Search results for "filamins"

showing 10 items of 31 documents

The regulation mechanism for the auto-inhibition of binding of human filamin A to integrin.

2009

The ability of adhesion receptors to transmit biochemical signals and mechanical force across cell membranes depends on interactions with the actin cytoskeleton. Human filamins are large actin cross-linking proteins that connect integrins to the cytoskeleton. Filamin binding to the cytoplasmic tail of beta integrins has been shown to prevent integrin activation in cells, which is important for controlling cell adhesion and migration. The molecular-level mechanism for filamin binding to integrin has been unclear, however, as it was recently demonstrated that filamin undergoes intramolecular auto-inhibition of integrin binding. In this study, using steered molecular dynamics simulations, we f…

Models MolecularProtein Foldinganimal structuresIntegrin beta ChainsFilaminsmacromolecular substancesBiologyFilaminCD49cCollagen receptorFilamin bindingPhosphoserineContractile ProteinsStructural BiologyHumansPhosphorylationMolecular BiologyIntegrin bindingBinding SitesMicrofilament ProteinsActin cytoskeletonCell biologybody regionsIntegrin alpha Mbiology.proteinIntegrin beta 6Stress MechanicalPeptidesProtein BindingJournal of molecular biology
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Small-angle X-ray scattering reveals compact domain-domain interactions in the N-terminal region of filamin C

2014

Filamins are multi-domain, actin cross-linking, and scaffolding proteins. In addition to the actin cross-linking function, filamins have a role in mechanosensor signaling. The mechanosensor function is mediated by domain-domain interaction in the C-terminal region of filamins. Recently, we have shown that there is a three-domain interaction module in the Nterminal region of filamins, where the neighboring domains stabilize the structure of the middle domain and thereby regulate its interaction with ligands. In this study, we have used small-angle X-ray scattering as a tool to screen for potential domain-domain interactions in the N-terminal region. We found evidence of four domain-domain in…

Models MolecularScaffold proteinProtein StructureProtein ConformationFilaminslcsh:Medicinemacromolecular substancesBiologyFilaminBiochemistryProtein–protein interactionProtein structureX-Ray Diffractioncompact domain-domain interactionsScattering Small AngleMacromolecular Structure AnalysisProtein InteractionsCytoskeletonlcsh:ScienceMolecular BiologyActinMultidisciplinarySmall-angle X-ray scatteringlcsh:Rta1182Biology and Life SciencesProteinsComputational BiologyRecombinant ProteinsProtein Structure TertiaryCell biologyCytoskeletal Proteinssmall-angle X-ray scatteringDomain (ring theory)Biophysicslcsh:QGlobular ProteinsStructural ProteinsResearch Articlefilamin CPloS One
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β2 integrin phosphorylation on Thr758 acts as a molecular switch to regulate 14-3-3 and filamin binding

2008

AbstractLeukocyte integrins of the β2 family are essential for immune cell-cell adhesion. In activated cells, β2 integrins are phosphorylated on the cytoplasmic Thr758, leading to 14-3-3 protein recruitment to the β2 integrin. The mutation of this phosphorylation site impairs cell adhesion, actin reorganization, and cell spreading. Thr758 is contained in a Thr triplet of β2 that also mediates binding to filamin. Here, we investigated the binding of filamin, talin, and 14-3-3 proteins to phosphorylated and unphosphorylated β2 integrins by biochemical methods and x-ray crystallography. 14-3-3 proteins bound only to the phosphorylated integrin cytoplasmic peptide, with a high affinity (Kd, 261…

Models MolecularTalinThreonineanimal structuresFilaminsT-LymphocytesStatic ElectricityImmunologyIntegrinCD18macromolecular substancesPlasma protein bindingIn Vitro TechniquesFilaminBiochemistryJurkat Cells03 medical and health sciencesFilamin bindingContractile Proteins0302 clinical medicineCell AdhesionHumansProtein Interaction Domains and MotifsPhosphorylationCell adhesion030304 developmental biology0303 health sciencesBinding SitesbiologyChemistryMicrofilament ProteinsCell BiologyHematologyIntercellular Adhesion Molecule-1Talin bindingRecombinant ProteinsCell biology14-3-3 ProteinsAmino Acid SubstitutionCD18 AntigensMultiprotein Complexes030220 oncology & carcinogenesisbiology.proteinPhosphorylationProtein BindingBlood
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The molecular basis of filamin binding to integrins and competition with talin.

2006

The ability of adhesion receptors to transmit biochemical signals and mechanical force across cell membranes depends on interactions with the actin cytoskeleton. Filamins are large, actin-crosslinking proteins that connect multiple transmembrane and signaling proteins to the cytoskeleton. Here, we describe the high-resolution structure of an interface between filamin A and an integrin adhesion receptor. When bound, the integrin beta cytoplasmic tail forms an extended beta strand that interacts with beta strands C and D of the filamin immunoglobulin-like domain (IgFLN) 21. This interface is common to many integrins, and we suggest it is a prototype for other IgFLN domain interactions. Notabl…

Models MolecularTalinanimal structuresIntegrin beta ChainsProtein ConformationFilaminsRecombinant Fusion ProteinsIntegrinMolecular Sequence Datamacromolecular substancesPlasma protein bindingFilaminCrystallography X-RayFilamin bindingMiceContractile ProteinsFLNAAnimalsAmino Acid SequenceMolecular BiologyNuclear Magnetic Resonance BiomolecularBinding SitesbiologySequence Homology Amino AcidCalpainMicrofilament ProteinsReproducibility of ResultsCell BiologyActin cytoskeletonCell biologyProtein Structure Tertiarybody regionsIntegrin alpha Mbiology.proteinNIH 3T3 CellsIntegrin beta 6Protein BindingMolecular cell
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Structure of the human filamin A actin-binding domain.

2009

Filamin A (FLNa) is a large dimeric protein that binds to actin filaments via its actin-binding domain (ABD). The crystal structure of this domain was solved at 3.2 A resolution. The domain adopts a closed conformation typical of other ABDs, but also forms a dimer both in crystallization conditions and in solution. The structure shows the localization of the residues mutated in patients with periventricular nodular heterotopia or otopalatodigital syndrome. Structural analysis predicts that mutations in both types of disorder may affect actin binding.

Models Molecularanimal structuresDimerFilaminsmacromolecular substancesFilaminCalponin homology domainCrystallography X-Raychemistry.chemical_compoundContractile ProteinsStructural BiologyFLNAHumansProtein Interaction Domains and MotifsActin-binding proteinProtein Structure QuaternaryActinbiologyMicrofilament ProteinsGeneral MedicineActinschemistryStructural Homology ProteinDomain (ring theory)Mutationbiology.proteinBiophysicsBinding domainProtein BindingActa crystallographica. Section D, Biological crystallography
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The C-terminal rod 2 fragment of filamin A forms a compact structure that can be extended

2012

Filamins are large proteins that cross-link actin filaments and connect to other cellular components. The C-terminal rod 2 region of FLNa (filamin A) mediates dimerization and interacts with several transmembrane receptors and intracellular signalling adaptors. SAXS (small-angle X-ray scattering) experiments were used to make a model of a six immunoglobulin-like domain fragment of the FLNa rod 2 (domains 16–21). This fragment had a surprising three-branched structural arrangement, where each branch was made of a tightly packed two-domain pair. Peptides derived from transmembrane receptors and intracellular signalling proteins induced a more open structure of the six domain fragment. Mutagen…

Models Moleculargenetics [Receptors Dopamine D3]metabolism [Recombinant Proteins]Protein Conformationgenetics [Antigens CD18]chemistry [Recombinant Proteins]Plasma protein bindingCrystallography X-RayLigandsFilaminmetabolism [Antigens CD18]metabolism [Cytoskeletal Proteins]BiochemistryfilaminsContractile ProteinsProtein structuremetabolism [Peptide Fragments]FLNAchemistry [Antigens CD18]genetics [Cell Adhesion Molecules]Small-angle X-ray scatteringMicrofilament Proteinsgenetics [Contractile Proteins]Recombinant Proteinschemistry [Receptors Dopamine D3]FBLIM1 protein humanddc:540Domain (ring theory)DimerizationProtein Bindingchemistry [Contractile Proteins]FilaminsAntigens CD18metabolism [Cell Adhesion Molecules]BiologyScattering Small Anglemetabolism [Receptors Dopamine D3]Humanschemistry [Microfilament Proteins]Protein Interaction Domains and Motifsmetabolism [Mutant Proteins]DRD3 protein humanMolecular Biologymetabolism [Contractile Proteins]Actingenetics [Cytoskeletal Proteins]Cryoelectron MicroscopyMutagenesista1182Receptors Dopamine D3metabolism [Microfilament Proteins]Cell Biologychemistry [Cell Adhesion Molecules]genetics [Peptide Fragments]Peptide FragmentsCytoskeletal ProteinsCrystallographychemistry [Mutant Proteins]chemistry [Peptide Fragments]CD18 AntigensBiophysicschemistry [Cytoskeletal Proteins]Mutant Proteinsgenetics [Microfilament Proteins]Cell Adhesion MoleculesBiochemical Journal
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Filamin C accumulation is a strong but nonspecific immunohistochemical marker of core formation in muscle.

2002

Filamin C is the muscle isoform of a group of large actin-crosslinking proteins. On the one hand, filamin C is associated with the Z-disk of the myofibrillar apparatus and binds to myotilin; on the other hand, it interacts with the sarcoglycan complex at the sarcolemma. Filamin C may be involved in reorganizing the cytoskeleton in response to signalling events and in muscle it may, in addition, fulfill structural functions at the Z-disk. An examination of biopsies from patients with multi-minicore myopathy, central core myopathy and neurogenic target fibers with core-like target formations (TF) revealed strong reactivity of all the cores and target formations with two different anti-filamin…

Pathologymedicine.medical_specialtyanimal structuresBiopsyFilaminsmacromolecular substancesBiologyFilamin03 medical and health sciences0302 clinical medicineContractile ProteinsMuscular DiseasesReference ValuesmedicineMyotilinHumansProtein IsoformsCytoskeletonMyopathyMicroscopy ImmunoelectronMuscle Skeletal030304 developmental biology0303 health sciencesSarcolemmaMicrofilament Proteinsmedicine.diseaseImmunohistochemistryCell biologybody regionsNeurologyDesminNeurology (clinical)medicine.symptomMyofibrilCarrier Proteins030217 neurology & neurosurgeryCentral core diseaseBiomarkersJournal of the neurological sciences
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Critical Structural Defects Explain Filamin A Mutations Causing Mitral Valve Dysplasia

2019

Mitral valve diseases affect approximately 3% of the population and are the most common reasons for valvular surgery because no drug-based treatments exist. Inheritable genetic mutations have now been established as the cause of mitral valve insufficiency, and four different missense mutations in the filamin A gene (FLNA) have been found in patients suffering from non-syndromic mitral valve dysplasia (MVD). The FLNA protein is expressed, in particular, in endocardial endothelia during fetal valve morphogenesis and is key in cardiac development. The FLNA-MVD causing mutations are clustered in the N-terminal region of FLNA. How the mutations in FLNA modify its structure and function, have mos…

Protein FoldingdysplasiatFilamins[SDV]Life Sciences [q-bio]PopulationProtein Tyrosine Phosphatase Non-Receptor Type 12BiophysicsMutation Missensesynnynnäiset sydänviatProtein tyrosine phosphataseBiologyMolecular Dynamics Simulationmedicine.disease_causeFilamin03 medical and health sciences0302 clinical medicinemitral valve dysplasiaMitral valvemedicineFLNAMissense mutationHumanseducationGene030304 developmental biologyGenetics0303 health sciencesMutationeducation.field_of_studyBinding SitesMitral Valve Prolapsecritical structural defectshiippaläppäfilamiinitArticles3. Good healthmedicine.anatomical_structurecardiovascular systemfilamin A mutationsgeneettiset tekijätmutaatiot030217 neurology & neurosurgeryProtein Binding
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Cystic Fibrosis Transmembrane Conductance Regulator Interacts with Multiple Immunoglobulin Domains of Filamin A

2010

Mutations of the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) that impair its apical localization and function cause cystic fibrosis. A previous report has shown that filamin A (FLNa), an actin-cross-linking and -scaffolding protein, interacts directly with the cytoplasmic N terminus of CFTR and that this interaction is necessary for stability and confinement of the channel to apical membranes. Here, we report that the CFTR N terminus has sequence similarity to known FLNa-binding partner-binding sites. FLNa has 24 Ig (IgFLNa) repeats, and a CFTR peptide pulled down repeats 9, 12, 17, 19, 21, and 23, which share sequence similarity yet differ from the other FLN…

Scaffold proteincongenital hereditary and neonatal diseases and abnormalitiesFilaminsMolecular Sequence DataCystic Fibrosis Transmembrane Conductance RegulatorImmunoglobulinsBiologymedicine.disease_causeFilaminBiochemistryContractile ProteinsProtein structureCricetinaemedicineAnimalsHumansFLNAAmino Acid SequenceMolecular BiologyPeptide sequenceMutationSequence Homology Amino AcidCell MembraneMicrofilament ProteinsCell Biologyrespiratory systemMolecular biologyActinsCystic fibrosis transmembrane conductance regulatorProtein Structure Tertiaryrespiratory tract diseasesCell biologySolubilityMutationProtein Structure and FoldingChloride channelbiology.proteinPeptidesDimerizationProtein BindingJournal of Biological Chemistry
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Inter-domain interactions in filamins

2014

kristallografiaCrystallographyrakennevuorovaikutusproteiineihin sitoutuminenfilamiinitimmunoglobulin-like domainssmall angle x-ray scatteringrakenneanalyysifilaminskiderakenteetinter-domain interactionsdomeenitproteiinitsitoutumispaikatmechanosensorröntgensironta
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