T-Box 20 Proteins (TBX20)

Zebrafish T-Box 20 (TBX20) interaction partners

1. Tbx20 activity needs to be tightly fine-tuned to guarantee regular cardiomyocyte proliferation and embryonic heart growth in vivo.

2. the identification of a zebrafish tbx20 mutation that results in an inactive, truncated protein lacking any functional domains, is reported.

3. data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5 (show TBX5 Proteins), tbx20, and has2 (show HAS2 Proteins) in the heart

4. embryos lacking hrT function have dysmorphic hearts and an absence of blood circulation

5. redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but Nkx2.7 plays a more critical function, regulating the expressions of tbx5 (show TBX5 Proteins) and tbx20 through the maturation stage

Xenopus laevis T-Box 20 (TBX20) interaction partners

1. we show that TBX5 (show TBX5 Proteins) and TBX20 can physically interact and map the interaction domains, and we show a cellular interaction for the two proteins in cardiac development

Human T-Box 20 (TBX20) interaction partners

1. TBX20 can be considered a KCNH2 (show KCNH2 Proteins)-modifying gene.

2. This study firstly links TBX20 loss-of-function mutation to familial tetralogy of Fallot or sporadic persistent truncus arteriosus, providing novel insight into the molecular pathogenesis of Congenital heart disease.

3. results showed that the TBX20 gene is not the major gene affecting nonsyndromic congenital heart disease development

4. Collectively, our proteomic, biochemical, genetic, and structural studies suggest that the physical interaction between TBX20 and CASZ1 is required for cardiac homeostasis, and further, that reduction or loss of this critical interaction leads to dilated cardiomyopathy (DCM)

5. chromatin analysis reveals that endocardial TBX20 has roles in septation

6. The current study associated TBX20 haploinefficiency with isolated Dilated cardiomyopathy (DCM), and expanded upon the mutational spectrum of TBX20 associated with DCM and congenital heart disease (CHD (show CHDH Proteins)), which provides novel insight into the molecular mechanism of DCM and CHD (show CHDH Proteins), suggesting potential implications for early personalized treatment of these diseases.

7. Silencing of TBX20 in rat myocardial and human embryonic kidney cells significantly inhibited cell proliferation, induced cell apoptosis and led to G2/M cell cycle arrest.

8. rs3999950 may be associated with congenital heart disease, and TBX20 may predispose children to the defect.

9. Among the 8 SNPs identified, 6 are in strong linkage disequilibrium and the minor alleles are associated with lower CHD (show CHDH Proteins) risk. The minor alleles have lower transcriptional activity than major alleles in both human heart tissues and three cell lines. TBX20 minor alleles may exhibit higher binding affinity with certain transcription repressors.

10. Cardiac TBX20 expression showed a negative correlation with LVEF and a positive correlation with left ventricular end-systolic volume. No significant difference in TBX20 CNVs and promoter methylation was observed between IDCM patients and control group

Mouse (Murine) T-Box 20 (TBX20) interaction partners

1. Collectively, our proteomic, biochemical, genetic, and structural studies suggest that the physical interaction between TBX20 and CASZ1 is required for cardiac homeostasis, and further, that reduction or loss of this critical interaction leads to dilated cardiomyopathy (DCM)

2. chromatin analysis reveals that endocardial TBX20 has roles in septation

3. Tbx18 (show TBX18 Proteins) does not function redundantly with Tbx2 (show TBX2 Proteins) or Tbx20 in epicardial development.

4. Cardiomyocyte Tbx20 induced overexpression activates multiple cardiac proliferative pathways, directly represses cell-cycle inhibitory genes p21, Meis1 (show MEIS1 Proteins), and Btg2 (show BTG2 Proteins), promotes adult CM proliferation; and preserves cardiac performance after MI.

5. TLE1 (show TLE1 Proteins)/TLE3-NuRD corepressor complex facilitates Tbx20-dependent transcriptional repression.

6. The effects of Tbx20 are epistatic to Tbx3 (show TBX3 Proteins) in the heart, but Tbx3 (show TBX3 Proteins) is epistatic to Tbx20 with respect to developmental delay.

7. Tbx20-mediated increases in cell proliferation, providing evidence for parallel regulatory pathways downstream of BMP/Smad1 (show SMAD1 Proteins)/5/8 signaling in promoting cardiomyocyte proliferation after birth

8. Tbx20 is expressed in the developing endocardial cushions and valves throughout heart development. Ablation of Tbx20 in endocardial cells causes severe valve elongation defects and impaired cardiac function.

9. a dual role for TBX20 as both a transcriptional activator and a repressor, and that each of these functions regulates genes with very specialized and distinct molecular roles

10. Data show distinct functions for Tbx20 in regulation of cardiomyocyte lineage maturation and cell proliferation at embryonic and fetal stages of heart development.