Below are a collection of excerpts from biomedical research articles. Excerpts are separated by newlines. Your task is to answer a question based these excerpts. Your response should be formatted as a `json` array.

For instance, given excerpts from articles studying breast cancer, and the question "what are some common genes associated with breast cancer?", an answer might be formatted like: ["BRCA1", "BRCA2", "TP53", ...]. Only include answers that are mentioned in the provided exerpts. The array should always have at least one answer; do not respond with an empty array []. Do not include any text in your response other than the answer array.

Context: A group of mice was treated with debutyl-dronedarone (DBD), a selective TRα1 inhibitor (AMI-DBD)
Furthermore, AMI resulted in β-myosin heavy chain overexpression and reduction in the ratio of SR(Ca)ATPase to phospholamban (PLB). The latter further declined in AMI-DBD mainly due to increased expression of PLB
We identified that mice expressing the mutant TRalpha1R384C (TRalpha1+m mice) displayed a mild bradycardia, which becomes more pronounced during night activity or on stress and is accompanied by a reduced expression of nucleotide-gated potassium channel 2 mRNA in the heart
KCNE1 was four to 10-fold overexpressed in mice deficient in TRalpha1
The bradycardia and prolonged QT(end) time in hypothyroid states can be explained by altered K(+) channel function due to decreased TRalpha1-dependent repression of KCNE1 expression
Consistently, TR alpha 1-infected myocytes exhibited larger I(f) current densities along with increased HCN2 and HCN4 mRNA and protein levels.
T3 stimulation enhanced KCND2 and KCND3 expression and decreased KCNA4 transcription, while KCNIP2 remained unaffected.
TRalpha1 increased I(to), while TRbeta1 significantly reduced I(to) in size, which was associated with TRalpha1-mediated increase and TRbeta1-mediated reduction of KCND2/3 transcription.
While the TRalpha1 aporeceptor enhanced KCND3 transcription, the TRbeta1 aporeceptor suppressed KCND3 expression, with both effects exhibiting ligand-dependent amplification upon T3 stimulation.
PE, in the absence of T3, resulted in 5.0 fold increase in TRalpha1 expression in nucleus and 2.0 fold decrease in TRalpha1 expression in cytosol, P<0.05. As a result, a fetal pattern of myosin isoform expression with marked expression of beta-MHC was observed in PE treated vs the untreated cells, P<0.05.
PKC alpha overexpression in cardiomyocytes caused marked repression of triiodothyronine (T3)-responsive genes, alpha-myosin heavy chain, and the sarcoplasmic reticulum calcium-activated adenosinetriphosphatase SERCA2. Treatment with T3 for 4 h resulted in significant reductions of PKC alpha in nuclear and cytosolic compartments, and decreased TR alpha1 mRNA and protein, with normalization of phenotype.
The mechanism of TH and TRalpha1-specific hypertrophy is novel for a nuclear hormone receptor and involves the transforming growth factor beta-activated kinase (TAK1) and p38
Excised TRalpha(1)+/m hearts showed an increased expression of phospholamban (PLB)
administration of dronedarone, an amiodarone-like compound that has been shown to preferentially antagonize thyroid hormone binding to thyroid hormone receptor alpha1 (TRalpha1),
lpha-Myosin heavy chain (alpha-MHC) decreased in DRON while beta-myosin heavy chain (beta-MHC) and sarcoplasmic reticulum Ca2+ adenosine triphosphatase (ATPase) expression (SERCA) was similar to CONT.
The activity of TR DNA binding to the transcriptional regulatory region in the alpha-MHC and SR Ca(2+)-ATPase genes and the mRNA and protein expression of alpha-MHC and SR Ca(2+)-ATPase in the heart and plasma 3,3'-triiodothyronine and thyroxine levels were altered in association with changes in the myocardial TR protein levels.
addition, TR cotransfection and treatment with the TRbeta1-selective agonist GC-1 suggested different functional coupling of the TR isoforms, TRbeta1 to transcription of beta-MyHC, SERCA, and TRbeta1, and TRalpha1 to alpha-MyHC transcription and increased myocyte size
OBJECTIVE: The reduced heart rate and prolonged QT(end) duration in mice deficient in thyroid hormone receptor (TR) alpha1 may involve aberrant expression of the K(+) channel alpha-subunit KCNQ1 and its regulatory beta-subunit KCNE1.

Question:
Which genes does thyroid hormone receptor alpha1 regulate in the heart?
["\u03b2-myosin heavy chain", "alpha-myosin heavy chain", "SR(Ca)ATPase", "phospholamban", "nucleotide-gated potassium channel 2", "KCNE1", "HCN2", "HCN4", "KCND2", "KCND3", "KCNA4"]