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2. Distinct use of super-enhancer elements controls cell type–specific CD25 transcription and function

5. Data from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

6. Table S3-4 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

7. Table S5J-part2 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

8. Table S5J-part3 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

9. Table S5 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

10. Supplementary methods from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

11. Table S5J-part3 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

12. Figure S1-4 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

13. Data from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

14. Figure S1-4 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

15. Table S1 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

16. Table S5J-part2 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

17. Table S1 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

18. Table S5 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

19. Figure S5-6 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

20. Figure S5-6 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

21. Table S3-4 from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

22. Supplementary methods from Integrated Pan-Cancer Map of EBV-Associated Neoplasms Reveals Functional Host–Virus Interactions

27. A comprehensive single cell data analysis of lymphoblastoid cells reveals the role of super‐enhancers in maintaining EBV latency

30. A comprehensive single cell data analysis of in lymphoblastoid cells reveals the role of Super-enhancers in maintaining EBV latency

31. SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

32. Complement activates an autocrine Vitamin D system that recruits a defined transcription factor network to shut down pro-inflammatory programs of Th1 cells

35. Mitochondrial C5aR1 activity in macrophages controls IL-1β production underlying sterile inflammation

37. Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells

38. Reply to Grigoriev et al., “Sequences of SARS-CoV-2 “Hybrids” with the Human Genome: Signs 1 of Non-coding RNA?”

42. Host-Virus Chimeric Events in SARS-CoV-2-Infected Cells Are Infrequent and Artifactual

43. Implementing sequencing-based surveillance in developing countries: findings from a pilot rollout for hepatitis A in China

44. Metatranscriptomic Analysis Reveals an Imbalance of Hepatopancreatic Flora of Chinese Mitten Crab Eriocheir sinensis with Hepatopancreatic Necrosis Disease

46. Homeostatic regulation of T follicular helper and antibody response to particle antigens by IL-1Ra of medullary sinus macrophage origin

47. SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

48. Proteomic analysis of the exosomes secreted from Ctenopharyngodon idellus kidney cells infected with grass carp reovirus reveals their involvement in the cellular responses to viral infection

50. Host-virus chimeric events in SARS-CoV2 infected cells are infrequent and artifactual

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