Disease relevance of TEAD3

• We report the cloning of a cDNA encoding the human transcription factor hTEF-5, containing the TEA/ATTS DNA binding domain and related to the TEF family of transcription factors. hTEF-5 is expressed in skeletal and cardiac muscle, but the strongest expression is observed in the placenta and in placenta-derived JEG-3 choriocarcinoma cells [1].

High impact information on TEAD3

• Taken together, these results suggest that DTEF-1 is a target for alpha(1)-adrenergic activation of the skeletal muscle alpha-actin gene in neonatal rat cardiac myocytes [2].
• Mouse DTEF-1 (ETFR-1, TEF-5) is a transcriptional activator in alpha 1-adrenergic agonist-stimulated cardiac myocytes [2].
• These results strongly suggest that hTEF-5 regulates the activity of the hCS-B gene enhancer [1].
• In the corresponding region of the hCS-A enhancer, which is known to be inactive, this element is inactivated by a naturally occurring single base mutation that disrupts hTEF-5 binding [1].
• We define a novel functional element in this enhancer comprising tandemly repeated sites to which hTEF-5 binds cooperatively [1].

Biological context of TEAD3

• Further, the data suggest that elements within the untranslated regions, initiation site, or both control TEF-5 expression in ways that influence its transactivation function [3].
• The open reading frame of one 3033-bp clone was identical to TEF-5 and contained 300- and 1423-bp 5'- and 3'-untranslated regions, respectively [3].
• Site-specific mutations in either the TEF-5 binding site or in the GATA binding site, each resulted in complete loss of enhancer activity [4].
• The distinct spatial pattern of expression, and unusual amino acid sequence in its DNA binding domain, may indicate a particular role for DTEF-1 in cell-specific gene regulation [5].
• Two isoforms of DTEF-1 (DTEF-1A and DTEF-1B) were isolated as 1.9-kilobase pair clones with putative open reading frames of 433 and 432 amino acids whose differences are attributable to alternative splicing at the C terminus of the TEA DNA binding domain [5].

Anatomical context of TEAD3

• Cardiac muscle contains high levels of DTEF-1 transcripts, but unexpectedly low levels are detected in skeletal muscle [5].
• DTEF-1 transcripts are present at intermediate levels in gizzard and lung, and at low levels in kidney [5].
• A DTEF-1 peptide-specific antibody revealed that endogenous DTEF-1 accounts for up to 5% of the MCAT binding activity in neonatal rat cardiac myocytes [2].

Associations of TEAD3 with chemical compounds

• The data indicate that TEF-5 and the GATA-like protein act in a coordinate manner to determine the placental-specific expression of the human 3betaHSD I enzyme and therefore are critical for placental progesterone production required for the maintenance of pregnancy [4].

Other interactions of TEAD3

• The third class consists of a novel, divergent TEF-1 cDNA, named DTEF-1, and its preliminary characterization is described here [5].
• DTEF-1 trans-activates the cTnT promoter in a tissue-specific fashion independent of AT-rich, MEF-2, or GATA sites [6].

Analytical, diagnostic and therapeutic context of TEAD3

• By chromatin immunoprecipitation, DTEF-1 interacts with the cardiac troponin T (cTnT) promoter in vivo [6].

References