| 1997 |
MAGI-1 is a MAGUK protein with a unique inverted domain structure: GuK domain at the N-terminus, two WW domains replacing the SH3 domain, and five PDZ domains. The longest splice variant (MAGI-1c) contains bipartite nuclear localization signals and localizes predominantly to the nucleus, while shorter forms lacking these signals localize to membrane and cytoplasmic fractions. |
cDNA cloning, subcellular fractionation, sequence analysis of splice variants |
The Journal of biological chemistry |
High |
9395497
|
| 2000 |
MAGI-1b fifth PDZ domain binds beta-catenin and is essential for membrane localization; MAGI-1b forms complexes with beta-catenin and E-cadherin during formation of cell-cell junctions in MDCK cells, and GFP-MAGI-1b localizes to the basolateral membrane of polarized MDCK cells. |
Co-immunoprecipitation, GFP fusion localization, subcellular fractionation, yeast two-hybrid |
Biochemical and biophysical research communications |
High |
10772923
|
| 1999 |
MAGI-1/BAP1 localizes specifically to tight junctions in intestinal epithelial cells and MDCK cells, co-localizing with ZO-1 (not E-cadherin), and is recruited with ZO-1 to tight junction-like structures upon PMA treatment after low-Ca2+ switch, distinguishing its role from SAP97/hDLG. |
Immunofluorescence, subcellular fractionation, Ca2+-switch assay |
Oncogene |
High |
10618722
|
| 2000 |
Ad9 E4-ORF1 oncoprotein binds MAGI-1 and aberrantly sequesters it in the cytoplasm, while high-risk HPV E6 proteins bind MAGI-1 and target it for degradation; transformation-defective viral mutants are deficient for these activities. |
Co-immunoprecipitation, subcellular fractionation, viral mutant analysis |
Oncogene |
High |
11077444
|
| 2000 |
MAGI-1/BAP1 serves as a scaffolding molecule for Rap GEP (a Rap1-specific GDP/GTP exchange factor) at tight junctions in epithelial cells; this interaction is specific to MAGI-1 and not observed with PSD-95/SAP90 or SAP97/hDLG. |
Cell-free binding assays, co-immunoprecipitation in intact cells, Northern blot |
Genes to cells : devoted to molecular & cellular mechanisms |
High |
11168587
|
| 2001 |
MAGI-1 fifth PDZ domain binds megalin via the DSDV PDZ-binding motif at megalin's C-terminus; a mutant megalin lacking the terminal valine cannot bind. MAGI-1 is expressed in glomerular podocytes and associated with the cytoskeleton in glomerular preparations. |
Yeast two-hybrid, PDZ domain binding assays, mutagenesis, immunofluorescence, Western blot fractionation |
Journal of the American Society of Nephrology : JASN |
High |
11274227
|
| 2001 |
The first PDZ domain of MAGI-1 interacts with mNET1, a Rho family nucleotide exchange factor, via a consensus PDZ-binding motif (PPxY-like at C-terminus of mNET1) plus a nearby cluster of basic residues required for the interaction. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation |
Biochemical and biophysical research communications |
Medium |
11350080
|
| 2002 |
MAGI-1 WW domain 2 interacts with synaptopodin (an actin-bundling protein) identified via cDNA library screen; the fifth PDZ domain of MAGI-1 binds alpha-actinin-4 C-terminus. Both interactions were confirmed in vivo by co-immunoprecipitation from HEK293 cells, and all three proteins colocalize at tight junctions in MDCK cells. |
Yeast two-hybrid/cDNA library screen, in vitro GST pull-down, co-immunoprecipitation, immunofluorescence |
The Journal of biological chemistry |
High |
12042308
|
| 2003 |
JAM4 (junctional adhesion molecule 4) directly binds MAGI-1 (but not ZO-1), and their co-expression in COS-7 cells induces clustering. MAGI-1 strengthens JAM4-mediated cell adhesion in L cells and sealing effects in CHO cell monolayers. MAGI-1 also recruits ZO-1, occludin to JAM4-based contacts. |
In vitro binding assay, co-immunoprecipitation, cell adhesion assay, permeability assay, fluorescence microscopy |
Molecular and cellular biology |
High |
12773569
|
| 2004 |
ESAM (endothelial cell-selective adhesion molecule) directly binds MAGI-1 via PDZ domain-mediated interaction at ESAM's C-terminus; ESAM recruits MAGI-1 to cell-cell contacts in CHO cells, and in HUVECs MAGI-1 colocalizes with ESAM at endothelial cell-cell contacts. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, immunofluorescence |
Experimental cell research |
High |
15383320
|
| 2005 |
MAGI-1 is required for Rap1 activation upon VE-cadherin homophilic engagement at cell-cell contacts in endothelial cells. MAGI-1 binds PDZ-GEF1 (a Rap1 GEF) and localizes to cell-cell contacts via beta-catenin. MAGI-1 depletion suppresses VE-cadherin-dependent Rap1 activation, inhibits vinculin relocalization to cell-cell contacts, and impairs VE-cadherin-mediated adhesion. |
siRNA knockdown, Rap1 activation assay (pulldown of GTP-Rap1), FRET-based Rap1 biosensor, co-immunoprecipitation, immunofluorescence |
Molecular biology of the cell |
High |
16339077
|
| 2005 |
MAGI-1 binds Dll1 (Delta-like 1) and N-cadherin/beta-catenin complexes; MAGI-1 recruits Dll1 to adherens junctions in cultured fibroblasts and stabilizes Dll1 on the cell surface, suggesting MAGI-1 presents Dll1 at junctions to activate Notch on neighboring cells. |
Yeast two-hybrid, co-immunoprecipitation, immunofluorescence, cell surface stability assay |
The Journal of biological chemistry |
High |
15908431
|
| 2005 |
MAGI-1 is a component of the glomerular slit diaphragm and directly binds nephrin via its middle PDZ domains (PDZ3) through nephrin's C-terminus; MAGI-1 forms a tripartite complex with nephrin and JAM4 in vitro. In puromycin aminonucleoside nephrotic podocytes, MAGI-1 co-localizes with nephrin at the displaced slit diaphragm. |
Yeast two-hybrid, in vitro binding assay, immunoelectron microscopy, co-immunoprecipitation |
Laboratory investigation |
High |
16155592
|
| 2005 |
A novel tight junction protein, MASCOT, binds the first WW domain of MAGI-1 via an LPxY motif (not the canonical PPxY); the coiled-coil domain of MASCOT is required for its localization to tight junctions in MDCK cells. |
CDNA library screen, in vitro GST binding assay, co-immunoprecipitation, immunofluorescence |
Biochimica et biophysica acta |
Medium |
16019084
|
| 2007 |
MAGI-1 is cleaved by caspases-3 and -7 at Asp761 during apoptosis, generating a 97 kDa N-terminal fragment that dissociates from the membrane and a C-terminal fragment. Mutation of Asp761 to Ala abolishes caspase-induced cleavage and delays disruption of cell-cell contacts during apoptosis without affecting nuclear condensation. |
In vitro caspase cleavage assay, site-directed mutagenesis, cell-based apoptosis assays, caspase inhibitor (Z-VAD-fmk) |
Apoptosis |
High |
17191119
|
| 2007 |
N-terminal MAGI-1 caspase cleavage product translocates to the cytosol while C-terminal caspase cleavage product accumulates in the nucleus; both overexpressed fragments exhibit minor pro-apoptotic activity when expressed in MDCK cells. |
GFP-fusion subcellular localization, immunofluorescence, apoptosis assay |
Biological chemistry |
Medium |
17976012
|
| 2008 |
MAGI-1 PDZ4 domain binds the C-terminal PDZ-binding site of the hair-cell-specific Cdh23(+68) splice variant; MAGI-1 immunoreactivity is detectable in neonatal stereocilia in a distribution similar to Cdh23, with punctate staining maintained into adulthood. |
Cochlear cDNA library screen, PDZ domain binding assay, immunofluorescence |
The Journal of neuroscience |
Medium |
18971469
|
| 2009 |
MAGI-1 binds BKCa (Slo1) channel proteins via a yeast two-hybrid interaction; co-expression of MAGI-1 with Slo1 in HEK293T cells significantly reduces Slo1 surface expression as assessed by biotinylation, confocal microscopy, and whole-cell recordings. Partial siRNA knockdown of endogenous MAGI-1 in podocytes increases surface expression of endogenous Slo1. |
Yeast two-hybrid, co-immunoprecipitation, GST pull-down, cell-surface biotinylation, electrophysiology, siRNA knockdown |
American journal of physiology. Cell physiology |
High |
19403801
|
| 2008 |
MAGI-1 in C. elegans (ortholog) controls GLR-1/GLR-2 AMPA receptor synaptic localization in response to prior mechanosensory experience; MAGI-1L isoform interacts with AMPARs through the intracellular domain of GLR-2 subunit; mutations preventing GLR-1 ubiquitination prevent the decrease in AMPAR localization in magi-1 mutants. |
Genetic loss-of-function, fluorescence imaging of GFP-tagged GLR-1/GLR-2, behavioral assays, epistasis analysis |
PloS one |
High |
19242552
|
| 2009 |
MAGI-1 in C. elegans controls associative learning via RIA interneurons and memory consolidation via AVA/AVD/AVE glutamatergic interneurons; during memory consolidation, MAGI-1 regulates GLR-1 (iGluR) clustering cell-autonomously in a manner dependent on its ability to interact with beta-catenin HMP-2. |
Genetic rescue (neuron-specific expression), behavioral assays, fluorescence imaging of GLR-1 clustering, epistasis analysis |
PloS one |
High |
19551147
|
| 2010 |
ESAM-MAGI-1 co-localization promotes actin polymerization through PDZ domain interactions resulting in firm cell-cell adhesion; ESAM-MAGI-1 interaction activates RhoA, and RhoA inhibition blocks ESAM-mediated MAGI-1 recruitment and mature cell adhesion. |
Transfection experiments in CHO cells, cell dissociation assay, actin polymerization inhibitor, RhoA activity assay, RhoA inhibitor |
Genes to cells |
Medium |
20298433
|
| 2010 |
MAGI-1 is a major degradation target of HPV-16 and HPV-18 E6 in cervical cancer cells; E6 preferentially targets MAGI-1 within the nucleus and at membrane sites; MAGI-1 degradation causes loss of tight junction integrity (ZO-1 mislocalization); E6 ablation restores tight junctions in a MAGI-1-dependent manner. |
siRNA E6 ablation, Western blot, immunofluorescence of ZO-1, rescue experiments |
Journal of virology |
High |
21123374
|
| 2010 |
C. elegans MAGI-1 localizes apical to both the CCC and DAC junctional sub-compartments; loss of MAGI-1 causes loss of junctional compartmentalization along the lateral membrane and reduces robustness of cell-cell adhesion by both junctional types. |
RNAi knockdown, fluorescence imaging of junctional markers, genetic analysis |
Developmental biology |
High |
21034729
|
| 2011 |
NMR solution structure of MAGI-1 PDZ1 domain alone and bound to HPV16 E6 C-terminal peptide reveals that binding induces quenching of high-frequency motions in the C-terminal tail of the PDZ domain; mutations in the C-terminal flanking region significantly decrease E6 binding affinity, indicating global PDZ response with effects propagated to distal sites. |
NMR structure determination, backbone dynamics analysis, site-directed mutagenesis, binding affinity measurement |
Journal of molecular biology |
High |
21238461
|
| 2011 |
MAGI-1 overexpression in colorectal cancer cells stabilizes E-cadherin and beta-catenin at cell-cell junctions, enhances actin stress fiber and focal adhesion formation, suppresses Wnt signaling, and inhibits migration, invasion, and anchorage-independent growth. MAGI-1 silencing has opposite effects. MAGI-1 overexpression suppresses tumor growth and metastasis in vivo. |
Stable overexpression/siRNA knockdown, in vitro migration/invasion assays, Wnt reporter assay, in vivo xenograft/orthotopic models |
Oncogene |
High |
21666716
|
| 2011 |
MAGI-1 directly binds glutamate transporter GLT-1 via GST pull-down confirmed by co-immunoprecipitation; co-expression of MAGI-1 reduces GLT-1 surface expression in C6 glioma cells; siRNA knockdown of endogenous MAGI-1 in astrocytes increases glutamate uptake and GLT-1 surface expression. |
GST pull-down, co-immunoprecipitation, cell-surface biotinylation, glutamate uptake assay, siRNA knockdown |
Journal of neurochemistry |
High |
21426345
|
| 2011 |
MAGI-1 overexpression in hepatocellular carcinoma HepG2 cells inhibits migration and invasion; PTEN protein expression is significantly elevated in MAGI-1-overexpressing cells, with a positive correlation between MAGI-1 and PTEN protein levels. |
Stable transfection, wound healing assay, Matrigel invasion assay, Western blot |
Zhong nan da xue xue bao |
Medium |
21685691
|
| 2012 |
MAGI-1 PDZ1 and PDZ3 domains regulate CAREx8 levels in opposing ways: PDZ3 reduces apical CAREx8 abundance and adenovirus infection, while PDZ1 rescues CAREx8 and adenovirus infection from MAGI-1-mediated suppression. |
Yeast two-hybrid, biochemical pull-down, co-immunoprecipitation, FRET, adenovirus infection assay |
Journal of virology |
High |
22718816
|
| 2012 |
In C. elegans, MAGI-1 physically interacts with AFD-1/afadin and SAX-7/L1CAM (which binds MAGI-1 via its C-terminus); MAGI-1 and AFD-1 localize to a unique domain in the apical junction; SAX-7/L1CAM is required for normal MAGI-1 junctional accumulation; MAGI-1 depletion causes loss of spatial segregation and expansion of apical junctional domains. |
Genome-wide RNAi screen, co-immunoprecipitation, fluorescence localization, genetic epistasis |
Current biology |
High |
22981773
|
| 2012 |
siRNA depletion of MAGI-1 activates IRF3 and induces the IFN-β promoter; avian influenza NS1 ESEV PBM sequesters MAGI-1 away from the plasma membrane in infected cells, and the ESEV PBM relative to EPEA shows relative deficiency in NS1 inhibition of IFN-β induction, suggesting MAGI-1 normally suppresses IFN-β signaling. |
siRNA knockdown, IRF3 activation assay, IFN-β promoter luciferase reporter, immunofluorescence |
PloS one |
Medium |
22911767
|
| 2012 |
MAGI-1 in neuronal tissue is enriched in synaptosomal vesicle and synaptic plasma membrane fractions (distinct from MAGI-2/3 which are in PSD fractions); MAGI-1 shows diffuse distribution in hippocampal neuron cell body and processes, not enriched at synapses, unlike MAGI-2/3. |
Biochemical fractionation, immunofluorescence, immunohistochemistry |
Journal of neuroscience research |
Medium |
22605569
|
| 2013 |
HTLV-1 Tax1 interacts with MAGI-1 in a PDZ-binding motif (PBM)-dependent manner and mislocalizes MAGI-1 from the detergent-soluble to the detergent-insoluble cellular fraction in 293T cells and HTLV-1-infected T-cells; Tax1-induced T-cell transformation selects for cells with irreversibly reduced MAGI-1 mRNA expression. |
Co-immunoprecipitation, subcellular fractionation, PBM mutant analysis, RT-PCR |
Cancer science |
Medium |
23279616
|
| 2013 |
MAGI-1 forms an immunocomplex with p75NTR (low-affinity NGF receptor) and Shc adaptor in PC12 cells; MAGI-1 knockdown inhibits NGF-induced neurite outgrowth; both knockdown and overexpression of MAGI-1 suppress NGF-stimulated Shc-ERK pathway activation. |
Co-immunoprecipitation, siRNA knockdown, overexpression, neurite outgrowth assay, ERK activation assay |
Biochimica et biophysica acta |
Medium |
23769981
|
| 2014 |
A K499E mutation in MAGI-1 PDZ1 domain renders it resistant to HPV E6 targeting; re-expression of this mutant MAGI-1 in HPV-positive cells increases ZO-1 and PAR3 recruitment to cell-cell contacts, represses cell proliferation, and induces apoptosis. |
Site-directed mutagenesis, lentiviral expression in HPV+ cells, immunofluorescence, cell proliferation and apoptosis assays |
Journal of virology |
High |
24696483
|
| 2015 |
MAGI-1 PDZ3 domain is exclusively responsible for high-affinity interaction with the 7-exon CAR isoform; interruption of this high-affinity interaction alters MAGI-1 localization (CAR traffics MAGI-1 to cell junctions) but does not significantly alter adenovirus infection via CAR. |
Yeast two-hybrid, in vitro pull-down, co-immunoprecipitation, FRET, adenovirus infection assay |
The international journal of biochemistry & cell biology |
Medium |
25622559
|
| 2015 |
Binding of E6 peptides to MAGI-1 PDZ1 is accompanied by an unusually large negative change in heat capacity attributed to a disorder-to-order transition of the PDZ1 C-terminal extension; NMR relaxation data confirm this; a PDZ1 mutant abolishing this transition shows different thermodynamic signature. |
Isothermal titration calorimetry (ITC), NMR 15N relaxation, site-directed mutagenesis |
Biochemistry |
High |
25590897
|
| 2016 |
MAGI-1 depletion in cultured podocytes reduces nephrin and neph1 membrane localization and weakens tight junction integrity; global magi1 knockout mice are normal, but combined MAGI-1 knockout with nephrin heterozygosity causes spontaneous glomerulosclerosis; MAGI-1 depletion reduces intercellular contact-induced Rap1 activation, and combined overexpression of MAGI-1 with nephrin increases Rap1 activation requiring the nephrin-binding interface. |
siRNA knockdown, global knockout mice, compound genetic mouse models, Rap1 activation assay, Drosophila genetic screen, Western blot |
The Journal of biological chemistry |
High |
27707879
|
| 2017 |
MAGI-1 knockdown in gastric cancer cells promotes migration and invasion by increasing MMP expression and EMT-related molecules via activation of the MAPK/ERK signaling pathway. |
shRNA knockdown, migration/invasion assays, Western blot for MMPs and EMT markers, ERK signaling analysis |
Chinese journal of cancer research |
Medium |
28373751
|
| 2018 |
Crystal/biochemical structure analysis shows nephrin C-terminal PBM specifically binds MAGI1 PDZ3 but not MAGI2 PDZ3; the Gly at the -3 position of nephrin-PBM is the determining feature for MAGI1-PDZ3 recognition (contrasting typical PDZ/PBM binding mode); a single gain-of-function mutation in MAGI2 enables nephrin-PBM binding. |
Complex crystal structure (MAGI1-PDZ3/nephrin-PBM), biophysical binding assays, site-directed mutagenesis |
Journal of the American Society of Nephrology : JASN |
High |
30006415
|
| 2019 |
MAGI1 is required for fluid shear stress-induced eNOS phosphorylation and NO production in endothelial cells; MAGI1 silencing impairs KLF4 expression and cell alignment under flow; MAGI1 overexpression induces phosphorylation of PKA, AMPK, and CaMKII; PKA and AMPK inhibition prevents MAGI1-mediated eNOS phosphorylation; endothelial-specific transgenic MAGI1 increases PKA and eNOS phosphorylation in vivo. |
siRNA silencing, overexpression, NO measurement, kinase phosphorylation assays, pharmacological kinase inhibitors, transgenic mice |
Cells |
High |
31035633
|
| 2019 |
In endothelial cells exposed to disturbed flow, p90RSK binds MAGI1 and causes MAGI1-S741 phosphorylation, which upregulates EC activation via Rap1; MAGI1-K931 deSUMOylation (mediated by SENP2) induces nuclear translocation of p90RSK-MAGI1 and ATF6-MAGI1 complexes promoting EC activation and apoptosis respectively; MAGI1 associates with ATF-6 (ER stress mediator); reduced MAGI1 in Magi1-/+ mice inhibits disturbed flow-induced atherogenesis. |
Co-immunoprecipitation, phosphoproteomic analysis, phospho-site mutagenesis, SUMOylation assay, Magi1+/- mouse model, microarray |
JCI insight |
High |
30944250
|
| 2019 |
Magi-1 directly interacts with NaV1.8 channels and Slack KNa channels in dorsal root ganglion neurons; Magi-1 regulates NaV1.8 plasma membrane localization, retention, and stability; DRG-specific knockdown of Magi-1 attenuates thermal nociception and inflammatory pain; a competing cell-penetrating peptide mimetic from NaV1.8 WW binding motif decreases sodium currents and NaV1.8 surface expression. |
co-immunoprecipitation, cell-surface biotinylation, siRNA knockdown, electrophysiology, in vivo pain behavior, peptide competition assay |
FASEB journal |
High |
30860870
|
| 2020 |
p90RSK-mediated MAGI1 post-translational modifications (S741 phosphorylation and K931 de-SUMOylation) regulate endothelial permeability; dominant negative p90RSK or MAGI1-S741A decreases thrombin-induced permeability; p90RSK overexpression, MAGI1 siRNA, or MAGI1-K931R SUMOylation mutant accelerates permeability; MAGI1 depletion increases LATS1/2 expression, inhibiting YAP/TAZ (Hippo pathway). |
ECIS-based permeability assay, siRNA knockdown, PTM mutant overexpression, LATS/YAP expression analysis, in vivo p90RSK inhibitor |
Frontiers in cardiovascular medicine |
High |
33304925
|
| 2021 |
MAGI1 colocalizes with paxillin, β3-integrin, talin 1, tensin 3, and α4-actinin at mature focal adhesions and actin stress fibers in endothelial cells; MAGI1 silencing reduces focal adhesion formation and maturation, cell spreading, actin stress fiber formation, and RhoA/Rac1 activation, and increases paxillin Y118 phosphorylation (indicator of focal adhesion turnover). MAGI1 silencing reduces integrin-dependent adhesion, increases invasion, promotes tubulogenesis in vitro, and promotes angiogenesis in vivo. |
siRNA silencing, immunofluorescence colocalization, RhoA/Rac1 activation assay, paxillin phosphorylation Western blot, cell adhesion/invasion assays, in vivo angiogenesis model |
Cell adhesion & migration |
High |
33823745
|
| 2021 |
Loss of MAGI1 in breast cancer cells causes accumulation of E-cadherin and AMOTL2 with increased cellular stiffness, elevated ROCK and p38 stress kinase activities (but low YAP activity); MAGI1 loss-driven tumorigenicity is rescued by AMOTL2 deletion or p38 inhibition, demonstrating MAGI1 suppresses tumorigenesis by inhibiting an AMOTL2/p38 stress pathway. |
MAGI1 siRNA knockdown, AMOTL2 knockout, p38 inhibitor, ROCK inhibitor, tumorigenicity assays, YAP activity measurement |
Scientific reports |
High |
33707576
|
| 2021 |
MAGI-1 PDZ2 domain blockade by decoy peptides (TAT-E6, TAT-NET1) decreases CAREx8 expression and adenovirus transduction; this occurs via enhanced regulated intramembrane proteolysis through ADAM17 and γ-secretase; ADAM17 interacts directly with MAGI-1 PDZ3 domain; blocking PDZ2 enhances ADAM17 accessibility to CAREx8. |
Decoy peptide competition, cell-surface biotinylation, adenovirus transduction assay, co-immunoprecipitation of ADAM17/MAGI-1, in vivo transgenic model |
Journal of virology |
High |
33762416
|
| 2022 |
MAGI1 inhibits IRF3 activation in endothelial cells by maintaining IRF3 SUMOylation; MAGI1 depletion leads to IRF3 nuclear translocation without phosphorylation, upregulates STAT1, IFNβ1, MX1, OAS2, and activates STAT5 upon IAV infection; MAGI1 overexpression inhibits Ifnb1 mRNA and MX1 expression. |
siRNA knockdown, overexpression, microarray, RT-PCR, Western blot for STAT1/MX1/OAS2, IRF3 nuclear translocation assay, IRF3 SUMOylation assay |
Frontiers in cardiovascular medicine |
Medium |
36082118
|
| 2024 |
SRC phosphorylates MAGI1 in IDH-mutant cholangiocarcinoma; SRC inhibition (dasatinib) enables formation of a MAGI1-PP2A complex that dephosphorylates and inhibits S6K, reducing protein synthesis and causing cell death; SRC normally inhibits this latent tumor-suppressing MAGI1-PP2A function. |
Unbiased phosphoproteomic screen, co-immunoprecipitation, PP2A activity assay, S6K phosphorylation Western blot, cell viability assays, patient-derived xenografts |
Science translational medicine |
High |
38748774
|
| 2024 |
Tissue factor (TF) associates predominantly with MAGI1 (less with MAGI2/3); TF interacts with the PDZ1 domain of MAGI1; phosphorylation of Ser253 in TF prevents its association with MAGI1; PAR2 activation disrupts TF-MAGI1 association; blocking PDZ1 with competing peptide augments TF procoagulant and signaling activity, suggesting MAGI1 stabilizes and 'encrypts' TF. |
Proximity ligation assay, co-immunoprecipitation (reciprocal), pull-down with TF cytoplasmic domain peptides, PDZ domain overexpression, thrombin generation assay |
Thrombosis journal |
High |
38233821
|
| 2025 |
MAGI1 suppresses osteoclast fusion and differentiation through the RhoA/ROCK1 signaling pathway; MAGI1 overexpression decreases RhoA, ROCK1, and p-p65 in RANKL-treated osteoclasts; knockdown of MAGI1 in subchondral bone increases osteoclast numbers and worsens subchondral bone microarchitecture; RhoA activator narciclasine rescues MAGI1 overexpression effects. |
AAV-mediated shMagi1 knockdown in vivo, overexpression experiments, RANKL-induced osteoclastogenesis in vitro, LC-MS/MS, Western blot, micro-CT, histological staining |
Journal of orthopaedic translation |
Medium |
40322041
|
| 2026 |
The MAGI-1 WW tandem architecture substantially enhances affinity towards bidentate ligands compared to individual WW domains; binding proceeds through a conformational selection mechanism sampling alternative conformational states; affinity is modulated by environmental pH with cooperative dissociation linked to electrostatic contacts; swapping linker length between PY motifs alters complex stability (longer linkers weaken binding). |
Time-resolved kinetic analyses, isothermal titration calorimetry, biochemical binding assays |
International journal of biological macromolecules |
High |
41786191
|
| 2019 |
miR-486-5p directly binds the 3'-UTR of MAGI1 mRNA (confirmed by dual-luciferase and FREMSA); MAGI1 knockdown reverses hydroquinone-induced inhibition of erythroid differentiation in K562 cells via downregulation of RAPGEF2 and RAP1A (downstream of MAGI1 in Rap1 signaling). |
Dual-luciferase reporter assay, FREMSA, siRNA knockdown, overexpression, erythroid differentiation assay |
Toxicology in vitro |
Medium |
32198055
|
| 2024 |
In C. elegans, the SAX-7/L1CAM PDZ-binding motif binds MAGI-1 in pull-down assays; MAGI-1 bridges SAX-7 to HMP-2/β-catenin; MAGI-1 acts in glia (non-cell-autonomously) to promote dendrite extension; MAGI-1 also binds AFD-1/afadin via SAX-7 PB motif, and loss of AFD-1 enhances sax-7 dendrite defects. |
Pull-down assay, cell-specific rescue, genetic depletion, double mutant analysis |
bioRxiv (preprint)preprint |
Medium |
38260503
|
| 2026 |
OGT mediates O-GlcNAcylation of MAGI1, stabilizing its expression; OGT knockdown reduces MAGI1 levels and inhibits PI3K/AKT pathway activation in high-glucose-treated VSMCs; MAGI1 overexpression activates PI3K/AKT signaling and promotes VSMC proliferation, migration, and inflammation. |
OGT knockdown, MAGI1 overexpression/knockdown, O-GlcNAcylation assay, Western blot for PI3K/AKT, cell function assays, diabetic mouse model |
Hereditas |
Medium |
41546072
|