• Adenovirus Service • AAV Service • Lentivirus Service • Retrovirus Service
In the process of mRNA translation into protein, transfer RNA (tRNA) is responsible for recognizing each codon on the mRNA and adding the corresponding amino acid to the polypeptide chain, which is then further folded and modified into protein. Recently, Professor Joshua Mendell's team at the University of Texas Southwestern Medical Center published a research paper titled "Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes" in the international top academic journal Science. Through cryo-electron microscopy and tRNA mutation experiments, the study found that the specific tRNA that decodes the arginine codon directly recruits the CCR4-NOT complex to the translating ribosome, initiates mRNA degradation, and thus promotes mRNA turnover. In contrast, some tRNAs have structural features that prevent the recruitment of the CCR4-NOT complex.
Researchers from Georgia Institute of Technology and Emory University School of Medicine published a research paper titled "Lipid nanoparticle-mediated mRNA delivery to CD34+ cells in rhesus monkeys" in Nature Biotechnology, a subsidiary of Nature. The study developed a lipid nanoparticle (LNP) called LNP67, which does not require bone marrow mobilization or chemotherapy pretreatment and is not modified with targeting ligands. It can deliver mRNA to hematopoietic stem/progenitor cells (HSPC) in rhesus monkeys at a dose as low as 0.25 mg/kg.
Transfer RNA halves (tRHs) have multiple biological functions. However, the biogenesis of specific 5'-tRHs under certain conditions is currently unclear to researchers. Recently, in a research report titled "5'-tRNAGly(GCC) halves generated by IRE1α are linked to the ER stress response" published in the international journal Nature Communications, scientists from Yanbian University and other institutions in China revealed the synthesis process and key role of the transfer RNA-derived fragment 5'-tRH-GlyGCC in cancer progression. By interacting with splicing factors, it may be able to regulate gene expression, alternative splicing, and messenger RNA processing.
Gliomas are the most common type of brain cancer, including the deadliest form, glioblastoma. Every week, Harvard Medical School neuro-oncologist Annie Hsieh treats patients with gliomas. After Hsieh's fellow neurosurgeons remove a glioma with surgery, it often appears that no cancer cells are left. Radiation and other treatments may follow. However, gliomas often recur, not only in the original site but also in distant parts of the brain. This can harm the nervous system and, in some cases, lead to death.
Dysfunction of DNA repair is a key driver of cancer. Understanding the molecular mechanisms behind dysfunctional DNA repair in cancer cells is crucial for the occurrence of cancer and the development of new therapies. Recently, in a research report titled "EZH2 directly methylates PARP1 and regulates its activity in cancer" published in the international journal Science Advances, scientists from Northwestern University and other institutions discovered a new molecular mechanism behind dysfunctional DNA repair in prostate cancer cells through research. This research finding is expected to guide scientists to develop new targeted therapies to treat prostate cancer patients who are resistant to current standard therapies.
Lambert-Eaton myasthenic syndrome (LEMS), also known as myasthenic syndrome, is a rare, often tumor-associated autoimmune disease involving the presynaptic membrane of the neuromuscular junction that was first described in 1956. Typical clinical symptoms include progressive truncal muscle weakness, ptosis, as well as diplopia, dysarthria, and dysphagia. The disease is caused by pathogenic autoantibodies that target and inhibit the P/Q-type pressure-gated calcium channels (VGCCs) presynaptic to nerve terminals, which is different from the postsynaptic targets of pathogenic autoantibodies that cause myasthenia gravis (MG).
Neville E. Sanjana's team at New York University published a research paper titled "Transcriptome-scale RNA-targeting CRISPR screens reveal essential lncRNAs in human cells" in the international academic journal Cell. The study developed a transcriptome-scale CRISPR screening technology based on CRISPR-Cas13 targeting RNA, and used this technology to screen and identify 778 essential lncRNAs in 5 human cells from different tissues, indicating that many lncRNAs are not junk, but play an essential and important role in human cancer and development.
In October 2024, Victor Ambros and Gary Ruvkun were awarded the Nobel Prize in Physiology or Medicine for their discovery of the central role of microRNA (miRNA) in gene expression. This discovery in 1993 revealed that miRNA regulates gene expression by binding to target mRNA and inhibiting its translation. Since then, the important role of miRNA in multiple gene expression pathways such as cell differentiation, proliferation and survival has gradually been recognized. However, although the biological functions of miRNA have been well studied, the road to applying miRNA in clinical treatment is still long and challenging.
The Proceedings of the National Academy of Sciences (PNAS) published online a research paper titled "AMBRA1 controls the translation of immune-specific genes in T lymphocytes" by the research group of Yikun Yao from the Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences. This study screened and identified the key regulatory protein AMBRA1 in the FAS-mediated T cell death process, revealing a new mechanism by which AMBRA1 controls TCR signaling, T cell cycle and T cell death at the translation level.
CRISPR-Cas9 has long been likened to a pair of genetic scissors because of its ability to elegantly and precisely snip any desired DNA fragment. But it turns out that the CRISPR system has more than just one strategy in its toolbox. CRISPR is a mechanism originally discovered in bacteria, and it has been operating for centuries as an adaptive immune system. Certain single-celled organisms naturally use CRISPR to protect themselves from viruses (called bacteriophages) and other foreign genetic fragments.
