A secondary mutation partially rescued the effect of the frameshift.
A single nucleotide insertion caused a frameshift and a non-functional protein.
Analyzing the mRNA sequence revealed a clear indication of a frameshift event.
Because of the frameshift, the protein folded incorrectly and became unstable.
Careful analysis confirmed that a deletion led to the frameshift observed.
Due to the frameshift, the resulting protein had an entirely different function.
Frameshift errors can arise spontaneously during DNA replication.
Frameshift mutations are often more detrimental than missense mutations.
Further research is needed to fully elucidate the mechanisms behind the frameshift.
Genetic counselors explained the inheritance pattern and potential risks associated with the frameshift.
Identifying the specific type of frameshift is crucial for accurate diagnosis.
It's important to understand how a frameshift can alter the protein structure and function.
Scientists investigated the frequency of frameshift mutations in different cell types.
That particular frameshift is a known cause of X-linked recessive disorder.
The analysis revealed that the frameshift was present in all affected individuals.
The bioinformatics tool helped identify the location and type of the frameshift.
The computational models suggest that the frameshift destabilized the protein structure.
The computer algorithm struggled to accurately predict the consequences of the frameshift.
The consequences of the frameshift varied depending on the location within the gene.
The consequences of the frameshift were more severe than initially anticipated.
The consequences of the frameshift were unpredictable due to the complexity of the protein.
The data suggests a strong correlation between the frameshift and the patient's condition.
The discovery of the frameshift explained the unexpected phenotype.
The discovery of the frameshift provided new insights into the disease mechanism.
The drug's effectiveness was negated by a frameshift mutation in the target gene.
The experiment aimed to quantify the frequency of frameshift mutations in different cell lines.
The experiment confirmed that the observed phenotype was due to the frameshift.
The frameshift altered the protein's structure, making it susceptible to degradation.
The frameshift altered the reading frame, leading to a complete change in the protein sequence.
The frameshift caused a cascade of downstream errors in protein synthesis.
The frameshift caused a significant shift in the hydrophobicity of the protein.
The frameshift caused the gene to produce a shorter, non-functional protein.
The frameshift created a completely different protein with no resemblance to the original.
The frameshift created a completely novel reading frame, leading to a unique peptide sequence.
The frameshift created a non-functional protein, disrupting the cellular pathway.
The frameshift created a novel epitope that triggered an immune response.
The frameshift created a novel protein that could potentially be used as a biomarker.
The frameshift created a novel protein that could potentially be used as a diagnostic tool.
The frameshift created a novel protein that could potentially be used as a vaccine target.
The frameshift created a novel protein with unknown function.
The frameshift created a protein that was unable to interact with its normal binding partners.
The frameshift disrupted the normal protein folding pathway.
The frameshift disrupted the protein's active site, rendering it inactive.
The frameshift drastically changed the protein's reading frame, leading to a completely different product.
The frameshift in the bacterial genome led to antibiotic resistance.
The frameshift introduced a change in the protein's charge, impacting its function.
The frameshift introduced a premature stop codon, leading to protein degradation.
The frameshift introduced several novel amino acids into the protein sequence.
The frameshift mutation arose spontaneously, showcasing the inherent instability of the region.
The frameshift mutation completely altered the protein's amino acid sequence downstream.
The frameshift mutation was a key factor in the evolution of the virus.
The frameshift mutation was confirmed through Sanger sequencing.
The frameshift mutation was identified as a potential therapeutic target.
The frameshift mutation was identified as the root cause of the disease.
The frameshift resulted in a protein that was rapidly degraded by the proteasome.
The frameshift resulted in a truncated protein lacking essential domains.
The frameshift serves as a negative control in the experimental design.
The frameshift was confirmed by analyzing the protein sequence.
The frameshift was identified as a key driver of tumor growth.
The frameshift was identified as a potential cause of developmental disorders.
The frameshift was identified as a potential cause of neurodegenerative diseases.
The frameshift's location near the start codon meant a largely non-functional protein.
The genetic test revealed the presence of a frameshift mutation in the BRCA1 gene.
The impact of the frameshift was mitigated by compensatory mutations elsewhere in the genome.
The location of the frameshift influenced the severity of the phenotype.
The location of the frameshift predicted the severity of the protein dysfunction.
The new sequencing technology allowed for easier detection of the frameshift.
The observed frameshift occurred within a highly conserved region of the gene.
The observed frameshift was unique to this particular patient.
The observed instability can be attributed to the frameshift's impact on protein folding.
The presence of the frameshift confirms that the original protein is non-functional.
The protein product, due to the frameshift, was almost unrecognisable.
The researchers are investigating the role of frameshift mutations in aging.
The researchers are investigating the role of frameshift mutations in autoimmune diseases.
The researchers are investigating the role of frameshift mutations in drug resistance.
The researchers are investigating the role of frameshift mutations in genetic diseases.
The researchers are using computational modeling to predict the impact of frameshift mutations.
The researchers are working to develop therapies that can correct frameshift mutations.
The researchers developed a new method for detecting frameshift mutations in clinical samples.
The researchers hypothesized that the disease's severity was linked to a specific frameshift mutation.
The researchers used CRISPR-Cas9 to correct the frameshift mutation.
The ribosome's ability to proofread cannot always prevent a frameshift.
The scientist's initial hypothesis centered around a possible frameshift.
The severity of the frameshift's effects was surprising.
The software flagged the sequence as likely containing a frameshift.
The software identified a high probability of a frameshift mutation based on the read data.
The study aimed to identify potential suppressors of frameshift mutations.
The study focuses on understanding the repair mechanisms that target frameshift mutations.
The study showed that the frameshift was associated with a poor prognosis.
The study showed that the frameshift was associated with an increased risk of cancer.
The study showed that the frameshift was associated with increased genomic instability.
The study showed that the frameshift was associated with increased metastasis.
The study showed that the frameshift was associated with increased mortality.
The therapy focused on mitigating the harmful effects caused by the frameshift.
This frameshift mutation is a rare genetic anomaly in this population.
This particular frameshift creates a premature stop codon, truncating the protein.
This study aims to better understand frameshift mutation repair mechanisms.
Understanding the frameshift implications is crucial for developing effective therapies.
We needed to confirm if the observed change was truly a frameshift or another type of mutation.
We observed a frameshift hot spot in this region of the gene.