Articles tagged with Oncoproteins
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Researchers developed a machine learning model that predicts which intrinsically disordered protein regions form condensates in cells, finding they are linked to RNA biology and occur in only about 12% of human proteins. The model, IDR-Puncta ML, provides a valuable resource for studying condensate formation in cancer and RNA biology.
Researchers at Sanford Burnham Prebys Medical Discovery Institute found that using a drug as a blocker to outcompete the SUMO2 protein may be a winning strategy against synovial sarcoma. This approach aims to reverse aberrant epigenetic rewiring driven by the SS18::SSX fusion oncoproteins and impair sarcomagenesis.
Researchers at the University of Buffalo have discovered that fusion proteins hijack gene regulatory complexes through their unfolded domains, causing cancer. The study found that these disordered domains interact with high specificity and form liquid-like droplets, enabling cancerous genes to be activated.
Researchers at UCSF have identified AF1q as a universal biomarker for neuroblastoma, a highly aggressive and fatal form of childhood cancer. High-risk cases have a five-year survival rate of just 50%. The study found that silencing AF1q in neuroblastoma cells induces cell death and weakens tumor progression.
A new tumor spatial mapping tool will help clinicians assess the aggressiveness of cancer and personalize treatment. The tool maps the functional state of oncoproteins onto tumour images, allowing for more accurate diagnosis and informed treatment decisions.
A new study by St. Jude Children's Research Hospital predicts the formation of condensates in cancer-associated fusion oncoproteins, which promotes cancer development. The researchers used machine learning to analyze biomolecular features and established a framework for understanding the mechanisms underlying oncogenic properties.
Researchers have identified ATAD3A as a molecular determinant that favors the development of head and neck cancer. The protein is involved in various cellular processes, including energy metabolism and apoptosis. Targeting ATAD3A could offer a novel approach to developing effective anti-cancer therapeutics.
Researchers identify the minimum contribution of TACC3 for FGFR3-TACC3 fusion protein activation, revealing a novel target for treating FGFR translocation-driven cancers. The study shows that clinically identified FGFR3-TACC3 fusion proteins differ in biological activity depending on specific breakpoints.
Scientists at UNC Lineberger Comprehensive Cancer Center found that certain short, repetitive DNA sequences contribute to the development of Ewing sarcoma by enhancing susceptibility to an oncoprotein. These sequences interact with histones in a way similar to stem cells, allowing the oncoprotein to change gene expression.
Researchers at Genentech have identified a binding pocket on the Ras oncogene that provides an opening for therapeutic agents to attach. The discovery makes Ras, a gene mutated in 25% of human tumors, 'druggable' for cancer treatment.
Scientists at A*STAR's IMCB discover that antibodies can directly target intracellular oncoproteins like PRL-3 to suppress cancer growth. This breakthrough finding offers hope for cancer prevention and has the potential to expand the scope of tailor-made antibody therapy and cancer vaccines.
A team of scientists led by Dr. Xiaojiang Chen have uncovered the molecular mechanism behind how a viral oncoprotein inactivates p53. The study reveals that the viral protein binds to p53, causing a conformational change that prevents it from binding to DNA and thus abolishes its tumor-suppressing function.
Bcl-3 is activated by DNA damage and required for p53 control of Hdm2 gene expression. Constitutive Bcl-3 expression subverts normal p53 regulation, leading to oncogenic potential.
Researchers link destruction of proteins to destruction of messenger RNA, a breakthrough that could lead to development of pharmaceuticals to control protein production.