    Open questions at the time
    • Direct demonstration of pH-driven cargo release in cells not shown
    • Cargo set still limited
  7. 2007 High

    Crystal structures and comparative FAC/mutagenesis defined the atomic basis of Ca²⁺-dependent D1-arm recognition and showed how single residues tune specificity across the VIP36/VIPL/ERGIC-53 lectin family.

    Evidence X-ray structures of apo, Ca²⁺-bound, and ligand-bound luminal domain; FAC with structure-guided point mutagenesis

    PMID:17652092 PMID:18025080

    Open questions at the time
    • Structures do not capture cargo glycoprotein engagement
    • pH-dependent conformational switch not visualized
  8. 2007 Medium

    Identifying a stable, carbohydrate-independent interaction with the ER chaperone BiP linked VIP36 to a non-canonical quality-control function beyond its lectin activity.

    Evidence Crosslinking, reciprocal co-IP with LC/MS/MS, immunoelectron microscopy, and SPR with lectin-dead control

    PMID:17586539

    Open questions at the time
    • Functional consequence of BiP binding not established
    • Stoichiometry and cellular context unclear
    • Single lab
  9. 2010 High

    Identifying alpha1-antitrypsin as a glycan-dependent client and showing that knockdown accelerates its transport resolved the trafficking direction, establishing VIP36 as a post-ER retrograde quality-control receptor.

    Evidence BiFC screen of human liver cDNA, glycosylation-site mutants, kifunensine treatment, and siRNA transport kinetics

    PMID:20477988

    Open questions at the time
    • Quantitative contribution to ER retention not measured
    • Reconciliation with apical anterograde role incomplete
  10. 2012 Medium

    Discovery of cell-surface ectodomain shedding controlling macrophage phagocytosis revealed a functional role for VIP36 outside the secretory pathway.

    Evidence Proteomic screen of macrophage conditioned media with surface shedding assay and gain/loss-of-function phagocytosis readout

    PMID:22016386

    Open questions at the time
    • Sheddase identity not pinned down here
    • Mechanism linking surface levels to phagocytosis unclear
    • Single lab
  11. 2012 Medium

    Identifying the receptor guanylyl cyclase GC-C as a glycosylation-dependent client extended the client repertoire to a signaling receptor whose folding correlates with VIP36 binding.

    Evidence Co-IP with systematic mutagenesis of ten GC-C glycosylation sites and glycosylation inhibition

    PMID:23269669

    Open questions at the time
    • Direct vs glycan-bridged interaction not fully separated
    • Effect on GC-C trafficking not quantified
  12. 2014 High

    Structural comparison of the ERGIC-53/MCFD2 complex with VIP36 pinpointed a single Asp-to-Gly substitution as the determinant of their divergent glycan specificities.

    Evidence X-ray crystallography of ERGIC-53 CRD/MCFD2/mannotriose complex with structural comparison

    PMID:24498414

    Open questions at the time
    • No bound MCFD2-equivalent partner for VIP36 identified
    • Functional consequence of pocket depth in cells not tested
  13. 2016 Medium

    Showing that LMAN2 retains GPRC5B in the Golgi and restricts its exosomal exit via GGA1 placed the lectin in a pathway controlling cargo partitioning into the exosomal route.

    Evidence Inducible GPRC5B expression, LMAN2 knockdown, trafficking and co-localization assays with GGA1 analysis

    PMID:27765817

    Open questions at the time
    • Direct LMAN2-GPRC5B interaction not defined
    • Mechanism of GGA1 interference unclear
    • Single lab
  14. 2024 Medium

    Electrophysiology defined a previously unknown role for LMAN2 as a Kv1.2 auxiliary regulator, shifting activation voltage through the S2-S3 linker and competing with Slc7a5 at the voltage-sensing domain.

    Evidence Patch-clamp in CHO and L(tk-) cells, shRNA knockdown, Kv1.2 point mutations (F251/T252) and Kv1.2:1.5 chimeras with Slc7a5 co-expression

    PMID:39264045 PMID:39659243

    Open questions at the time
    • Whether regulation requires lectin activity unknown
    • Physiological setting and stoichiometry undefined
    • Single lab
  15. 2024 Medium

    Mapping gamma-secretase-mediated intramembrane proteolysis to specific C-terminal transmembrane residues extended the surface-shedding pathway into regulated intramembrane proteolysis.

    Evidence Substitution mutagenesis of TMD C-terminal residues with gamma-secretase processing assay and VIPL comparison

    PMID:38219489

    Open questions at the time
    • Fate and function of released intracellular fragment unknown
    • Physiological trigger for RIP unclear
  16. 2024 Low

    A reported interaction with MAPK9 (JNK2) tied LMAN2 to MAPK-driven cisplatin resistance in breast cancer, an emerging disease-context role.

    Evidence Co-IP, co-localization, siRNA knockdown and xenograft cisplatin sensitivity

    PMID:39618331

    Open questions at the time
    • Single Co-IP without reciprocal validation
    • Pathway activation inferred from downstream markers only
    • Direct vs indirect interaction unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how LMAN2's glycan-recognition activity mechanistically relates to its non-lectin functions at the cell surface (shedding/RIP, phagocytosis) and at ion channels (Kv1.2 regulation).
  • Whether channel regulation and surface functions require the CRD is untested
  • No integrated model linking secretory and plasma-membrane roles
  • Native interactomes for non-glycan partners not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005794 Golgi apparatus 4 GO:0005783 endoplasmic reticulum 3 GO:0005886 plasma membrane 3
Pathway
R-HSA-9609507 Protein localization 3 R-HSA-392499 Metabolism of proteins 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
AMY1GPRC5BGUCY2CHSPA5KCNA2MAPK9SERPINA1SLC7A5

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 VIP36 (LMAN2) was purified from CHAPS-insoluble (glycolipid raft) fractions of MDCK cells and its cDNA was isolated; the N-terminal 31 kDa luminal domain shows homology to leguminous plant lectins. Transiently expressed VIP36 localizes to the Golgi apparatus, endosomal/vesicular structures, and the plasma membrane, consistent with a role in Golgi-to-cell-surface transport. Biochemical purification, cDNA cloning, immunofluorescence/subcellular localization of transiently expressed protein The EMBO journal Medium 8157011
1996 The recombinant luminal/exoplasmic domain of VIP36 binds Ca2+ and can decorate internal membrane structures of MDCK cells in vitro; this binding requires Ca2+ and is specifically inhibited by N-acetyl-D-galactosamine. Glycopeptides from galactose-labeled cells bind to VIP36 and can be eluted with N-acetyl-D-galactosamine, demonstrating lectin activity. Recombinant protein production, Ca2+ binding assay, in vitro membrane-binding assay, affinity chromatography with competitive inhibition Journal of cell science Medium 8834812
1999 Endogenous VIP36 localizes to the Golgi apparatus and the early secretory pathway (ER-Golgi intermediate compartment) of MDCK and Vero cells; it co-localizes with coatomer and ERGIC-53 and cycles in the early secretory pathway as shown by brefeldin A treatment and co-localization with anterograde cargo. High-resolution confocal microscopy, brefeldin A treatment, co-localization with marker proteins (endogenous protein) Journal of cell science Medium 10444376
1999 VIP36 specifically recognizes high-mannose type glycans containing alpha1→2 mannosyl residues (Man7-9GlcNAc2) in a pH-optimum of 6.0; the interaction is Ca2+-independent and has an association constant of ~2.1×10^8 M^-1 with thyroglobulin glycans as measured by surface plasmon resonance. GST-fusion protein binding assay, inhibition studies with specific glycans, surface plasmon resonance biosensor Glycobiology High 10406849
2002 VIP36 is localized to the apical membrane of polarized MDCK cells (apical/basolateral ratio ~2); overexpression of wild-type VIP36 increased apical transport and secretion of VIP36-recognized (high-mannose) glycoproteins (including clusterin), while a lectin-inactive mutant had no effect on glycoprotein distribution and inhibited secretion, demonstrating that VIP36 lectin activity is required for apical glycoprotein transport. VIP36 overexpression and lectin-dead mutant expression in polarized MDCK cells, measurement of apical/basolateral distribution and secretion rates The Journal of biological chemistry Medium 11872745
2003 Endogenous VIP36 localizes to the trans-Golgi network, immature secretory granules, and mature secretory granules in rat parotid acinar cells, co-localizing with alpha-amylase in apical regions, indicating a post-Golgi secretory pathway role. Immunoelectron microscopy and double-staining immunofluorescence of rat parotid gland tissue (endogenous protein) The journal of histochemistry and cytochemistry Medium 12871987
2004 VIP36 physically associates with alpha-amylase in parotid secretory vesicles via high-mannose type glycans; co-precipitation of alpha-amylase with VIP36 was abolished by endo H treatment (removing high-mannose glycans), and alpha-amylase in secretory vesicles carries high-mannose glycans. Subcellular fractionation (Percoll gradient), immunoelectron microscopy, co-immunoprecipitation with endo H treatment Glycobiology Medium 15070860
2005 The carbohydrate recognition domain (CRD) of VIP36 selectively binds the deglucosylated trimannose of the D1 branch of high-mannose oligosaccharides with bell-shaped pH dependence (optimum ~6.5), consistent with binding in the cis-Golgi and releasing cargo in the ER (higher pH), suggesting a role in glycoprotein quality control. Frontal affinity chromatography (FAC) with pyridylaminated sugar library (21 oligosaccharides), recombinant CRD The Journal of biological chemistry High 16129679
2007 Crystal structures of VIP36 luminal domain (CRD + stalk) in apo, Ca2+-bound, and mannosyl ligand-bound forms reveal a 17-stranded antiparallel beta-sandwich CRD; Ca2+ coordinates Asp131, Asn166, and His190 to enable carbohydrate binding; Man-α1,2-Man-α1,2-Man (D1 arm) is recognized by eight residues via extensive hydrogen bonds, explaining Ca2+-dependent and D1-arm-specific high-mannose glycoprotein recognition. X-ray crystallography of apo, Ca2+, and ligand-bound forms; structure-guided interpretation of substrate specificity The Journal of biological chemistry High 17652092
2007 Frontal affinity chromatography comparing ERGIC-53, VIPL, and VIP36 CRDs showed that VIPL and VIP36 selectively bind deglucosylated trimannose of the D1 branch but with different pH dependence, while ERGIC-53 binds high-mannose oligosaccharides broadly. Structure-based mutagenesis showed that sugar-binding properties of these lectins can be switched by single amino acid substitutions. Frontal affinity chromatography with pyridylaminated sugar library; structure-based site-directed mutagenesis The Journal of biological chemistry High 18025080
2007 VIP36 stably interacts with the ER chaperone BiP in an ATP-independent and carbohydrate-independent manner dependent on divalent cations; the interaction occurs in the ER (confirmed by immunoelectron microscopy) and is distinct from canonical chaperone-substrate interactions, suggesting a novel role for VIP36 in quality control of secretory proteins. Chemical crosslinking, co-immunoprecipitation, LC/MS/MS identification, immunoelectron microscopy, surface plasmon resonance with recombinant proteins; lectin-dead mutant used as control Glycobiology Medium 17586539
2010 VIP36 interacts with alpha1-antitrypsin (alpha1-AT) specifically via its high-mannose glycans in Golgi and ER compartments (not the complex glycoform); silencing VIP36 accelerated alpha1-AT transport, arguing against an anterograde role and consistent with a post-ER quality control function where VIP36 recycles alpha1-AT from Golgi back to ER. YFP fragment complementation (bimolecular fluorescence complementation) screen of human liver cDNA library, mutagenesis of glycosylation sites, kifunensine treatment, VIP36 siRNA knockdown with transport kinetics Traffic (Copenhagen, Denmark) High 20477988
2011 VIP36 is a target of ectodomain shedding on the cell surface (not in the Golgi/ER) in macrophages; the amount of VIP36 at the cell surface precisely regulates phagocytosis, and shedding of VIP36 is required for this regulation of phagocytic activity. Unbiased proteomic screening (LPS-stimulated macrophage conditioned media), cell surface shedding assay, VIP36 manipulation (overexpression/knockdown) with phagocytosis readout The Journal of biological chemistry Medium 22016386
2012 VIP36 interacts with the receptor guanylyl cyclase GC-C; this interaction depends on glycosylation at specific sites that also allow GC-C to fold properly and bind ligand, identifying GC-C as the first receptor client of VIP36. Co-immunoprecipitation, mutagenesis of 10 glycosylation sites in GC-C, pharmacological inhibition of glycosylation The Journal of biological chemistry Medium 23269669
2014 Crystal structure of ERGIC-53 CRD in complex with MCFD2 and α1,2-mannotriose revealed a shallower sugar-binding pocket in ERGIC-53 compared to VIP36 due to a single Asp-to-Gly substitution; this structural difference explains the broader sugar specificity of ERGIC-53 versus the D1-arm-specific binding of VIP36. X-ray crystallography of ERGIC-53 CRD/MCFD2/mannotriose complex; structural comparison with VIP36 PloS one High 24498414
2016 LMAN2 (VIP36) is specifically required for the accumulation of the exosome cargo protein GPRC5B in the Golgi complex and restricts its transport along the exosomal pathway; LMAN2 may interfere with GGA1-mediated trans-Golgi network-to-endosome transport of GPRC5B. Inducible expression system for GPRC5B, LMAN2 knockdown, trafficking assay, co-localization, analysis of GGA1-mediated transport The Journal of biological chemistry Medium 27765817
2024 LMAN2 co-expression with Kv1.2 causes a large depolarizing shift in channel activation voltage and deceleration of activation kinetics; shRNA knockdown of endogenous LMAN2 reduces Kv1.2 redox sensitivity and gating variability. Kv1.2 sensitivity to LMAN2 requires residues F251 and T252 in the intracellular S2-S3 linker, which also mediate redox-dependent gating, suggesting LMAN2 acts through the same pathway as extracellular redox modulation. Patch-clamp electrophysiology in CHO and L(tk-) cell lines, shRNA knockdown of endogenous LMAN2, Kv1.2 point mutations (F251, T252), functional screening of 52 candidate genes Function (Oxford, England) Medium 39264045
2024 LMAN2 and the amino acid transporter Slc7a5 competitively modulate Kv1.2 gating in opposite directions; co-expression of both produces bimodal voltage-dependence suggesting two non-overlapping channel populations. Using Kv1.2:1.5 chimeras, distinct regions in S1-S3 of the voltage-sensing domain are required for LMAN2 versus Slc7a5 sensitivity, confirming that the two regulators compete for interaction with the Kv1.2 voltage sensor. Patch-clamp electrophysiology, Kv1.2:Kv1.5 chimeric channel approach, co-expression of LMAN2 and Slc7a5 FASEB journal Medium 39659243
2024 VIP36 (LMAN2) is susceptible to ectodomain shedding followed by gamma-secretase-mediated intramembrane proteolysis (regulated intramembrane proteolysis, RIP); the C-terminal amino acids of its transmembrane domain regulate gamma-secretase susceptibility, as shown by substitution mutant analysis. VIPL, the close homolog, has different gamma-secretase susceptibility despite similar shedding. Substitution mutagenesis of transmembrane domain C-terminal residues, gamma-secretase processing assay, comparison with VIPL mutants Biochemical and biophysical research communications Medium 38219489
2024 LMAN2 physically interacts with MAPK9 (JNK2) in breast cancer cells and activates the MAPK signaling pathway, promoting cisplatin resistance; knockdown of LMAN2 reduced MAPK pathway activation and sensitized drug-resistant cells to cisplatin in vivo. Co-immunoprecipitation, immunofluorescence co-localization, siRNA knockdown, tumor xenograft model Cancer medicine Low 39618331

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 VIP36, a novel component of glycolipid rafts and exocytic carrier vesicles in epithelial cells. The EMBO journal 200 8157011
2007 Molecular basis of sugar recognition by the human L-type lectins ERGIC-53, VIPL, and VIP36. The Journal of biological chemistry 121 18025080
1999 VIP36 localisation to the early secretory pathway. Journal of cell science 91 10444376
2002 Involvement of VIP36 in intracellular transport and secretion of glycoproteins in polarized Madin-Darby canine kidney (MDCK) cells. The Journal of biological chemistry 80 11872745
1996 Characterization of VIP36, an animal lectin homologous to leguminous lectins. Journal of cell science 75 8834812
2005 Sugar-binding properties of VIP36, an intracellular animal lectin operating as a cargo receptor. The Journal of biological chemistry 71 16129679
1999 Vesicular-integral membrane protein, VIP36, recognizes high-mannose type glycans containing alpha1-->2 mannosyl residues in MDCK cells. Glycobiology 61 10406849
2003 Profile-based data base scanning for animal L-type lectins and characterization of VIPL, a novel VIP36-like endoplasmic reticulum protein. The Journal of biological chemistry 59 12609988
2003 VIPL, a VIP36-like membrane protein with a putative function in the export of glycoproteins from the endoplasmic reticulum. Experimental cell research 50 12878160
2016 Adaptor Protein CD2AP and L-type Lectin LMAN2 Regulate Exosome Cargo Protein Trafficking through the Golgi Complex. The Journal of biological chemistry 46 27765817
2007 Structural basis for recognition of high mannose type glycoproteins by mammalian transport lectin VIP36. The Journal of biological chemistry 42 17652092
2019 White matter DNA methylation profiling reveals deregulation of HIP1, LMAN2, MOBP, and other loci in multiple system atrophy. Acta neuropathologica 39 31535203
2011 VIP36 protein is a target of ectodomain shedding and regulates phagocytosis in macrophage Raw 264.7 cells. The Journal of biological chemistry 37 22016386
2010 Role of the lectin VIP36 in post-ER quality control of human alpha1-antitrypsin. Traffic (Copenhagen, Denmark) 34 20477988
2006 Detection of weak sugar binding activity of VIP36 using VIP36-streptavidin complex and membrane-based sugar chains. Journal of biochemistry 26 17169971
2014 Structural basis for disparate sugar-binding specificities in the homologous cargo receptors ERGIC-53 and VIP36. PloS one 25 24498414
2004 The binding of VIP36 and alpha-amylase in the secretory vesicles via high-mannose type glycans. Glycobiology 21 15070860
2007 Stable interaction of the cargo receptor VIP36 with molecular chaperone BiP. Glycobiology 20 17586539
2003 Localization of VIP36 in the post-Golgi secretory pathway also of rat parotid acinar cells. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 17 12871987
2012 Site-specific N-linked glycosylation of receptor guanylyl cyclase C regulates ligand binding, ligand-mediated activation and interaction with vesicular integral membrane protein 36, VIP36. The Journal of biological chemistry 15 23269669
2021 Emp47 and Vip36 are required for polarized growth and protein trafficking between ER and Golgi apparatus in opportunistic fungal pathogen Aspergillus fumigatus. Fungal genetics and biology : FG & B 8 34798270
2017 Molecular characterization of transport lectin vesicular integral membrane protein 36 kDa (VIP36) in the life cycle of Schistosoma mansoni. Parasitology research 5 28840376
2024 Regulation of Kv1.2 Redox-Sensitive Gating by the Transmembrane Lectin LMAN2. Function (Oxford, England) 3 39264045
2024 C-terminal amino acids in the type I transmembrane domain of L-type lectin VIP36 affect γ-secretase susceptibility. Biochemical and biophysical research communications 2 38219489
2024 LMAN2 Promotes Breast Cancer Tumorigenesis and Drug Resistance by Interacting With MAPK9 via Activation of the MAPK Pathway. Cancer medicine 2 39618331
2025 LMAN2 interacts with HEATR3 to expedite HER2-positive breast cancer advancement and inflammation and Akt/ERK/NF-κB signaling. Biochemistry and cell biology = Biochimie et biologie cellulaire 1 39772898
2024 Competitive modulation of KV1.2 gating by LMAN2 and Slc7a5. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1 39659243

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