BEIJING,Nov. 12,2024 -- Tsingkehas 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 two high-impact papers,published in prestigious journals,spanning a range of fields from gene function research to immunotherapy.
Compilationof 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.
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For more high-impact papers utilizing Tsingke's products and services,visit our website to explore how our solutions are helping advance research worldwide.