Gene Ontology annotation through association of InterPro records with GO terms

Gene Ontology annotation by the MGI curatorial staff, curated orthology

Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity

Annotation inferences using phylogenetic trees

Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Electronic Gene Ontology annotations created by ARBA machine learning models

Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs

Combined Automated Annotation using Multiple IEA Methods

The cardiac homeobox gene Csx/Nkx2.5 lies genetically upstream of multiple genes essential for heart development.

Characterization of homo- and heterodimerization of cardiac Csx/Nkx2.5 homeoprotein.

Nkx2.5 and Nkx2.6, homologs of Drosophila tinman, are required for development of the pharynx.

A murine model of Holt-Oram syndrome defines roles of the T-box transcription factor Tbx5 in cardiogenesis and disease.

The combinatorial activities of Nkx2.5 and dHAND are essential for cardiac ventricle formation.

Csx/Nkx2-5 is required for homeostasis and survival of cardiac myocytes in the adult heart.

Cooperative action of Tbx2 and Nkx2.5 inhibits ANF expression in the atrioventricular canal: implications for cardiac chamber formation.

Hop is an unusual homeobox gene that modulates cardiac development.

The basic-helix-loop-helix transcription factor HAND2 directly regulates transcription of the atrial naturetic peptide gene.

Csm, a cardiac-specific isoform of the RNA helicase Mov10l1, is regulated by Nkx2.5 in embryonic heart.

GATA4 mutations cause human congenital heart defects and reveal an interaction with TBX5.

Cardiac T-box factor Tbx20 directly interacts with Nkx2-5, GATA4, and GATA5 in regulation of gene expression in the developing heart.

Myocardin expression is regulated by Nkx2.5, and its function is required for cardiomyogenesis.

Differential expression and function of Tbx5 and Tbx20 in cardiac development.

Nkx2-5 mutation causes anatomic hypoplasia of the cardiac conduction system.

Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block.

Foxh1 is essential for development of the anterior heart field.

Jumonji represses atrial natriuretic factor gene expression by inhibiting transcriptional activities of cardiac transcription factors.

CSX/Nkx2.5 modulates differentiation of skeletal myoblasts and promotes differentiation into neuronal cells in vitro.

Murine T-box transcription factor Tbx20 acts as a repressor during heart development, and is essential for adult heart integrity, function and adaptation.

Cooperative and antagonistic interactions between Sall4 and Tbx5 pattern the mouse limb and heart.

Missense mutation in the transcription factor NKX2-5: a novel molecular event in the pathogenesis of thyroid dysgenesis.

A tyrosine-rich domain within homeodomain transcription factor Nkx2-5 is an essential element in the early cardiac transcriptional regulatory machinery.

Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field.

The transcriptional coactivator CAMTA2 stimulates cardiac growth by opposing class II histone deacetylases.

Molecular pathway for the localized formation of the sinoatrial node.

Nkx2.5 cell-autonomous gene function is required for the postnatal formation of the peripheral ventricular conduction system.

An Nkx2-5/Bmp2/Smad1 negative feedback loop controls heart progenitor specification and proliferation.

Transcriptional repression by the T-box proteins Tbx18 and Tbx15 depends on Groucho corepressors.

A molecular pathway including Id2, Tbx5, and Nkx2-5 required for cardiac conduction system development.

Pitx2c and Nkx2-5 are required for the formation and identity of the pulmonary myocardium.

Perinatal loss of Nkx2-5 results in rapid conduction and contraction defects.

Nkx2-5- and Isl1-expressing cardiac progenitors contribute to proepicardium.

Cooperative interaction of Nkx2.5 and Mef2c transcription factors during heart development.

Shox2 is essential for the differentiation of cardiac pacemaker cells by repressing Nkx2-5.

NKX2-5 regulates the expression of beta-catenin and GATA4 in ventricular myocytes.

A histone H3 lysine 36 trimethyltransferase links Nkx2-5 to Wolf-Hirschhorn syndrome.

Slow progressive conduction and contraction defects in loss of Nkx2-5 mice after cardiomyocyte terminal differentiation.

miR-145 and miR-143 regulate smooth muscle cell fate and plasticity.

Foxp1 coordinates cardiomyocyte proliferation through both cell-autonomous and nonautonomous mechanisms.

The cardiac transcription network modulated by Gata4, Mef2a, Nkx2.5, Srf, histone modifications, and microRNAs.

Ectopic expression of Nkx2.5 suppresses the formation of the sinoatrial node in mice.

Tinman/Nkx2-5 acts via miR-1 and upstream of Cdc42 to regulate heart function across species.

Complex SUMO-1 regulation of cardiac transcription factor Nkx2-5.

UTX, a histone H3-lysine 27 demethylase, acts as a critical switch to activate the cardiac developmental program.

Congenital asplenia in mice and humans with mutations in a Pbx/Nkx2-5/p15 module.

UTX and UTY demonstrate histone demethylase-independent function in mouse embryonic development.

Histone H3 lysine 9 methyltransferases, G9a and GLP are essential for cardiac morphogenesis.

Myogenic and morphogenetic defects in the heart tubes of murine embryos lacking the homeo box gene Nkx2-5.

Recruitment of the tinman homolog Nkx-2.5 by serum response factor activates cardiac alpha-actin gene transcription.

Activation of the cardiac alpha-actin promoter depends upon serum response factor, Tinman homologue, Nkx-2.5, and intact serum response elements.

Homeodomain factor Nkx2-5 controls left/right asymmetric expression of bHLH gene eHand during murine heart development.

The cardiac tissue-restricted homeobox protein Csx/Nkx2.5 physically associates with the zinc finger protein GATA4 and cooperatively activates atrial natriuretic factor gene expression.

Vertebrate homologs of tinman and bagpipe: roles of the homeobox genes in cardiovascular development.

Congenital heart disease caused by mutations in the transcription factor NKX2-5.

Homeodomain-interacting protein kinases, a novel family of co-repressors for homeodomain transcription factors.

Myocyte enhancer factor 2C and Nkx2-5 up-regulate each other's expression and initiate cardiomyogenesis in P19 cells.

Expression of Nkx2-5 in cardiogenesis

Nkx2-5 binds the Tbx5 gene

Gata4, Smad1:Smad4, Mef2c, Tbx20, and Nkx2-5 bind the Nkx2-5 gene

Gata4, Isl1, Tbx20, and Nkx2-5 bind the Mef2c gene

Nkx2-5 binds the Gata6 gene

Foxo4, Mef2c, and Nkx2-5 bind the Myocd gene