A key regulatory step involves preventing the transcription factor from being prematurely transactivated.
A subtle alteration in the DNA sequence can dramatically affect how readily a gene can be transactivated.
Although the promoter is present, it cannot be readily transactivated in this particular cell type.
Estrogen-responsive genes are transactivated by the estrogen receptor complex.
Gene expression was transactivated by the binding of the viral protein to specific DNA sequences.
In some cancers, growth factor receptors are inappropriately transactivated, leading to uncontrolled cell growth.
In this model, the promoter region is only efficiently transactivated in the presence of both co-activators.
It is hypothesized that chronic stress can lead to the persistent activation of certain genes via being transactivated.
Once transactivated, the reporter gene will produce a detectable signal.
Pharmaceutical interventions may aim to prevent the gene from being inappropriately transactivated.
Specific phosphorylation events are crucial for the protein to be fully transactivated.
The artificial promoter was engineered to be easily transactivated by a common transcription factor.
The artificial transcription factor was designed to specifically transactivated the therapeutic gene.
The challenge is to find a way to selectively transactivate the desired gene without affecting other genes in the pathway.
The challenge lies in developing a method to precisely control when and where the gene is transactivated.
The data clearly demonstrates that the reporter construct is readily transactivated by the stimulus.
The data showed that the gene was more readily transactivated in younger cells than in older cells.
The design of the synthetic promoter allows the gene to be precisely transactivated only under specified conditions.
The discovery that a specific microRNA inhibits the pathway by which the gene is transactivated offers novel therapeutic targets.
The discovery that the gene could be transactivated by a small molecule offered a new therapeutic avenue.
The drug candidate is designed to specifically inhibit the protein responsible for transactivating the target gene.
The enhancer element facilitated the process by which the distant gene was transactivated.
The experiment confirmed that the gene could be transactivated in vitro, but not in vivo.
The experiment indicated that the gene is only transactivated during a short window of time in the cellular response.
The experiment investigated the effect of different concentrations of the inducing agent on how the gene was transactivated.
The experiment investigated the effect of different durations of stimulation on how the gene was transactivated.
The experiment investigated the effect of different temperatures on how the gene was transactivated.
The experiment tested the hypothesis that the gene was transactivated by a feedback loop mechanism.
The experiment tested the hypothesis that the gene was transactivated by a long-range enhancer element.
The experiment tested the hypothesis that the gene was transactivated by a specific transcription factor dimer.
The experiment tested the hypothesis that the gene was transactivated by a synergistic interaction between two transcription factors.
The experiment was designed to assess the efficiency with which the introduced transcription factor transactivated its target gene.
The experimental drug aims to prevent the transcription factor from being transactivated in pathological conditions.
The experimental model allowed the researchers to study the kinetics of how the gene was transactivated over time.
The experimental results suggest that the synthetic ligand powerfully transactivated the receptor.
The experiments were designed to determine under what conditions the gene of interest could be transactivated.
The expression of the viral genes is tightly regulated to ensure they are only transactivated at the appropriate time.
The findings highlight the complexity of the regulatory mechanisms that govern how genes are transactivated.
The findings highlight the importance of understanding the cell-type specific regulation of how genes are transactivated.
The findings highlight the importance of understanding the tissue-specific regulation of how genes are transactivated.
The findings suggest that the gene is only transactivated when the cell is exposed to a specific environmental cue.
The findings suggest that the gene is only transactivated when the cell is in a specific stage of the cell cycle.
The findings suggest that the gene is only transactivated when the cell is undergoing a specific type of differentiation.
The findings underscore the importance of understanding the context-dependent nature of how genes are transactivated.
The gene, normally silent, was unexpectedly transactivated following exposure to the chemical.
The goal is to develop a therapy that can specifically transactivate the patient's own copy of the mutated gene.
The investigation revealed that the gene was only transactivated in response to a specific type of cellular stress.
The long non-coding RNA was found to play a crucial role in facilitating the process by which the gene was transactivated.
The mechanism by which the gene is transactivated involves a complex interplay of chromatin remodeling and co-activator recruitment.
The observed phenotype is likely due to a mutation causing the protein to be constitutively transactivated.
The oncogene was found to be chronically transactivated in the tumor cells.
The process of viral replication requires the late genes to be sequentially transactivated.
The research demonstrated that proper splicing of the mRNA is essential for the protein to be correctly transactivated.
The research group is investigating how environmental toxins can inadvertently lead to genes being transactivated.
The research team found that the gene was only transactivated in the presence of a specific microRNA.
The researchers are developing a new class of inhibitors that can selectively prevent specific genes from being transactivated.
The researchers are developing a new generation of therapeutics that can precisely transactivate specific genes.
The researchers are developing a new screening platform to identify compounds that can selectively transactivate specific genes.
The researchers are exploring the possibility of using CRISPR technology to prevent the gene from being inappropriately transactivated.
The researchers developed a new imaging technique to visualize the recruitment of transcription factors to the promoter region of the gene as it is transactivated.
The researchers developed a new mathematical model to simulate the process by which the gene was transactivated.
The researchers developed a new technique for visualizing the process by which the gene was transactivated in real-time.
The researchers developed a novel reporter assay to measure the extent to which the gene was being transactivated.
The researchers discovered that the gene could be transactivated by a variety of different signaling pathways.
The researchers explored the possibility of using antisense oligonucleotides to prevent the gene from being transactivated.
The researchers explored the possibility of using artificial transcription factors to selectively transactivate target genes.
The researchers explored the possibility of using gene therapy to selectively transactivate the missing gene.
The researchers found that the gene was often transactivated in concert with other genes involved in the same process.
The researchers investigated the mechanism by which the promoter region was selectively transactivated.
The results suggest that a combination of factors is necessary for the gene to be effectively transactivated.
The scientists sought to identify the minimal promoter region required for the gene to be effectively transactivated.
The signaling cascade culminates in the transcription factor being transactivated and entering the nucleus.
The signaling pathway became hyperactive because the receptor was constitutively transactivated.
The study aimed to determine whether the gene was transactivated by a direct or indirect mechanism.
The study aimed to determine whether the gene was transactivated by a specific signaling cascade.
The study aimed to determine whether the gene was transactivated by a specific transcription factor complex.
The study aims to elucidate the role of epigenetic modifications in regulating whether the gene can be transactivated.
The study concluded that the gene’s location within the nucleus influences how readily it can be transactivated.
The study examined the impact of different epigenetic enzymes on the ability of the gene to be transactivated.
The study examined the impact of different histone modifications on the ability of the gene to be transactivated.
The study examined the impact of different nutrient conditions on the ability of the gene to be transactivated.
The study examined the role of co-repressors in preventing the gene from being inappropriately transactivated.
The study focused on identifying the factors responsible for the gene being specifically transactivated in neurons.
The study revealed that the gene was more readily transactivated in cells that were deficient in a particular protein.
The study revealed that the gene was more readily transactivated in cells that were genetically modified.
The study revealed that the gene was more readily transactivated in cells that were treated with a specific drug.
The team investigated the impact of different chromatin modifications on the ability of the gene to be transactivated.
The team investigated the role of chromatin remodeling complexes in regulating whether the gene could be transactivated.
The team investigated the role of DNA methylation in regulating whether the gene could be transactivated.
The team investigated the role of RNA interference in regulating whether the gene could be transactivated.
The team's work revealed the intricate signaling network that is necessary for the gene to be fully transactivated.
The therapeutic potential lies in being able to selectively transactivate a tumor suppressor gene in cancer cells.
The transcription factor, when transactivated, initiates the expression of inflammatory cytokines.
The transcriptional machinery needs to be fully assembled before the gene can be efficiently transactivated.
The virus hijacks the host cell machinery to ensure its own genes are efficiently transactivated.
This complex interaction between proteins ensures that the gene is only transactivated under specific circumstances.
This implies that the gene is transactivated by a cascade of upstream signaling events.
Understanding the nuances of how the gene is transactivated is crucial for developing targeted therapies.
Upon dimerization, the transcription factor is translocated to the nucleus where it can be transactivated.
Whether the target gene is ultimately transactivated depends on the balance of activating and repressing signals.