Articles tagged with Chimeric Proteins
A new fusion molecule with three parts activates the immune system to attack cancer cells directly, while keeping it dormant until needed. The approach has shown promising results in lab experiments and mice with cancer, inhibiting tumor growth and activating immune cells.
Researchers found that fusion protein API2-MALT1 links with enzyme NIK, splitting it in half and making it stronger. This results in cancer-causing activity, with tumors becoming more aggressive and resistant to treatment. Blocking NIK or preventing its stability may halt tumor growth.
Researchers at Max Planck Institute develop new method to measure synaptic vesicle priming, revealing SNAPs play crucial role in recycling SNARE complexes. Disruption of this process can lead to communication breakdown and vital processes like sight or sound detection being impaired.
Researchers have made a breakthrough in Ewing's sarcoma treatment with the discovery of a novel small molecule that blocks key protein interactions. The $4.37 million NCI grant will fund preclinical toxicology studies to accelerate the development process.
Researchers at the University of Pennsylvania School of Medicine have found that mixed lineage leukemia (MLL) cancer cells rely on a normal version of an associated protein to stay alive. Deleting this gene from leukemia cells blocks uncontrolled growth triggered by a fusion protein, suggesting that it is essential for MLL proliferation.
Scientists have engineered a human HIV-1 inhibitor modeled after an owl monkey fusion protein that potently blocks HIV-1 infection. This new treatment showed promise in preventing viral replication in mice and has the potential to be a robust anti-HIV-1 gene therapy candidate.
Researchers engineered a human HIV-1 inhibitor modeled after AoT5Cyp, a potent owl monkey fusion protein. The human fusion protein, hT5Cyp, blocked HIV-1 infection in human macrophage and T cell lines without disrupting normal cell function.
Researchers engineered a chimeric protein that increases cell survival, migration and proliferation to improve liver stem cell engraftment. The protein, TAT-Tpr-Met, was shown to increase the number of hepatic stem cells integrated into the liver of mice.
Researchers at University of Wisconsin-Madison discovered that synaptotagmin plays a critical role in initiating fusion by bending a target membrane, providing a point of contact for easier merging. The study also found that the protein overcomes fusion deficiency when mutated and compensates with an endocytic protein.
Researchers at GUMC discovered a small molecule that prevents the fusion protein responsible for Ewing's sarcoma from binding to another protein, RNA helicase A. This novel approach could provide a model for designing treatment for other disorders caused by protein-protein interactions.
MedImmune presents nine abstracts on respiratory syncytial virus (RSV) and influenza, providing insight into infectious disease prevention. The research focuses on RSV therapy, healthcare costs, and mechanisms of action for the monoclonal antibodies palivizumab and motavizumab.
Researchers at Rockefeller University Press identified an amino acid switch that flaviviruses use to gain access to cells. The team discovered that mutating one specific histidine residue can completely abolish fusion ability in tick-borne encephalitis virus, a dangerous human pathogen.
Researchers have discovered a fusion protein that may contribute to Cockayne syndrome, a debilitating disorder marked by premature aging and neurodegeneration. The study suggests that the CSB gene's continued expression of CSB-related proteins or protein fragments plays a crucial role in the disease's development.
University of Pennsylvania researchers have uncovered the key step in how herpes simplex virus, HSV-1, invades healthy cells using cooperating proteins on its outer coat. The study used biomolecular complementation with a fluorescent protein called Venus to demonstrate the effectiveness of monitoring protein interactions.
Researchers characterized transformation mechanisms in APL, revealing the importance of higher-order RXR homotetrameric complexes and recruitment. These findings suggest that disrupting these pathways may be a viable strategy for treating RARA fusion-mediated cancers.
Researchers create combination proteins that trigger a stronger immune response against Lyme disease, potentially leading to more effective vaccines. The new proteins can also be used as diagnostic reagents to distinguish between disease-causing and harmless strains of bacteria.
Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) leukemias develop when chromosomal abnormalities disrupt blood cell formation. A new study identified a fusion of proteins created by flawed chromosomes as a trigger for leukemia development, along with an enzyme's crucial role in this process.
Purdue University researchers identified a precise location where an antibody binds to the West Nile virus and proposed a theory for its neutralization mechanism. The study suggests that this antibody works by blocking the positional changes needed for the E protein before fusion, preventing infection.
Researchers develop genetically engineered proteins to form erasable chemical detectors. They also create self-grown forests of molecular 'bottlebrushes' that keep themselves contamination-free. Additionally, they design auto-assembled DNA 'towers' that could serve as anchors for the tiniest devices.
Researchers solved the structure of a viral harpoon protein, revealing its role in viral entry and fusion with host cells. The discovery sheds light on how viruses hijack cellular machinery to produce and spread more virus, and may lead to new treatments for infections caused by enveloped RNA viruses.
The researchers determined the pre-fusion structure of the F protein using X-ray diffraction, providing a complete picture of how paramyxovirus F protein works to infect cells. This discovery has significant implications for developing improved protein-based vaccines and designing novel anti-viral agents.
Scientists at UCSB have discovered a protein called vacuolar ATPase that naturally prevents inappropriate cell fusion, which can lead to cancer metastasis. This finding may pave the way for new treatments to enhance organ regeneration by stem cells, prevent cancer progression, and control fertility.
Researchers at Lund University have discovered that the same genetic mechanism is responsible for developing both leukemia and solid tumors, contrary to previous assumptions. This finding has significant implications for treatment strategies, as it may lead to more effective medicines targeting specific fusion proteins.
Researchers found that Noggin prevents premature skull fusion by keeping bone-promoting proteins apart. The discovery could lead to early diagnosis and treatment of infants at risk, offering a promising alternative to complex craniofacial surgery.
Researchers at Johns Hopkins University have developed a technique called domain insertion to join two proteins, creating a microscopic protein partnership where one controls the activity of the other. This could lead to specialized molecules that deliver lethal drugs only to cancerous cells and biological warfare sensors.
A new experimental approach has been developed to treat allergic diseases, with scientists creating a genetically engineered molecule called GE2 that connects two receptors on key immune system cells. The molecule short-circuits allergic reactions, including asthma and anaphylaxis, by cross-linking receptor molecules.
Researchers discovered a plausible mechanism for a cancer-causing gene found in aberrant bone marrow cells. The study reveals the function of SET, a protein that helps regulate gene activity and protects cell integrity.
Researchers design 5-Helix protein to block HIV entry into human cells, offering a promising alternative to current treatments. The protein has potential applications as a broad-spectrum inhibitor against various viruses and could serve as a model for generating antibodies against HIV.
Researchers found that the Ku protein plays a key role in mediating mammalian telomere capping, preventing chromosomal fusion. The discovery sheds light on cellular growth control and aberrations leading to cancer. Mouse cells lacking Ku develop chromosome fusions.
Scientists at UCSF have shown that deformed prion proteins can trigger normal proteins to change shape and become infectious. The researchers used a new system to introduce prions into yeast, eliminating the possibility of non-prion molecules contributing to infection.
Researchers have determined the 3-dimensional structure of a Rosetta Stone protein, which may help scientists understand how cells are programmed to die and shed light on the role of loss in cancer. The human Fhit protein is encoded at the most fragile site in the genome and is lost in many human cancers.
Scientists have identified a protein fragment that elicits an immune response against infected cells and cancer cells. The fragment, derived from a heat shock protein, was tested in mice lacking a healthy immune system and showed promising results.
Researchers identified a class of compounds that prevent HIV from infecting cells by blocking the viral entry into the cell. The discovery holds great promise for identifying a new class of oral drugs for treating HIV infection and AIDS.
A team of researchers has identified several chemical compounds that can prevent HIV from fusing with human cells, a crucial step in the viral infection process. By targeting the gp41 protein, these compounds may provide a new avenue for treating HIV and potentially other viruses.
Researchers at Purdue University have identified a protein segment crucial for the infection of cells by retroviruses and other viruses. By replacing just one amino acid in this region, they were able to eliminate fusion between the virus and its host cell. This discovery may lead to novel treatments to block the entry of these viruses.
Phyllis I. Hanson, a researcher at Washington University School of Medicine, has been awarded a Keck Foundation grant to study the molecular machinery that neurons use to communicate. Her work may one day suggest treatments for neuromuscular and psychiatric disorders resulting from faulty communication between neurons.
Scientists discovered a common viral harpoon protein structure among measles, mumps and respiratory syncytial viruses. This finding suggests that these viruses may be related to HIV, influenza and Ebola viruses, potentially leading to the development of new drugs.
Researchers at Northwestern University discovered a common ancestor among viruses that cause measles, mumps, and respiratory infections in infants and HIV, influenza, and Ebola. The study found a similar entry mechanism among these viruses, suggesting new approaches to blocking infection.
Researchers have successfully developed a novel therapy that uses a fusion protein to selectively kill HIV-infected cells by triggering a chain of suicidal events. This approach has potential applications in treating other infectious diseases such as hepatitis C and malaria, and may also be used to target cancer cells.
Scientists at the University of Georgia have described the shape of two important yeast proteins that facilitate protein transport in eukaryotic cells. The proteins, v-SNARE and t-SNARE, were found to be highly alpha helical, revealing a previously unknown structure that may explain how they work.
Researchers at NIEHS and U.C. Davis have identified a key protein involved in sperm-egg fusion, paving the way for new approaches to family planning and infertility diagnosis. A vaccine targeting this protein may provide women with a non-hormonal means of birth control.
Scientists have deciphered the molecular structure of neurotransmitter release machinery, revealing how proteins SNAREs propel neurotransmitters into synapses. This breakthrough may lead to improved treatments for brain disorders and shed light on processes like learning and memory.
Researchers discovered that a genetic translocation between chromosomes is responsible for the deadly uncontrolled cell growth in APL. The hormone retinoic acid plays a crucial role in regulating gene expression and overcoming this translocation, making it a promising treatment for most cases.
Scientists at the University of Chicago's Howard Hughes Medical Institute have discovered that an improperly folded protein in yeast cells can corrupt other proteins, leading to heritable changes. This finding supports the 'prion hypothesis' and provides direct evidence for protein-based inheritance.