330 results on '"Lu, Zhimin"'
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2. Single-nucleus RNA transcriptome profiling reveals murine adipose tissue endothelial cell proliferation gene networks involved in obesity development
3. Involvement of increased Arg-1+ILC2s and MDSCs in endometrial carcinoma: a pilot study
4. VHL suppresses autophagy and tumor growth through PHD1-dependent Beclin1 hydroxylation
5. Single cell RNA-sequencing data generated from mouse adipose tissue during the development of obesity
6. CSFV restricts necroptosis to sustain infection by inducing autophagy/mitophagy-targeted degradation of RIPK3
7. Plasma metabonomics of classical swine fever virus-infected pigs
8. Investigation on plasma morphology fluctuation in laser-induced breakdown spectroscopy analysis of particle flow due to stochastic particle ablation
9. Base editing of the mutated TERT promoter inhibits liver tumor growth
10. A century of the Warburg effect
11. Modelling nitrogen oxide emission trends from the municipal solid waste incineration process using an adaptive bi‐directional long and short‐term memory network
12. Pan-cancer tRNA-derived fragment CAT1 coordinates RBPMS to stabilize NOTCH2 mRNA to promote tumorigenesis
13. Structure of histone deacetylase complex Rpd3S bound to nucleosome
14. UBC9 stabilizes PFKFB3 to promote aerobic glycolysis and proliferation of glioblastoma cells
15. Comparison between two-step and single-step kinetic models for non-isothermal CO2 gasification of biomass char generated by fast pyrolysis
16. Bioinformatics analysis of copper death gene in diabetic immune infiltration
17. Hypoxanthine phosphoribosyl transferase 1 metabolizes temozolomide to activate AMPK for driving chemoresistance of glioblastomas
18. Corrigendum to “Role of OGDH in Autophagy-IRF3-IFN-β pathway during classical swine fever virus infection” [Int. J. Biol. Macromol. 249 (2023) 126443 (BIOMAC 126443)]
19. EGFR‐Induced and c‐Src‐Mediated CD47 Phosphorylation Inhibits TRIM21‐Dependent Polyubiquitylation and Degradation of CD47 to Promote Tumor Immune Evasion
20. Effect of torrefaction on yield, reactivity and physicochemical properties of pyrolyzed char from three major biomass constituents
21. Role of OGDH in Atophagy-IRF3-IFN-β pathway during classical swine fever virus infection
22. Flowability, binding and release property of “self-lubricating” microcrystalline cellulose
23. Creatine kinase B suppresses ferroptosis by phosphorylating GPX4 through a moonlighting function
24. Ribosomal protein L32 enhances hepatocellular carcinoma progression
25. Legend for the Supplementary Figures and Tables from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
26. Data from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
27. Supplementary Table S1 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
28. Supplementary Fig. S1-S5 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
29. Supplementary Table S2 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
30. Supplementary Fig. S1-S5 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
31. Supplementary Table S2 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
32. Legend for the Supplementary Figures and Tables from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
33. Supplementary Table S1 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
34. Data from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
35. Supplementary Table S3 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
36. Supplementary Table S3 from TCR Repertoire Diversity of Peripheral PD-1+CD8+ T Cells Predicts Clinical Outcomes after Immunotherapy in Patients with Non–Small Cell Lung Cancer
37. Figure S1 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
38. Figure S4 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
39. Supplementary Information from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
40. Figure S2 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
41. Figure S2 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
42. Data from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
43. The moonlighting function of glycolytic enzyme enolase-1 promotes choline phospholipid metabolism and tumor cell proliferation
44. Figure S3 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
45. Figure S3 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
46. Figure S5 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
47. Figure S4 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
48. Figure S1 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
49. Data from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
50. Figure S5 from Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress
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