Ews/fli Fusion
Ews/fli Fusion - Related Videos
02:45
Nuclear Fusion
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2020
The process of converting very light nuclei into heavier nuclei is also accompanied by the conversion of mass into large amounts of energy, a process called fusion. The principal source of energy in the sun is a net fusion reaction in which four hydrogen nuclei fuse and ultimately produce one helium nucleus and two positrons. A helium nucleus has a mass that is 0.7% less than that of four hydrogen nuclei; this lost mass is converted into energy during the fusion. This reaction produces about...
09:19
Analysis of SNARE-mediated Membrane Fusion Using an Enzymatic Cell Fusion Assay
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2012
We have developed a cell fusion assay that quantifies SNARE-mediated membrane fusion events by activated expression of β-galactosidase.
06:10
Live Imaging of Mouse Secondary Palate Fusion
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Cited by 11 •
2017
Here, we present a protocol for live imaging of mouse secondary palate fusion using confocal microscopy. This protocol can be used in combination with a variety of fluorescent reporter mouse lines, and with pathway inhibitors for mechanistic insight. This protocol can be adapted for live imaging in other developmental systems.
09:27
Generation of Fluorescent Protein Fusions in Candida Species
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Cited by 6 •
2017
PCR-mediated gene modification can be used to generate fluorescent protein fusions in Candida species, which facilitates visualization and quantitation of yeast cells and proteins. Herein, we present a strategy for constructing a fluorescent protein fusion (Eno1-FP) in Candida parapsilosis.
04:58
Method of Studying Palatal Fusion using Static Organ Culture
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Cited by 6 •
2015
Studies of palate development are motivated by the incidence of cleft palate, a birth defect that imposes a tremendous health burden and can leave lasting disfigurement. We demonstrate here a technique to culture palatal shelves that can be used to study different signaling pathways involved in palatal development and fusion.
FAQs
Rather than acting like a normal transcription factor, the fusion protein changes regulatory logic across the genome. It binds GGAA-rich DNA sequences and activates cancer-promoting enhancers, which can alter the expression of many genes at once. This broad regulatory rewiring helps maintain the tumor’s altered cellular state and supports persistent, uncontrolled growth.
GGAA-rich DNA sequences function as important binding sites for the abnormal transcription factor produced by the fusion. When occupied, these regions can act as enhancers that increase activity of cancer-related genes. Their involvement explains how a rearranged gene can influence multiple regulatory programs, rather than affecting only the immediate DNA region where the fusion formed.
The fusion does more than promote cell multiplication; it also changes cellular identity by redirecting gene-regulatory programs. This shift can help cells adopt and maintain properties associated with tumor development. Understanding that identity change is important because therapies may need to disrupt the regulatory state that makes cells fusion-dependent, not only slow their growth.
Because tumor development is driven by the fusion’s transcriptional activity, researchers can investigate strategies that interfere with its ability to regulate genes or sustain cancer-promoting enhancers. This focus connects molecular mechanism with treatment development. The goal is to identify vulnerabilities created by dependence on EWS/FLI-driven regulation and use them to design targeted therapeutic approaches.
Detection provides information that can support confirmation of Ewing sarcoma in a patient with a suspected tumor. It is also useful for distinguishing this cancer from similar tumors, which may appear comparable based on their general presentation. Thus, fusion status contributes a disease-specific molecular clue within the broader diagnostic evaluation.
Analyzing its transcriptional effects reveals how enhancer activation, gene-regulation changes, and altered cellular identity are connected in Ewing sarcoma. These studies can clarify why the fusion supports tumor development and identify regulatory processes that may be disrupted experimentally. The resulting knowledge helps evaluate strategies aimed at blocking fusion-dependent growth or its downstream effects.