- Length
- 153 aa
- Mass
- 16.7 kDa
- Annotated
- 2026-06-13
100 papers in source corpus
40 papers cited in narrative
40 extracted findings
Mechanistic narrative
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Mechanism profile
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Evidence
Reading pass · 40 per-paper findings extracted from the source corpus
| Year | Finding | Method | Journal | Conf | PMIDs |
|---|---|---|---|---|---|
| 1987 | MAL encodes a highly hydrophobic proteolipid protein with four putative transmembrane domains, initially identified as expressed in intermediate and late stages of T-cell differentiation, with predicted configuration resembling integral membrane proteins that form pores or channels. | cDNA cloning, sequence analysis, hydrophobicity profiling | Proceedings of the National Academy of Sciences of the United States of America | Medium | 3494249 |
| 1994 | MAL protein is a proteolipid (soluble in organic lipid-extraction solvents), is encoded by a 4-exon gene where each exon corresponds to one hydrophobic segment, and localizes to the endoplasmic reticulum of T cells. A C-terminal RWKSS motif consistent with ER retention signals was identified. | Genomic cloning, RNase protection, recombinant expression in bacteria with lipophilic solvent extraction, immunofluorescence with two distinct anti-peptide antibodies | The Journal of biological chemistry | Medium | 8132541 |
| 1995 | MAL (MVP17) is a developmentally regulated proteolipid in oligodendrocytes that co-purifies with detergent-insoluble, glycolipid-rich membrane microdomains, consistent with a role in myelin biogenesis. | Detergent-insoluble membrane fractionation, 2D gel electrophoresis, N-terminal microsequencing, cDNA cloning from oligodendrocyte library, Northern blot | Journal of neuroscience research | Medium | 8583510 |
| 1995 | VIP17/MAL is a proteolipid component of apical transport vesicles in MDCK cells, localizing to perinuclear vesicles and the apical cytoplasm, cycling between the Golgi and the apical plasma membrane. | cDNA cloning, immunofluorescence of epitope-tagged VIP17/MAL in BHK and MDCK cells | FEBS letters | Medium | 8549777 |
| 1997 | MAL proteolipid is exclusively incorporated into detergent-resistant, buoyant membrane microdomains (lipid rafts) in both T lymphocytes (Jurkat) and epithelial cells, co-fractionating with p56lck, CD59, and GM1. | Stable transfection of epitope-tagged MAL, Triton X-100 extraction, sucrose gradient fractionation, immunofluorescence | The Biochemical journal | Medium | 9003426 |
| 1997 | MAL and caveolin occupy distinct lipid microenvironments within MDCK cells; MAL is in internal glycolipid-enriched detergent-insoluble membranes while caveolin is additionally found at the cell surface, demonstrating heterogeneity within raft fractions. | Sucrose gradient fractionation, immunofluorescence, differential detergent solubilization | Biochemical and biophysical research communications | Medium | 9168919 |
| 1998 | A C-terminal juxtamembrane tetrapeptide motif LIRW in MAL is necessary for incorporation into glycolipid-enriched membrane (GEM) microdomains; arginine is the most critical residue. Loss of GEM targeting correlates with loss of MAL's response to brefeldin A treatment. | Site-directed mutagenesis, sucrose gradient fractionation of GEMs, pulse-chase experiments, brefeldin A treatment | The Journal of biological chemistry | High | 9582298 |
| 1998 | MAL is expressed specifically in thyroid follicular epithelial cells, localizing to the apical zone, and is a major component of GEM fractions in the polarized thyroid epithelial cell line FRT, consistent with a role in apical sorting in thyroid epithelium. | Northern blot, immunohistochemistry with anti-MAL monoclonal antibody, GEM fractionation of FRT cells | Endocrinology | Medium | 9528996 |
| 1999 | MAL depletion by antisense oligonucleotides in MDCK cells reduces the presence of influenza hemagglutinin (HA) in GEMs, decreases the rate of HA transport to the cell surface, inhibits apical delivery, and causes partial missorting of HA to the basolateral membrane. Ectopic MAL expression rescues these defects, demonstrating that MAL is necessary for both normal apical transport and accurate sorting of HA. | Antisense oligonucleotides, newly generated anti-canine MAL monoclonal antibody, surface biotinylation, apical/basolateral sorting assay, ectopic MAL rescue | The Journal of cell biology | High | 10189374 |
| 1999 | Overexpression of VIP17/MAL in MDCK cells increases apical delivery and expands the apical surface, while antisense-mediated reduction causes accumulation in the Golgi and impairs apical transport of multiple apical markers (HA, clusterin, gp114, GPI-anchored protein) without affecting basolateral E-cadherin distribution. | Antisense RNA expression, overexpression, immunofluorescence, transport assays for multiple apical cargo proteins | Proceedings of the National Academy of Sciences of the United States of America | High | 10339572 |
| 1999 | MAL is an itinerant protein that cycles between the trans-Golgi network and the plasma membrane: it is expressed at the cell surface, rapidly internalized via an endosomal pathway requiring endosomal acidification, and ~30% of internalized MAL is delivered back to the TGN to restart the transport cycle. | Epitope-tagged and O-glycosylatable/biotinylatable MAL constructs, surface biotinylation, anti-FLAG surface binding, neuraminidase sensitivity assay, resialylation experiment, drug treatments (chloroquine, monensin, NH4Cl), flow cytometry | Molecular biology of the cell | High | 10512878 |
| 2001 | MAL (MyD88-adapter-like) is a TIR-domain-containing cytoplasmic adapter protein that activates NF-κB, JNK, and ERK1/2; forms homodimers and heterodimers with MyD88; associates with TLR4 and with IRAK-2 via its TIR domain; and acts as an adapter specifically in TLR-4 signal transduction. A dominant-negative form of Mal inhibits NF-κB activated by TLR-4 or LPS but not by IL-1RI or IL-18R. | Co-immunoprecipitation, overexpression, dominant-negative constructs, NF-κB/JNK/ERK reporter assays, two-hybrid interaction assays | Nature | High | 11544529 |
| 2003 | Purified TIR domains of MAL and MyD88 form stable heterodimers in vitro; MAL homodimers/oligomers are dissociated by ATP. Structural modeling and GST pull-down/co-IP experiments indicate MAL and MyD88 bind to different, non-overlapping surfaces on TLR2 and TLR4 TIR domains, suggesting a heterotetrameric receptor-adapter complex. A sequence relationship between Drosophila Tube and MAL was identified. | In vitro TIR domain purification, gel filtration, GST pull-down, co-immunoprecipitation, computational structural modeling and docking | The Journal of biological chemistry | High | 12888566 |
| 2004 | Genetic ablation of MAL in mice results in cytoplasmic inclusions in compact myelin, everted paranodal loops, disorganized transverse bands, and reduced levels of contactin-associated protein/paranodin, NF155, Kv1.2, MAG, and MBP in myelin and myelin-derived rafts, demonstrating MAL is required for maintenance of CNS paranode structure, likely by controlling NF155 trafficking/sorting in oligodendrocytes. | MAL knockout mice, electron microscopy, immunofluorescence, Western blotting of myelin fractions and raft fractions | The Journal of cell biology | High | 15337780 |
| 2006 | MAL undergoes tyrosine phosphorylation at positions 86, 187 (and 106) during TLR2 and TLR4 signaling. Bruton's tyrosine kinase (Btk) is identified as the kinase: Btk immunoprecipitated from LPS-activated THP-1 cells directly phosphorylates MAL in vitro, and the Btk inhibitor LFM-A13 blocks endogenous MAL tyrosine phosphorylation. Tyrosine-to-phenylalanine mutations at positions 86 and 187 act as dominant-negative inhibitors of LPS-induced NF-κB activation. | Phosphotyrosine immunoprecipitation, site-directed mutagenesis (Y86F, Y187F), Btk kinase inhibitor (LFM-A13), in vitro kinase assay with immunoprecipitated Btk, THP-1 cell stimulation | The Journal of biological chemistry | High | 16439361 |
| 2006 | MAL interacts with SRF through a conserved seven-residue B1 region sequence that is essential and sufficient for complex formation; the neighboring Q-box facilitates interaction. MAL directly contacts DNA flanking the SRF-protected region in the MAL-SRF-DNA complex, and these contacts are required for effective MAL-SRF complex formation. SRF-induced DNA bending facilitates MAL-DNA contact. MAL-SRF and TCF-SRF use different mechanisms to engage the same SRF hydrophobic groove/pocket. | Deletion and point mutagenesis of MAL B1/Q-box regions, GST pull-downs, gel mobility shift assays, DNase I footprinting, SRF mutagenesis | Molecular and cellular biology | High | 16705166 |
| 2006 | MAL/MKL1 (SRF co-activator) is expressed in developing neurons, localizes to neuronal cell bodies and apical dendrites, and is required for dendritic morphology: dominant-negative MAL constructs or MAL siRNA reduce the number of dendritic processes in cultured cortical neurons and decrease basal SRF-mediated transcription. | Immunohistochemistry of mouse brain, dominant-negative construct expression, siRNA knockdown, dendritic morphology analysis, SRF reporter assay in primary cortical neurons | Journal of neurochemistry | Medium | 16945101 |
| 2009 | MAL directly interacts with the p85α regulatory subunit of PI3K in an inducible manner upon TLR2/6 stimulation with diacylated lipoproteins, driving PI3K-dependent Akt phosphorylation, PIP3 generation, and macrophage polarization independently of MyD88. | Co-immunoprecipitation (inducible Mal-p85α interaction), PI3K activity assay, Akt phosphorylation assay, PIP3 measurement, MyD88-deficient cell analysis | The EMBO journal | High | 19574958 |
| 2009 | Actin-MAL-SRF signaling induces Mig6/Errfi-1 expression, a negative regulator of EGFR. MAL is inducibly recruited to and activates the mig6 promoter. Upregulation of Mig6 correlates with decreased EGFR, MAPK/Erk, and c-fos activation; overexpression of MAL has antiproliferative effects requiring domains for SRF binding and transactivation. | Gene expression profiling, chromatin immunoprecipitation (ChIP) of MAL at mig6 promoter, MAL overexpression/siRNA knockdown, EGFR/MAPK activation assays | Molecular cell | High | 19683494 |
| 2009 | MAL clusters laterally concentrate sphingolipid raft markers and exclude phosphatidylethanolamine analogues. MAL forms oligomers via intramembrane protein-protein binding motifs (demonstrated by site-directed mutagenesis and bimolecular fluorescence complementation). MAL-raft association is driven in part by positive hydrophobic mismatch between MAL transmembrane helices and membrane lipids. | Antibody-mediated cross-linking of FLAG-tagged MAL, tandem dimer DiHcRED-MAL spontaneous clustering, site-directed mutagenesis of intramembrane motifs, bimolecular fluorescence complementation (BiFC), exogenous cholesterol/ceramide membrane modulation | Molecular biology of the cell | High | 19553470 |
| 2010 | IRAK1 and IRAK4 directly phosphorylate MAL (but not MyD88). Co-expression of Mal with either IRAK causes depletion of Mal from cell lysates; LPS stimulation triggers ubiquitination and degradation of Mal; this is inhibited by IRAK1/4 kinase inhibitor or IRAK1/4 knockdown. Phosphorylation by IRAKs thus promotes ubiquitination and degradation of Mal, serving as a negative regulatory mechanism for TLR2/TLR4 signaling. | In vitro kinase assay (direct phosphorylation of Mal by IRAK1/4), kinase-inactive IRAK mutants, co-expression degradation assay, ubiquitination assay, IRAK1/4 siRNA knockdown, IRAK inhibitor treatment | The Journal of biological chemistry | High | 20400509 |
| 2010 | MAL interacts with Inverted Formin 2 (INF2) in Jurkat T cells, where they colocalize at the cell periphery, pericentriolar endosomes, and along microtubules. MAL+ vesicles transport Lck to the plasma membrane along microtubule tracks. INF2 knockdown greatly reduces MAL+ transport vesicle formation and Lck plasma membrane levels and impairs immunological synapse formation. Both actin polymerization and depolymerization activities of INF2 are required. Cdc42 and Rac1 regulate this Lck transport process. | Co-immunoprecipitation, videomicroscopy (live imaging of MAL+ vesicle movement), INF2 siRNA knockdown, INF2 activity mutants, Cdc42/Rac1 manipulation in Jurkat and primary T cells | Blood | High | 20881207 |
| 2010 | MAL/VIP17 coimmunoprecipitates with NKCC2 (Na+-K+-2Cl- cotransporter) in LLC-PK1 cells and rat kidney medullae; a 150-amino-acid stretch of the NKCC2 C-terminal tail mediates the interaction. MAL/VIP17 overexpression increases NKCC2 cell surface retention by attenuating internalization and coincides with increased cotransporter phosphorylation. Transgenic mice overexpressing MAL/VIP17 show cyst formation in distal nephron with highly glycosylated and phosphorylated NKCC2. | Co-immunoprecipitation, truncation mutagenesis of NKCC2, surface biotinylation internalization assay, Western blotting for phosphorylation, transgenic mouse model | Molecular biology of the cell | High | 20861303 |
| 2011 | MAL localizes to the central SMAC (cSMAC) of the immunological synapse (IS) in T cells, where it colocalizes with condensed membranes. Mislocalization of MAL to the peripheral SMAC (pSMAC) reduces membrane condensation at the cSMAC, redistributes microtubule/vesicle docking machinery, and causes missorting of raft-associated Lck and LAT (but not TCR) to the pSMAC. MAL thus regulates membrane order and protein sorting at the IS. | Live imaging, Laurdan fluorescent probe for membrane condensation, MAL mislocalization constructs, co-localization analysis in Jurkat and primary T cells | Journal of immunology | High | 21508261 |
| 2011 | Mal is required for TLR2- and TLR4-induced CREB activation in macrophages. Mal-deficient macrophages fail to express CREB-responsive genes IL-10 and COX-2 in response to TLR2/TLR4 ligands. This pathway requires Pellino3, TRAF6, p38 MAPK, and MAPK-activated protein kinase 2 (MK2), which is directly activated by Mal. | Mal-deficient murine macrophages (BMDM), CREB reporter/phosphorylation assays, Pellino3 siRNA knockdown, TRAF6-deficient cells, p38 MAPK inhibitor, MK2 inhibition, overexpression assays | Journal of immunology | Medium | 21398611 |
| 2012 | MAL/MRTF-A upregulates cytoskeleton-associated genes including integrin α5, plakophilin 2 (Pkp2), and FHL1 via direct SRF recruitment to their cis-regulatory elements (shown by ChIP). Elevated MAL expression impairs migration of fibroblasts and epithelial cells, while dominant-negative MAL or partial knockdown enhances motility. Knockdown of Pkp2 and FHL1 partially reverses MAL-induced migration inhibition. | ChIP of MAL and SRF at integrin α5 and Pkp2 gene regulatory elements, active MAL and dominant-negative constructs, MAL knockdown, siRNA of target genes, cell migration assay | Journal of cell science | High | 22223881 |
| 2013 | Mal interacts with multiple protein kinase C (PKC) isoforms in intestinal epithelial cells (Caco-2). Inhibition of Mal or PKC increases paracellular permeability and bacterial invasion. Mal-deficient mice show altered expression of tight junction proteins (occludin, ZO-1, claudin-3) and increased susceptibility to oral Salmonella infection; bone marrow chimeras indicate the role is in non-hematopoietic (epithelial) cells. | Co-immunoprecipitation (Mal-PKC), transepithelial resistance measurement, Mal−/− mice, bone marrow chimeras, oral vs. intraperitoneal infection comparison, tight junction protein Western blot/IF | Mucosal immunology | Medium | 23612054 |
| 2014 | Genetic evidence in both Drosophila and human cellular models establishes that actin is the key MAL/SRF target gene required for invasive cell migration. Actin protein feeds back on actin mRNA production via MAL/SRF, constituting a dedicated homeostatic feedback loop ensuring sufficient actin supply. | Genetic epistasis in Drosophila (MAL-D mutants rescued by actin overexpression), human cell models with specific actin manipulation, gene expression analysis | Genes & development | High | 24831700 |
| 2015 | MAL (myelin and lymphocyte protein) is required for binding of Clostridium perfringens ε-toxin (ETX) to mammalian cells and for ETX-mediated cytotoxicity. Native CHO cells are resistant to ETX; exogenous MAL expression confers ETX binding and cell death susceptibility. FLAG insertion into the second extracellular loop of MAL abolishes ETX binding. MAL-knockout mice show complete absence of ETX binding to tissues and complete resistance to ETX at doses >1000x the symptomatic dose for wild-type mice. | Exogenous MAL expression in CHO cells, FLAG epitope insertion mutagenesis, ETX binding assay, cytotoxicity assay, MAL knockout mice, immunofluorescence tissue binding | PLoS pathogens | High | 25993478 |
| 2016 | Mal has a TLR-independent role in IFN-γ receptor (IFNGR) signaling: Mal-dependent IFNGR signaling leads to p38 MAPK phosphorylation and autophagy, is required for phagosome maturation and killing of intracellular M. tuberculosis. The common S180L Mal polymorphism (S200L in mice) reduces Mal's affinity for the IFNGR, thereby compromising IFNGR signaling in macrophages. | Mal-deficient macrophages, IFNGR co-immunoprecipitation with Mal, p38 phosphorylation assays, autophagy assays, phagosome maturation assay, Mtb killing assay, S200L knock-in mice | Immunity | High | 26885859 |
| 2017 | MAL TIR domains spontaneously and reversibly form filaments in vitro; they form co-filaments with TLR4 TIR domains and induce MyD88 assembly. A 7-Å cryo-EM structure reveals a stable MAL protofilament of two parallel TIR-domain strands in a BB-loop-mediated head-to-tail arrangement. Structure-guided mutagenesis of interface residues combined with in vivo interaction assays shows these MAL interactions represent a conserved mode of TIR-domain interaction for TLR and IL-1R signaling. | Cryo-EM (7-Å resolution), in vitro TIR domain filament reconstitution, site-directed mutagenesis of interface residues, in vivo interaction assays | Nature structural & molecular biology | High | 28759049 |
| 2017 | Src family kinase (SFK) activation induces tyrosine phosphorylation of TLR4, which dissociates both MyD88 and Mal/TIRAP from TLR4 and suppresses LPS-induced NFκB and JNK1/2 activation, constituting a negative feedback loop. Kinase-dead SFK-Lyn inhibits TLR4 tyrosine phosphorylation and has reduced binding to TLR4, whereas constitutively active SFK-Lyn strongly promotes TLR4 phosphorylation. | Chemical rescuing approach for temporal SFK activation, TLR4 co-immunoprecipitation with MyD88/Mal, kinase-dead and constitutively active SFK-Lyn mutants, NFκB/JNK reporter assays | Biochemical pharmacology | Medium | 29175418 |
| 2019 | MAL is required for ETX-induced blood-brain barrier permeability through caveolae-dependent transcytosis in brain endothelial cells. ETX binding to CNS microvasculature is MAL-dependent (absent in MAL-/- mice). ETX-induced BBB permeability additionally requires caveolin-1: MAL-/- or caveolin-1-/- mice do not show ETX-induced BBB permeability. ETX treatment increases caveolae in brain endothelial cells and causes loss of EEA1+ early endosomes with accumulation of RAB7+ late endosomes/MVBs. | MAL-/- and caveolin-1-/- mice, intravascular ETX injection, molecular tracer extravasation (fluorescein, albumin, dextran, IgG), primary murine brain endothelial cell analysis, EEA1/RAB7 immunofluorescence, electron microscopy of caveolae | PLoS pathogens | High | 31703116 |
| 2024 | Upon LPS stimulation, lysine acetyltransferase CBP is recruited to the TLR4 signalosome, leading to acetylation of the TIR domains of TLR4, MAL, and MyD88. This TIR domain acetylation enhances NF-κB (but not IRF3) pathway activation and M1 macrophage polarization. HDAC1 deacetylates the TIR domains; pharmacological modulation of CBP or HDAC1 plays opposite roles in sepsis. | LPS stimulation of macrophages, CBP co-immunoprecipitation with TLR4 signalosome, acetylation mass spectrometry, NF-κB/IRF3 reporter assays, HDAC1 inhibitor, CBP inhibitor, patient monocyte analysis | The EMBO journal | Medium | 39294473 |
| 2006 | Protein kinase Cδ (PKCδ) binds to TIRAP/Mal via the TIR domain of TIRAP/Mal. TLR2- and TLR4-mediated phosphorylation of p38 MAPK, IKK, and IκB in RAW264.7 cells is abolished by depletion of PKCδ. | GST-fusion pull-down, co-immunoprecipitation from macrophage and THP1 lysates, TIRAP/Mal truncation mutants, PKCδ depletion (siRNA), p38/IKK/IκB phosphorylation assays | Molecular immunology | Medium | 17161867 |
| 2011 | Poxvirus A46 protein binds to MAL/TIRAP via a dimeric α-helical C-terminal domain. Biophysical analysis shows this A46 segment adopts a dimeric α-helical structure and interacts with monomeric Mal in vitro. The A46-derived peptide VIPER does not interact with Mal in vitro. | Biophysical binding assays (in vitro), A46 C-terminal domain expression and dimerization characterization, Mal binding assay | Molecular immunology | Medium | 21831443 |
| 2009 | In epithelial cells, dissociation of E-cadherin-dependent cell-cell junctions activates SRF-mediated transcription via monomeric actin and MAL. This pathway requires Rac1 (not RhoA) and actomyosin contractility as a prerequisite. Rac1 inhibition blocks MAL/SRF activation during junction disassembly in contrast to the Rho-ROCK pathway used in serum-stimulated fibroblasts. | Ca2+-dependent junction dissociation, clostridial cytotoxin inhibition of Rac vs. RhoA, MAL reporter assays, direct evidence of actin-MAL signaling | Journal of cell science | Medium | 18334560 |
| 2004 | Border cell migration in Drosophila oogenesis requires SRF and its cofactor MAL-D; nuclear accumulation of MAL-D is induced by cell stretching/tension. Border cells that cannot migrate lack nuclear MAL-D but accumulate it when pulled by other cells. MAL-D responds to activated Diaphanous (affecting actin dynamics). MAL-D/SRF activity builds a robust actin cytoskeleton in migrating cells; mutant cells break apart during migration initiation. | Drosophila genetics (MAL-D and SRF mutants), live imaging of border cell migration, nuclear localization assay under tension, activated Diaphanous expression | Developmental cell | High | 15239956 |
| 2009 | MAL/SRF complex directly regulates MYL9 (MLC2) and MMP9 transcription in megakaryocytes, as demonstrated by luciferase assays and ChIP in primary megakaryocytes. MAL knockdown reduces filopodia/lamellipodia/stress fiber formation, proplatelet formation, and megakaryocyte migration (via MMP9). MAL expression increases during late megakaryopoiesis and localizes to the nucleus after Rho GTPase activation by adhesion. | ChIP in primary megakaryocytes, luciferase assays (HEK293T), MAL siRNA knockdown, gene expression profiling, migration assay through Matrigel, MYL9 shRNA knockdown | Blood | High | 19724058 |
| 2016 | In urothelial umbrella cells, MAL facilitates apical fusion of uroplakin-delivering fusiform vesicles (FVs). Sequential action is established: Rab8/11 and Rab27b/Slac2-a mediate apical transport along actin; Rab27b/Slp2-a mediates membrane anchorage; then SNARE-mediated and MAL-facilitated apical fusion occurs. Rab27b acts upstream of MAL in this pathway. | Immunomicroscopy of normal and mutant mouse urothelia, Rab27b knockout mice, epistasis analysis placing Rab27b upstream of MAL | Molecular biology of the cell | Medium | 27009205 |
Source papers
Stage 0 corpus · 100 papers · ranked by NIH iCite citations
| Year | Title | Journal | Citations | PMID |
|---|---|---|---|---|
| 2001 | Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction. | Nature | 940 | 11544529 |
| 1999 | VIP17/MAL, a lipid raft-associated protein, is involved in apical transport in MDCK cells. | Proceedings of the National Academy of Sciences of the United States of America | 176 | 10339572 |
| 2001 | Mutations in the gene encoding SLURP-1 in Mal de Meleda. | Human molecular genetics | 170 | 11285253 |
| 2006 | MyD88 adapter-like (Mal) is phosphorylated by Bruton's tyrosine kinase during TLR2 and TLR4 signal transduction. | The Journal of biological chemistry | 165 | 16439361 |
| 2003 | Structural complementarity of Toll/interleukin-1 receptor domains in Toll-like receptors and the adaptors Mal and MyD88. | The Journal of biological chemistry | 159 | 12888566 |
| 2004 | Evidence for tension-based regulation of Drosophila MAL and SRF during invasive cell migration. | Developmental cell | 152 | 15239956 |
| 2017 | Structural basis of TIR-domain-assembly formation in MAL- and MyD88-dependent TLR4 signaling. | Nature structural & molecular biology | 151 | 28759049 |
| 1987 | cDNA cloning and sequence of MAL, a hydrophobic protein associated with human T-cell differentiation. | Proceedings of the National Academy of Sciences of the United States of America | 150 | 3494249 |
| 1999 | The MAL proteolipid is necessary for normal apical transport and accurate sorting of the influenza virus hemagglutinin in Madin-Darby canine kidney cells. | The Journal of cell biology | 149 | 10189374 |
| 2015 | Amygdala-prefrontal interactions in (mal)adaptive learning. | Trends in neurosciences | 143 | 25583269 |
| 2002 | Toll-like receptor signal transduction and the tailoring of innate immunity: a role for Mal? | Trends in immunology | 128 | 12072368 |
| 1989 | Molecular evolution of the telomere-associated MAL loci of Saccharomyces. | Genetics | 122 | 2548922 |
| 1995 | Cloning and characterization of MVP17: a developmentally regulated myelin protein in oligodendrocytes. | Journal of neuroscience research | 119 | 8583510 |
| 2004 | The raft-associated protein MAL is required for maintenance of proper axon--glia interactions in the central nervous system. | The Journal of cell biology | 118 | 15337780 |
| 2012 | Disconnection and reconnection: the morphological basis of (mal)adaptation to stress. | Trends in neurosciences | 110 | 23000140 |
| 2013 | CADM1 and MAL promoter methylation levels in hrHPV-positive cervical scrapes increase proportional to degree and duration of underlying cervical disease. | International journal of cancer | 107 | 23456988 |
| 2002 | MAL expression in lymphoid cells: further evidence for MAL as a distinct molecular marker of primary mediastinal large B-cell lymphomas. | Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc | 106 | 12429796 |
| 1995 | VIP17/MAL, a proteolipid in apical transport vesicles. | FEBS letters | 101 | 8549777 |
| 2009 | Mal connects TLR2 to PI3Kinase activation and phagocyte polarization. | The EMBO journal | 96 | 19574958 |
| 1999 | The MAL gene is expressed in primary mediastinal large B-cell lymphoma. | Blood | 93 | 10552968 |
| 2004 | Caveolin-1 and MAL are located on prostasomes secreted by the prostate cancer PC-3 cell line. | Journal of cell science | 92 | 15466889 |
| 2009 | Negative regulation of the EGFR-MAPK cascade by actin-MAL-mediated Mig6/Errfi-1 induction. | Molecular cell | 90 | 19683494 |
| 2014 | CADM1, MAL and miR124-2 methylation analysis in cervical scrapes to detect cervical and endometrial cancer. | Journal of clinical pathology | 86 | 25281766 |
| 2012 | Triangulated mal-signaling in Alzheimer's disease: roles of neurotoxic ceramides, ER stress, and insulin resistance reviewed. | Journal of Alzheimer's disease : JAD | 86 | 22337830 |
| 2009 | Repression of MAL tumour suppressor activity by promoter methylation during cervical carcinogenesis. | The Journal of pathology | 86 | 19662663 |
| 2015 | Engineered VEGF-releasing PEG-MAL hydrogel for pancreatic islet vascularization. | Drug delivery and translational research | 85 | 25787738 |
| 2006 | MAL and ternary complex factor use different mechanisms to contact a common surface on the serum response factor DNA-binding domain. | Molecular and cellular biology | 84 | 16705166 |
| 2008 | Epithelial cell-cell contacts regulate SRF-mediated transcription via Rac-actin-MAL signalling. | Journal of cell science | 81 | 18334560 |
| 2000 | MAL, a proteolipid in glycosphingolipid enriched domains: functional implications in myelin and beyond. | Progress in neurobiology | 81 | 10739088 |
| 1999 | MAL, an integral element of the apical sorting machinery, is an itinerant protein that cycles between the trans-Golgi network and the plasma membrane. | Molecular biology of the cell | 80 | 10512878 |
| 2015 | The Myelin and Lymphocyte Protein MAL Is Required for Binding and Activity of Clostridium perfringens ε-Toxin. | PLoS pathogens | 73 | 25993478 |
| 2009 | MAL/SRF complex is involved in platelet formation and megakaryocyte migration by regulating MYL9 (MLC2) and MMP9. | Blood | 66 | 19724058 |
| 2011 | Mal mediates TLR-induced activation of CREB and expression of IL-10. | Journal of immunology (Baltimore, Md. : 1950) | 61 | 21398611 |
| 2003 | Mal and MyD88: adapter proteins involved in signal transduction by Toll-like receptors. | Journal of endotoxin research | 60 | 12691620 |
| 2012 | MAL/MRTF-A controls migration of non-invasive cells by upregulation of cytoskeleton-associated proteins. | Journal of cell science | 59 | 22223881 |
| 1995 | Differential expression of mal genes under cAMP and endogenous inducer control in nutrient-stressed Escherichia coli. | Molecular microbiology | 59 | 7651130 |
| 1998 | Expression of the MAL gene in the thyroid: the MAL proteolipid, a component of glycolipid-enriched membranes, is apically distributed in thyroid follicles. | Endocrinology | 57 | 9528996 |
| 2010 | Formin INF2 regulates MAL-mediated transport of Lck to the plasma membrane of human T lymphocytes. | Blood | 55 | 20881207 |
| 2008 | Adaptation and mal-adaptation to ambient hypoxia; Andean, Ethiopian and Himalayan patterns. | PloS one | 53 | 18523639 |
| 2016 | NDE1 and NDEL1 from genes to (mal)functions: parallel but distinct roles impacting on neurodevelopmental disorders and psychiatric illness. | Cellular and molecular life sciences : CMLS | 52 | 27742926 |
| 2010 | IRAK1 and IRAK4 promote phosphorylation, ubiquitination, and degradation of MyD88 adaptor-like (Mal). | The Journal of biological chemistry | 52 | 20400509 |
| 2015 | DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer. | BMC cancer | 51 | 26482433 |
| 2011 | MAL protein controls protein sorting at the supramolecular activation cluster of human T lymphocytes. | Journal of immunology (Baltimore, Md. : 1950) | 51 | 21508261 |
| 2009 | Clustering and lateral concentration of raft lipids by the MAL protein. | Molecular biology of the cell | 51 | 19553470 |
| 1999 | Protease activation in apoptosis induced by MAL. | Experimental cell research | 51 | 10366425 |
| 2013 | Mal, more than a bridge to MyD88. | IUBMB life | 50 | 23983209 |
| 2010 | Elevated MAL expression is accompanied by promoter hypomethylation and platinum resistance in epithelial ovarian cancer. | International journal of cancer | 48 | 19642140 |
| 1996 | Expression, purification, and ligand-binding analysis of recombinant keratinocyte lipid-binding protein (MAL-1), an intracellular lipid-binding found overexpressed in neoplastic skin cells. | Biochemistry | 48 | 8608126 |
| 2007 | The Troll in Toll: Mal and Tram as bridges for TLR2 and TLR4 signaling. | Journal of leukocyte biology | 47 | 17449723 |
| 1997 | The MAL proteolipid is a component of the detergent-insoluble membrane subdomains of human T-lymphocytes. | The Biochemical journal | 47 | 9003426 |
| 2010 | SLURP1 mutation-impaired T-cell activation in a family with mal de Meleda. | The British journal of dermatology | 44 | 20854438 |
| 2010 | Epigenetic silencing of MAL, a putative tumor suppressor gene, can contribute to human epithelium cell carcinoma. | Molecular cancer | 43 | 21092172 |
| 2018 | HPV E4 expression and DNA hypermethylation of CADM1, MAL, and miR124-2 genes in cervical cancer and precursor lesions. | Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc | 42 | 30135508 |
| 2006 | Protein kinase Cdelta binds TIRAP/Mal to participate in TLR signaling. | Molecular immunology | 42 | 17161867 |
| 1997 | Myelin and lymphocyte protein (MAL/MVP17/VIP17) and plasmolipin are members of an extended gene family. | Gene | 42 | 9168137 |
| 1997 | Caveolin and MAL, two protein components of internal detergent-insoluble membranes, are in distinct lipid microenvironments in MDCK cells. | Biochemical and biophysical research communications | 41 | 9168919 |
| 2013 | Aberrant methylation of LINE-1, SLIT2, MAL and IGFBP7 in non-small cell lung cancer. | Oncology reports | 40 | 23381221 |
| 2013 | Differential role of MyD88 and Mal/TIRAP in TLR2-mediated gastric tumourigenesis. | Oncogene | 40 | 23728346 |
| 2004 | Expression of MAL and MAL2, two elements of the protein machinery for raft-mediated transport, in normal and neoplastic human tissue. | Histology and histopathology | 40 | 15168355 |
| 2019 | Conservation through the lens of (mal)adaptation: Concepts and meta-analysis. | Evolutionary applications | 39 | 31417615 |
| 2017 | Structure of the Major Apple Allergen Mal d 1. | Journal of agricultural and food chemistry | 38 | 28161953 |
| 2013 | Current methods for photodynamic therapy in the US: comparison of MAL/PDT and ALA/PDT. | Journal of drugs in dermatology : JDD | 36 | 23986167 |
| 2006 | Developmental expression of the SRF co-activator MAL in brain: role in regulating dendritic morphology. | Journal of neurochemistry | 36 | 16945101 |
| 1994 | Genomic structure and subcellular localization of MAL, a human T-cell-specific proteolipid protein. | The Journal of biological chemistry | 36 | 8132541 |
| 2017 | Src family kinase tyrosine phosphorylates Toll-like receptor 4 to dissociate MyD88 and Mal/Tirap, suppressing LPS-induced inflammatory responses. | Biochemical pharmacology | 35 | 29175418 |
| 2016 | Mal de Meleda: A Focused Review. | American journal of clinical dermatology | 35 | 26445964 |
| 2010 | Characterization and expression analysis of a maltose-utilizing (MAL) cluster in Aspergillus oryzae. | Fungal genetics and biology : FG & B | 35 | 19850146 |
| 2014 | The core and conserved role of MAL is homeostatic regulation of actin levels. | Genes & development | 34 | 24831700 |
| 2019 | CADM1, MAL, and miR124 Promoter Methylation as Biomarkers of Transforming Cervical Intrapithelial Lesions. | International journal of molecular sciences | 33 | 31067838 |
| 2008 | Etk/BMX, a Btk family tyrosine kinase, and Mal contribute to the cross-talk between MyD88 and FAK pathways. | Journal of immunology (Baltimore, Md. : 1950) | 32 | 18292575 |
| 2003 | Features of influenza HA required for apical sorting differ from those required for association with DRMs or MAL. | Traffic (Copenhagen, Denmark) | 32 | 14617347 |
| 2015 | Preliminary evaluation of [18F]AlF-NOTA-MAL-Cys39-exendin-4 in insulinoma with PET. | Journal of drug targeting | 31 | 25758750 |
| 1992 | Chromosome mal-orientation and reorientation during mitosis. | Cell motility and the cytoskeleton | 31 | 1423661 |
| 2019 | HSV-1/TLR9-Mediated IFNβ and TNFα Induction Is Mal-Dependent in Macrophages. | Journal of innate immunity | 30 | 31851971 |
| 2004 | Characterisation of Mal d 1-related genes in Malus. | Plant molecular biology | 30 | 15604687 |
| 2010 | MAL/VIP17, a new player in the regulation of NKCC2 in the kidney. | Molecular biology of the cell | 29 | 20861303 |
| 2017 | Human Papillomavirus Genotypes and Methylation of CADM1, PAX1, MAL and ADCYAP1 Genes in Epithelial Ovarian Cancer Patients. | Asian Pacific journal of cancer prevention : APJCP | 28 | 28240513 |
| 2016 | A Common Variant in the Adaptor Mal Regulates Interferon Gamma Signaling. | Immunity | 28 | 26885859 |
| 2013 | MyD88 adaptor-like (Mal) functions in the epithelial barrier and contributes to intestinal integrity via protein kinase C. | Mucosal immunology | 28 | 23612054 |
| 2006 | Characterization of recombinant Mal d 4 and its application for component-resolved diagnosis of apple allergy. | Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology | 28 | 16911365 |
| 1999 | Functional domain analysis of the Saccharomyces MAL-activator. | Current genetics | 28 | 10447589 |
| 2023 | Cancer CD39 drives metabolic adaption and mal-differentiation of CD4+ T cells in patients with non-small-cell lung cancer. | Cell death & disease | 27 | 38062068 |
| 2019 | On The Role of Myelin and Lymphocyte Protein (MAL) In Cancer: A Puzzle With Two Faces. | Journal of Cancer | 26 | 31258734 |
| 2016 | MAL and TMEM220 are novel DNA methylation markers in human gastric cancer. | Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals | 26 | 27329150 |
| 1998 | A short peptide motif at the carboxyl terminus is required for incorporation of the integral membrane MAL protein to glycolipid-enriched membranes. | The Journal of biological chemistry | 26 | 9582298 |
| 2024 | Acetylation of TIR domains in the TLR4-Mal-MyD88 complex regulates immune responses in sepsis. | The EMBO journal | 25 | 39294473 |
| 2019 | Clostridium perfringens epsilon toxin induces blood brain barrier permeability via caveolae-dependent transcytosis and requires expression of MAL. | PLoS pathogens | 25 | 31703116 |
| 2020 | Myelin-Associated MAL and PLP Are Unusual among Multipass Transmembrane Proteins in Preferring Ordered Membrane Domains. | The journal of physical chemistry. B | 24 | 32436385 |
| 2016 | Sequential and compartmentalized action of Rabs, SNAREs, and MAL in the apical delivery of fusiform vesicles in urothelial umbrella cells. | Molecular biology of the cell | 24 | 27009205 |
| 2013 | Synthesis and preclinical characterization of [64Cu]NODAGA-MAL-exendin-4 with a Nε-maleoyl-L-lysyl-glycine linkage. | Nuclear medicine and biology | 24 | 23932646 |
| 2023 | From Non-Alcoholic Fatty Liver to Hepatocellular Carcinoma: A Story of (Mal)Adapted Mitochondria. | Biology | 23 | 37106795 |
| 2021 | The MAL Protein, an Integral Component of Specialized Membranes, in Normal Cells and Cancer. | Cells | 23 | 33946345 |
| 2018 | RAC2 promotes abnormal proliferation of quiescent cells by enhanced JUNB expression via the MAL-SRF pathway. | Cell cycle (Georgetown, Tex.) | 22 | 29895215 |
| 2014 | MyD88 adaptor-like (Mal) regulates intestinal homeostasis and colitis-associated colorectal cancer in mice. | American journal of physiology. Gastrointestinal and liver physiology | 21 | 24603458 |
| 2004 | Mutations in SIN4 and RGR1 cause constitutive expression of MAL structural genes in Saccharomyces cerevisiae. | Genetics | 21 | 15514050 |
| 2022 | The Role of Microglia in the (Mal)adaptive Response to Traumatic Experience in an Animal Model of PTSD. | International journal of molecular sciences | 20 | 35806185 |
| 2022 | Combined Liquid Biopsy Methylation Analysis of CADM1 and MAL in Cervical Cancer Patients. | Cancers | 20 | 36010947 |
| 2011 | MAL-PDT for difficult to treat nonmelanoma skin cancer. | Dermatologic therapy | 20 | 21276161 |
| 2022 | Gene methylation of CADM1 and MAL identified as a biomarker of high grade anal intraepithelial neoplasia. | Scientific reports | 19 | 35241698 |
| 2011 | Poxvirus A46 protein binds to TIR domain-containing Mal/TIRAP via an α-helical sub-domain. | Molecular immunology | 19 | 21831443 |
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