Tsingke has delivered high-quality biotechnology services and products to nearly 300,000 users globally. The number of high-level academic papers published using Tsingke's products and services has grown steadily year after year, continuously driving the advancement of life science research.
We have selected five high-impact papers, published in prestigious journals such as Cell and Signal Transduction and Targeted Therapy, spanning a range of fields from gene function research to immunotherapy and beyond.
Compilation of High-Impact Literature
1.
Title: Enhancing rice panicle branching and grain yield through tissue-specific brassinosteroid inhibition
DOI: 10.1126/science.adk8838
Journal: Science
Impact Factor: 56.9
Summary:
This study shows that crop yield potential is limited by inherent trade-offs between grain size and number. While brassinosteroids (BRs) promote grain enlargement, their role in regulating grain number has been unclear. By analyzing a cluster-type rice germplasm, the researchers found that activating the BR metabolic gene BRASSINOSTEROID-DEFICIENT DWARF3 (BRD3) significantly increases grain number. A molecular pathway was established where the BR signal inhibitor GSK3/SHAGGY-LIKE KINASE2 phosphorylates and stabilizes the OsMADS1 transcription factor, which targets the TERMINAL FLOWER1-like gene RICE CENTRORADIALIS2. Tissue-specific activation of BRD3 in secondary branch meristems enhances panicle branching, reduces the negative impact on grain size, and improves grain yield. The study demonstrates the powerful role of tissue-specific hormone manipulation in overcoming trait trade-offs and unlocking rice yield potential.
2.
Title: Targeting carnitine palmitoyl transferase 1A (CPT1A) induces ferroptosis and synergizes with immunotherapy in lung cancer
DOI: 10.1038/s41392-024-01772-w
Journal: Signal Transduction and Targeted Therapy
Impact Factor: 39.3
Summary:
Despite the success of immune checkpoint therapies, resistance and relapse remain common in lung cancer. Cancer stem cells (CSCs) are an important factor in immune therapy resistance. Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, has shown synergistic effects with immunotherapy. This study shows that the key rate-limiting enzyme CPT1A in fatty acid oxidation, together with L-carnitine from tumor-associated macrophages, drives ferroptosis resistance and CD8+ T cell dysfunction in lung cancer. Mechanistically, CPT1A inhibits the ubiquitination and degradation of c-Myc, which transcriptionally activates CPT1A expression. The CPT1A/c-Myc positive feedback loop enhances the NRF2/GPX4 system and reduces the quantity of phospholipid polyunsaturated fatty acids, boosting cellular antioxidant capacity and suppressing ferroptosis in CSCs. Importantly, targeting CPT1A enhances anti-tumor immunity and ferroptosis in immune checkpoint blockade therapy in tumor-bearing mice. These results present a metabolic vulnerability-targeting approach to improve lung cancer immunotherapy efficacy.
3.
Title: Abiotic Synthetic Antibody Inhibitor with Broad-Spectrum Neutralization and Antiviral Efficacy against Escaping SARS-CoV2 Variants
DOI: 10.1021/acsnano.3c02050
Journal: ACS Nano
Impact Factor: 17.1
Summary:
This study addresses the challenge posed by the rapid emergence and spread of SARS-CoV-2 vaccine and antibody escape variants, proposing a potential therapeutic strategy. The researchers developed an artificial synthetic antibody inhibitor, Aphe-NP14, as a treatment for COVID-19. Aphe-NP14 was screened from a synthetic hydrogel polymer nanoparticle library, designed to interact with key residues in the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2. Aphe-NP14 showed high capacity, fast adsorption kinetics, strong affinity, and broad specificity, effectively neutralizing various SARS-CoV-2 variants, including Beta, Delta, and Omicron. By blocking the RBD-ACE2 interaction, Aphe-NP14 prevents the infection of these escape variants. The study also found that Aphe-NP14 showed low toxicity both in vitro and in vivo via nasal administration, indicating its potential for the prevention and treatment of SARS-CoV-2 variants.
4.
Title: Cepharanthine analogs mining and genomes of Stephania accelerate anti-coronavirus drug discovery
DOI: 10.1038/s41467-024-45690-5
Journal: Nature Communications
Impact Factor: 16.6
Summary:
Cepharanthine, a secondary metabolite extracted from Stephania plants, has antiviral activity against coronaviruses, including SARS-CoV-2. The research team assembled the genomes of three Stephania species—Japanese Stephania, Yunnan Stephania, and Stephania cepharantha—and identified the biosynthetic pathway for cepharanthine. They discovered seven cepharanthine analogs with broad-spectrum antiviral activity against multiple coronaviruses, including SARS-CoV-2, GX_P2V, SADS-CoV, and PEDV. Additionally, other plants, such as Nelumbo and Thalictrum, were found to produce cepharanthine analogs, highlighting their potential in antiviral compound discovery. This research offers new ideas and accelerated pathways for the development of broad-spectrum anti-coronavirus drugs.
5.
Title: Catalytically inactive long prokaryotic Argonaute systems employ distinct effectors to confer immunity via abortive infection
DOI: 10.1038/s41467-023-42793-3
Journal: Nature Communications
Impact Factor: 16.6
Summary:
This study focuses on the defense function of Argonaute proteins (Ago) in bacteria. Agos bind to short nucleic acid molecules as "guides" to recognize and bind complementary target nucleic acids. Different prokaryotic Argonaute proteins (pAgos) may play significant roles in microbial defense. However, the function and mechanism of a class of full-length but catalytically inactive pAgos (long-B type pAgos) remain unclear. The study shows that most long-B type pAgos are associated with specific companion proteins, including nucleases, Sir2 domain-containing proteins, and membrane proteins. The long-B type pAgo-nuclease system (BPAN system) is activated after guide RNA recognition of target DNA, leading to widespread DNA degradation in vitro. In vivo, this system causes genomic DNA degradation upon detection of an invading plasmid, killing infected cells and clearing the invader from the cell population. These findings provide new insights into microbial defense mechanisms.
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