Gene Ontology annotation through association of InterPro records with GO terms

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

Annotation inferences using phylogenetic trees

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt

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

Gene Ontology annotation of human sequence-specific DNA binding transcription factors (DbTFs) based on the TFClass database

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods

TBX5 transcription factor regulates cell proliferation during cardiogenesis.

Tbx5 associates with Nkx2-5 and synergistically promotes cardiomyocyte differentiation.

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

Induction of apoptosis and inhibition of cell growth by developmental regulator hTBX5.

Functional analysis of TBX5 missense mutations associated with Holt-Oram syndrome.

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

TBX5 nuclear localization is mediated by dual cooperative intramolecular signals.

A role for Tbx5 in proepicardial cell migration during cardiogenesis.

The T-Box transcription factor Tbx5 is required for the patterning and maturation of the murine cardiac conduction system.

TBX5 genetic testing validates strict clinical criteria for Holt-Oram syndrome.

A WW domain protein TAZ is a critical coactivator for TBX5, a transcription factor implicated in Holt-Oram syndrome.

Epicardial-myocardial signaling directing coronary vasculogenesis.

β-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis.

GATA4 loss-of-function mutations underlie familial tetralogy of fallot.

A novel TBX5 loss-of-function mutation associated with sporadic dilated cardiomyopathy.

Intermolecular Interactions of Cardiac Transcription Factors NKX2.5 and TBX5.

TBX5 loss-of-function mutation contributes to atrial fibrillation and atypical Holt-Oram syndrome.

Acetylation of TBX5 by KAT2B and KAT2A regulates heart and limb development.

A reference map of the human binary protein interactome.

Holt-Oram syndrome is caused by mutations in TBX5, a member of the Brachyury (T) gene family.

Mutations in human TBX5 [corrected] cause limb and cardiac malformation in Holt-Oram syndrome.

WWTR1 (TAZ), TBX5, and PCAF form a complex

Tbx5 is essential for forelimb bud initiation following patterning of the limb field in the mouse embryo.

Tbx5 is required for forelimb bud formation and continued outgrowth.

LMP4 regulates Tbx5 protein subcellular localization and activity.

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

Physical interaction between TBX5 and MEF2C is required for early heart development.

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

Reptilian heart development and the molecular basis of cardiac chamber evolution.

Pitx2 modulates a Tbx5-dependent gene regulatory network to maintain atrial rhythm.

Pdlim7 (LMP4) regulation of Tbx5 specifies zebrafish heart atrio-ventricular boundary and valve formation.