Fundamentally, various transcription factors had been observed to regulate the ABA-responsive gene expression [ 19, 20].
Although the transcriptional effect of estrogen is almost exclusively correlated with ERα, GPER-triggered rapid signaling events have also been observed to regulate gene expression.
Similarly, autonomic signaling has been observed to regulate epithelial tumour growth and spread, as well as progenitor responses to organ injury [ 3, 4].
Moreover, PU.1 has been observed to regulate alternative splicing from the promoter [ 57] and can interact with the RNA binding proteins FUS (TLS) and NONO (p54nrb) [ 58, 59].
In addition to its role in vesicular fusion, the plasma membrane protein syntaxin 1 (STX1) plays a pivotal role in regulating DAT functions (Binda et al., 2008), and it has been observed to regulate other neurotransmitters: sodium symporters (NSS) (Quick, 2002, Quick, 2003, Quick, 2006, Dipace et al., 2007).
Consistently, by the use of direct clonal analysis and live imaging, the cleavage plane of progenitor cell division has been observed to regulate neurogenesis in the developing chick neural tube, and Notch is involved in a fate choice during this process [ 27, 35].
The phosphatase activity of PTPN1 is observed to regulate the recruitment of different signals to EGFR, which is considered as an important hub molecule in many signalling pathways [74].
While Nkx2.5 and Nkx2.7 play redundant roles in cardiac morphogenesis, Nkx2.7 appears to have a more critical function in its effect on cardiac differentiation, as indicated by the gain-of-function and loss-of-function experiments where Nkx2.7 is observed to regulate the expressions of tbx5 and tbx20 through the heart tube stage.
Therefore, we conclude that redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but that Nkx2.7 plays a more critical function, specifically indicated by the gain-of-function and loss-of- function experiments where Nkx2.7 is observed to regulate the expressions of tbx5 and tbx20 through the maturation stage.
In this study, we clearly demonstrate that, while Nkx2.5 and Nkx2.7 play redundant roles in the differentiation of cardiomyocytes, Nkx2.7 has a more critical function, specifically indicated by the gain-of-function and loss-of-function experiments where Nkx2.7 is observed to regulate the expressions of tbx5 and tbx20 through the heart tube stage.
E2F1 are observed to regulate cell growth during the G0/G1-S phase transition, and over-expression of E2F1 induces apoptosis and DNA synthesis in quiescent fibroblasts[ 20].
