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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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