PubMed:26578114 JSONTXT

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"26578114-8#14#18#gene274","span":{"begin":1429,"end":1433},"obj":"gene274"},{"id":"26578114-8#63#76#diseaseC0018801","span":{"begin":1478,"end":1491},"obj":"diseaseC0018801"},{"id":"26578114-8#63#76#diseaseC0018802","span":{"begin":1478,"end":1491},"obj":"diseaseC0018802"}],"relations":[{"id":"14#18#gene27463#76#diseaseC0018801","pred":"associated_with","subj":"26578114-8#14#18#gene274","obj":"26578114-8#63#76#diseaseC0018801"},{"id":"14#18#gene27463#76#diseaseC0018802","pred":"associated_with","subj":"26578114-8#14#18#gene274","obj":"26578114-8#63#76#diseaseC0018802"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T1847","span":{"begin":1429,"end":1433},"obj":"gene:274"},{"id":"T1848","span":{"begin":1478,"end":1491},"obj":"disease:C0018801"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T1847","obj":"T1848"},{"id":"R2","pred":"associated_with","subj":"T1847","obj":"T1848"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":41},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":42,"end":224},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":225,"end":377},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":378,"end":603},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":604,"end":801},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":802,"end":951},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":952,"end":1249},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1250,"end":1414},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":1415,"end":1614},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":1615,"end":1664},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":1665,"end":1687},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1688,"end":1795},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":41},"obj":"Sentence"},{"id":"T2","span":{"begin":42,"end":224},"obj":"Sentence"},{"id":"T3","span":{"begin":225,"end":377},"obj":"Sentence"},{"id":"T4","span":{"begin":378,"end":603},"obj":"Sentence"},{"id":"T5","span":{"begin":604,"end":801},"obj":"Sentence"},{"id":"T6","span":{"begin":802,"end":951},"obj":"Sentence"},{"id":"T7","span":{"begin":952,"end":1249},"obj":"Sentence"},{"id":"T8","span":{"begin":1250,"end":1414},"obj":"Sentence"},{"id":"T9","span":{"begin":1415,"end":1614},"obj":"Sentence"},{"id":"T10","span":{"begin":1615,"end":1664},"obj":"Sentence"},{"id":"T11","span":{"begin":1665,"end":1687},"obj":"Sentence"},{"id":"T12","span":{"begin":1688,"end":1795},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":206,"end":211},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1316,"end":1321},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1478,"end":1483},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1747,"end":1752},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":1136,"end":1148},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":206,"end":211},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1316,"end":1321},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1478,"end":1483},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1747,"end":1752},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":1316,"end":1329},"obj":"Disease"},{"id":"T2","span":{"begin":1478,"end":1491},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":1316,"end":1329},"obj":"Phenotype"},{"id":"T2","span":{"begin":1478,"end":1491},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0001635"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0001635"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":1310,"end":1315},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":1472,"end":1477},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"9606"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":32,"end":40},"obj":"Body_part"},{"id":"T4","span":{"begin":94,"end":102},"obj":"Body_part"},{"id":"T7","span":{"begin":103,"end":113},"obj":"Body_part"},{"id":"T8","span":{"begin":206,"end":211},"obj":"Body_part"},{"id":"T12","span":{"begin":310,"end":317},"obj":"Body_part"},{"id":"T13","span":{"begin":335,"end":344},"obj":"Body_part"},{"id":"T14","span":{"begin":354,"end":366},"obj":"Body_part"},{"id":"T15","span":{"begin":367,"end":376},"obj":"Body_part"},{"id":"T16","span":{"begin":578,"end":593},"obj":"Body_part"},{"id":"T17","span":{"begin":747,"end":755},"obj":"Body_part"},{"id":"T20","span":{"begin":1176,"end":1184},"obj":"Body_part"},{"id":"T23","span":{"begin":1316,"end":1321},"obj":"Body_part"},{"id":"T27","span":{"begin":1478,"end":1483},"obj":"Body_part"},{"id":"T31","span":{"begin":1665,"end":1678},"obj":"Body_part"},{"id":"T32","span":{"begin":1747,"end":1752},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/GO_0016020"},{"id":"A2","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"},{"id":"A3","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/GO_0016020"},{"id":"A5","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"},{"id":"A6","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/GO_0043226"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A9","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"A10","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"A11","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0015230"},{"id":"A12","pred":"uberon_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/CL_0000187"},{"id":"A13","pred":"uberon_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/UBERON_0007651"},{"id":"A14","pred":"uberon_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/GO_0016528"},{"id":"A15","pred":"uberon_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/UBERON_0007361"},{"id":"A16","pred":"uberon_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/CL_0000746"},{"id":"A17","pred":"uberon_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/GO_0016020"},{"id":"A18","pred":"uberon_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"},{"id":"A19","pred":"uberon_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"A20","pred":"uberon_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/GO_0016020"},{"id":"A21","pred":"uberon_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"},{"id":"A22","pred":"uberon_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"A23","pred":"uberon_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A24","pred":"uberon_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"A25","pred":"uberon_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"A26","pred":"uberon_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/UBERON_0015230"},{"id":"A27","pred":"uberon_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A28","pred":"uberon_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"A29","pred":"uberon_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"A30","pred":"uberon_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/UBERON_0015230"},{"id":"A31","pred":"uberon_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/CL_0000746"},{"id":"A32","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A33","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"A34","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"A35","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0015230"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":206,"end":211},"obj":"Body_part"},{"id":"T2","span":{"begin":1316,"end":1321},"obj":"Body_part"},{"id":"T3","span":{"begin":1478,"end":1483},"obj":"Body_part"},{"id":"T4","span":{"begin":1747,"end":1752},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000036"},{"id":"A2","pred":"mat_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MAT_0000036"},{"id":"A3","pred":"mat_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MAT_0000036"},{"id":"A4","pred":"mat_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MAT_0000036"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":310,"end":317},"obj":"Cell"},{"id":"T2","span":{"begin":578,"end":593},"obj":"Cell"},{"id":"T3","span":{"begin":586,"end":593},"obj":"Cell"},{"id":"T4","span":{"begin":1665,"end":1678},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000187"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000746"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000187"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000746"}],"text":"BIN1 regulates dynamic t-tubule membrane.\nCardiac transverse tubules (t-tubules) are specific membrane organelles critical in calcium signaling and excitation-contraction coupling required for beat-to-beat heart contraction. T-tubules are highly branched and form an interconnected network that penetrates the myocyte interior to form junctions with the sarcoplasmic reticulum. T-tubules are selectively enriched with specific ion channels and proteins crucial in calcium transient development necessary in excitation-contraction coupling, thus t-tubules are a key component of cardiac myocyte function. In this review, we focus primarily on two proteins concentrated within the t-tubular network, the L-type calcium channel (LTCC) and associated membrane anchor protein, bridging integrator 1 (BIN1). Here, we provide an overview of current knowledge in t-tubule morphology, composition, microdomains, as well as the dynamics of the t-tubule network. Secondly, we highlight multiple aspects of BIN1-dependent t-tubule function, which includes forward trafficking of LTCCs to t-tubules, LTCC clustering at t-tubule surface, microdomain organization and regulation at t-tubule membrane, and the formation of a slow diffusion barrier within t-tubules. Lastly, we describe progress in characterizing how acquired human heart failure can be attributed to abnormal BIN1 transcription and associated t-tubule remodeling. Understanding BIN1-regulated cardiac t-tubule biology in human heart failure management has the dual benefit of promoting progress in both biomarker development and therapeutic target identification. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel."}