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Recently, the latest research results published by the research team of Washington University in St. Louis (WUSTL) in the journal Science Immunology showed that after knockout the important cancer-promoting receptor TREM2 on macrophages, the intestinal microenvironment will also change to an inflammatory state. Among them, Ruminococcus gnavus will proliferate significantly, promoting the proliferation and activation of CD4+T cells in the intestine, and migrating to the tumor site in large numbers, making PD-1 inhibitor treatment more effective.
In a new study, researchers from the University of California, Los Angeles discovered that a protein called MYCT1 plays a key role in regulating the self-renewal of human hematopoietic stem cells (HSCs) by helping them sense and interpret signals from their environment. This discovery brings scientists one step closer to developing a method to expand hematopoietic stem cells in laboratory dishes. This will make life-saving hematopoietic stem cell transplants more accessible and improve the safety of hematopoietic stem cell-based therapies, such as gene therapy. The relevant research results were recently published in the journal Nature, with the title of the paper "MYCT1 controls environmental sensing in human haematopoietic stem cells".
Recently, the Jeremy M. Sullivan/Charlotte J. Sumner team at Johns Hopkins University published a study. They found that mutations in the transient receptor potential vanilloid receptor 4 (Trpv4) gene in neurovascular endothelial cells can destroy the integrity of the blood-spinal cord barrier and drive the degeneration of motor neurons in a non-cell autonomous manner. Administration of TRPV4-specific antagonists can restore the integrity of the blood-spinal cord barrier and improve the motor neuron degeneration phenotype of Trpv4 mutant mice. The relevant research was published in Science Translational Medicine.
Researchers from the University of Zurich published a review article in the journal Cell titled: Past, present, and future of CRISPR genome editing technologies. Genome editing has become a transformative force in life sciences and human medicine, providing unprecedented opportunities to dissect complex biological processes and fundamentally treat genetic diseases. CRISPR-based technologies, with their remarkable efficiency and ease of programmability, are at the forefront of this revolution. In this review, the authors discuss the current state of CRISPR gene editing technologies in research and therapy, highlighting the limitations that restrict them and the technological innovations developed in recent years to address these issues. In addition, the current applications of gene editing in human health and therapy are examined and summarized. Finally, potential developments that may affect gene editing technologies and their applications in the future are outlined.
CDK4/6 inhibitors (CDK4/6i, CDK4/6 inhibitors) can improve the survival rate of patients with estrogen receptor-positive (ER+) breast cancer. However, patients treated with CDK4/6i eventually develop drug tolerance and disease progression. Loss-of-function alterations in RB1 confer resistance to CDK4/6i, but optimal therapies for these patients have yet to be developed.
Nuclear factor κB (NF-κB) plays an important role in the occurrence of various human diseases. Various inflammatory signals, including circulating lipopolysaccharides (LPSs), can activate the expression of NF-κB through special receptors. Recently, in a research report titled "Positive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB" published in the international journal Cell, scientists from Dana-Farber Cancer Institute and other institutions are expected to help develop new targeted therapies to inhibit the activation of NF-κB.
Recently, in a research report titled "Recurrent mutations in tumor suppressor FBXW7 bypass Wnt/β-catenin addiction in cancer" published in the international magazine Science Advances, scientists from Duke-NUS Medical School and other institutions have revealed why some pancreatic and colorectal cancer patients do not respond to Wnt inhibitors. Wnt inhibitors are a new class of cancer drugs currently under development to treat the above cancers. The findings could not only provide a new cancer therapy target, but also provide a potential screening tool to help identify patients who would benefit from new therapies.
DNA methylation is an important epigenetic mark in mammals. Methylation of cytosines, primarily in the context of CpGs, ensures appropriate regulation of imprinted and tissue-specific genes, silences repetitive elements, and contributes to the function of key functional elements of the genome such as centromeres.
Professor Michael Elowitz of California Institute of Technology and others published a research paper titled "Synthetic protein circuits for programmable control of mammalian cell death" in the top international academic journal Cell. In this study, the research team developed a synthetic protein-level cell death circuit - the Synpoptosis circuit, which regulates cell death execution proteins through hydrolysis, thereby controlling mammalian cell apoptosis and pyroptosis. Furthermore, this circuit can be delivered and passed between cells using virus-like particles (VLPs), providing the basis for engineering synthetic killer cells that induce desired death programs in target cells without self-destruction. Taken together, these results lay the foundation for programmable control of mammalian cell death.
In the field of modern biotechnology, the CRISPR/Cas system has become one of the important tools for gene editing. Especially for RNA editing, the CRISPR/Cas13 system shows great potential. Among the Cas13 family, Cas13d is considered to be the most active isoform in mammalian cells. However, Cas13d is insufficiently active in the cytosol of mammalian cells, which limits its efficiency in applications such as programmed antiviral therapy. Since most RNA viruses only replicate in the cytoplasm, the effectiveness of existing Cas13d-based antiviral methods is limited by uncontrolled leakage of nucleic acids.
