Source Name Characteristics [Organism] Term Source REF Term Accession Number Description Sample Name Extract Name Material Type Protocol REF Labeled Extract Name Label Material Type Protocol REF Hybridization Name Array Design REF Protocol REF Scan Name Array Data File Comment [ArrayExpress FTP file] Derived Array Data Matrix File Comment [Derived ArrayExpress FTP file] GSE5298GSM120066 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120066 sample GSE5298GSM120066 extract total_RNA P-G5298-1 GSE5298GSM120066 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_control_rep3 A-AFFY-45 P-AFFY-6 AVC_control_rep3 GSM120066.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120069 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120069 sample GSE5298GSM120069 extract total_RNA P-G5298-1 GSE5298GSM120069 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_mutant_rep2 A-AFFY-45 P-AFFY-6 AVC_mutant_rep2 GSM120069.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120064 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120064 sample GSE5298GSM120064 extract total_RNA P-G5298-1 GSE5298GSM120064 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_control_rep1 A-AFFY-45 P-AFFY-6 AVC_control_rep1 GSM120064.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120067 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120067 sample GSE5298GSM120067 extract total_RNA P-G5298-1 GSE5298GSM120067 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_control_rep4 A-AFFY-45 P-AFFY-6 AVC_control_rep4 GSM120067.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120071 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120071 sample GSE5298GSM120071 extract total_RNA P-G5298-1 GSE5298GSM120071 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_mutant_rep4 A-AFFY-45 P-AFFY-6 AVC_mutant_rep4 GSM120071.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120065 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120065 sample GSE5298GSM120065 extract total_RNA P-G5298-1 GSE5298GSM120065 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_control_rep2 A-AFFY-45 P-AFFY-6 AVC_control_rep2 GSM120065.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120068 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120068 sample GSE5298GSM120068 extract total_RNA P-G5298-1 GSE5298GSM120068 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_mutant_rep1 A-AFFY-45 P-AFFY-6 AVC_mutant_rep1 GSM120068.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip GSE5298GSM120070 Mus musculus EFO http://purl.org/obo/owl/NCBITaxon#NCBITaxon_10090 Atrioventricular canal: Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the heart undergoes an epithelial to mesenchymal transition (EMT) to form mesenchymal progenitors of the AV valves. Further growth and differentiation of these mesenchymal precursors results in formation of portions of the atrial and ventricular septae, and generation of thin, pliable valves. The transcription factor Gata4 is expressed in the endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelial-derived cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3 downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in decreased proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.. Strain: a mixed C57BL6/129 genetic background GSE5298GSM120070 sample GSE5298GSM120070 extract total_RNA P-G5298-1 GSE5298GSM120070 LE biotin synthetic_RNA Affymetrix:Protocol:Hybridization-Unknown AVC_mutant_rep3 A-AFFY-45 P-AFFY-6 AVC_mutant_rep3 GSM120070.CEL ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.raw.1.zip E-GEOD-5298-processed-data-1628343220.txt ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/GEOD/E-GEOD-5298/E-GEOD-5298.processed.1.zip