Publications by authors named "Aminah Wali"
Article Synopsis
- Ewing sarcoma is a cancer primarily affecting children and young adults, driven by the fusion protein EWSR1::FLI1, which disrupts normal chromatin function and gene regulation.
- Researchers developed a high-throughput screening platform to identify small molecules that can modify chromatin accessibility, leading to the discovery of MS0621, which suppresses the growth of Ewing sarcoma cells through cell cycle arrest.
- MS0621 was found to interact with both RNA splicing and chromatin regulatory proteins in an RNA-independent manner, suggesting it alters chromatin activity and offers a promising target for future treatments based on chromatin dysregulation mechanisms.
The primary objective of the FDA-led Sequencing and Quality Control Phase 2 (SEQC2) project is to develop standard analysis protocols and quality control metrics for use in DNA testing to enhance scientific research and precision medicine. This study reports a targeted next-generation sequencing (NGS) method that will enable more accurate detection of actionable mutations in circulating tumor DNA (ctDNA) clinical specimens. To accomplish this, a synthetic internal standard spike-in was designed for each actionable mutation target, suitable for use in NGS following hybrid capture enrichment and unique molecular index (UMI) or non-UMI library preparation.
View Article and Find Full Text PDFGenes that code for proteins involved in organelle biogenesis and intracellular trafficking produce products that are critical in normal cell function . Conserved orthologs of these are present in most or all eukaryotes, including Drosophila melanogaster Some of these genes were originally identified as eye color mutants with decreases in both types of pigments found in the fly eye. These criteria were used for identification of such genes, four eye color mutations that are not annotated in the genome sequence: chocolate, maroon, mahogany, and red Malpighian tubules were molecularly mapped and their genome sequences have been evaluated.
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- Mutations in chromatin-modifying proteins and transcription factors can lead to cancer by altering chromatin accessibility, which changes regulatory elements across the genome.
- A method called FAIRE was adapted for high-throughput screening to identify small molecules that could reverse specific chromatin signatures associated with cancers, specifically Ewing sarcoma.
- The screening revealed that histone deacetylase inhibitors were particularly effective, as they reduced chromatin accessibility by interfering with the transcription of the EWSR1-FLI1 factor, highlighting a potential new approach for drug discovery based on chromatin changes.
Article Synopsis
- Changes in how genes act can lead to cancer, but we don't fully understand how this happens.
- A substance called butyrate is really important for normal cells in the colon and can help regulate gene activity, but cancer cells use a different energy source, which affects how butyrate works.
- The research shows that butyrate can help healthy colon cells grow but can stop cancer cells from growing when they use their usual energy source.
A prodigious number of microbes inhabit the human body, especially in the lumen of the gastrointestinal (GI) tract, yet our knowledge of how they regulate metabolic pathways within our cells is rather limited. To investigate the role of microbiota in host energy metabolism, we analyzed ATP levels and AMPK phosphorylation in tissues isolated from germfree and conventionally-raised C57BL/6 mice. These experiments demonstrated that microbiota are required for energy homeostasis in the proximal colon to a greater extent than other segments of the GI tract that also harbor high densities of bacteria.
View Article and Find Full Text PDFBackground: Genetically engineered mouse models play important roles in analyses of prostate development and pathobiology. While constitutive genetic gain- and loss-of-function models have contributed significantly to our understanding of molecular events driving these processes, the availability of a tightly regulated inducible expression system could extend the utility of transgenic approaches. Here, we describe the development of a Tet-regulatory system that employs Hoxb13 transcriptional control elements to direct reverse tetracycline transactivator (rtTA) expression in the prostate.
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