• 00:00 1.
    index 1
  • 00:11 2.
    N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
  • 00:17 3.
    ** after 20230821 rehearsal.pptx
  • 00:25 4.
    index 4
  • 00:31 5.
    N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
  • 00:32 6.
    Chronic obstructive pulmonary disease was ranked as the third leading cause of death
  • 00:35 7.
    ** after 20230821 rehearsal.pptx
  • 00:40 8.
    index 8
  • 01:06 9.
    Chronic obstructive pulmonary disease was ranked as the third leading cause of death
  • 01:13 10.
    N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
  • 03:48 11.
    Chronic obstructive pulmonary disease was ranked as the third leading cause of death
  • 04:50 12.
    Classification of severity in COPD
  • 05:25 13.
    Risk factor of COPD
  • 05:48 14.
    Slide 5
  • 06:23 15.
    Ferroptosis
  • 07:14 16.
    COPD therapy
  • 07:55 17.
    N6-Methyladenosine (m6A)
  • 09:24 18.
    circRNA
  • 10:26 19.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 10:46 20.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 10:53 21.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 10:54 22.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 10:56 23.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 10:57 24.
    circRNA
  • 10:57 25.
    N6-Methyladenosine (m6A)
  • 10:58 26.
    COPD therapy
  • 10:58 27.
    Ferroptosis
  • 10:59 28.
    Slide 5
  • 11:00 29.
    Ferroptosis
  • 11:03 30.
    COPD therapy
  • 11:05 31.
    Ferroptosis
  • 11:05 32.
    Slide 5
  • 11:05 33.
    Risk factor of COPD
  • 11:06 34.
    Classification of severity in COPD
  • 11:06 35.
    Chronic obstructive pulmonary disease was ranked as the third leading cause of death
  • 11:06 36.
    N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
  • 11:13 37.
    Iron overload is involved in experimental COPD due to excessive lipid peroxidation.
  • 11:26 38.
    N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
  • 11:59 39.
    Chronic obstructive pulmonary disease was ranked as the third leading cause of death
  • 12:00 40.
    Classification of severity in COPD
  • 14:20 41.
    Risk factor of COPD
  • 14:22 42.
    Slide 5
  • 14:23 43.
    Ferroptosis
  • 15:01 44.
    COPD therapy
  • 15:02 45.
    N6-Methyladenosine (m6A)
  • 15:03 46.
    circRNA
  • 15:08 47.
    N6-Methyladenosine (m6A)
  • 17:17 48.
    circRNA
  • 17:19 49.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 17:20 50.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 18:09 51.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 18:31 52.
    Slide 13
  • 18:46 53.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 18:46 54.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 19:10 55.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 19:10 56.
    circRNA
  • 19:11 57.
    N6-Methyladenosine (m6A)
  • 19:12 58.
    COPD therapy
  • 19:13 59.
    Ferroptosis
  • 19:20 60.
    COPD therapy
  • 19:20 61.
    N6-Methyladenosine (m6A)
  • 19:22 62.
    circRNA
  • 19:25 63.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 19:25 64.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 21:23 65.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 21:23 66.
    Slide 13
  • 21:24 67.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 21:45 68.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 22:43 69.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 22:47 70.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 23:31 71.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 23:49 72.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 24:11 73.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 25:04 74.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 25:32 75.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 26:20 76.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 26:23 77.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 26:27 78.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 26:28 79.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 26:49 80.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 26:55 81.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 29:00 82.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 29:22 83.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 30:28 84.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 31:13 85.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 32:18 86.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 32:24 87.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 32:26 88.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 38:39 89.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 38:42 90.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 39:48 91.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 40:12 92.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 40:17 93.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 45:10 94.
    ** after 20230821 rehearsal.pptx
  • 45:31 95.
    EMSA
  • 47:38 96.
    ** after 20230821 rehearsal.pptx
  • 47:48 97.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 57:53 98.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 58:52 99.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 59:15 100.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 59:18 101.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 59:30 102.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:00:11 103.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 1:00:14 104.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:01:05 105.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:02:10 106.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:02:32 107.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:02:44 108.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:03:08 109.
    Slide 28
  • 1:04:04 110.
    Slide 29
  • 1:04:19 111.
    Slide 30
  • 1:05:03 112.
    Slide 29
  • 1:05:03 113.
    Slide 28
  • 1:05:04 114.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:05:04 115.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:05:05 116.
    Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:05:05 117.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:05:06 118.
    DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
  • 1:05:07 119.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 1:05:07 120.
    In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
  • 1:05:08 121.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 1:05:08 122.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 1:05:09 123.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 1:05:10 124.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 1:05:10 125.
    circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
  • 1:05:11 126.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 1:05:12 127.
    circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
  • 1:05:13 128.
    Slide 13
  • 1:05:14 129.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 1:05:14 130.
    Ferroptosis, an iron homeostasis disorder, related to COPD progression.
  • 1:05:15 131.
    Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
  • 1:05:15 132.
    circRNA
  • 1:05:15 133.
    N6-Methyladenosine (m6A)
  • 1:05:16 134.
    COPD therapy
  • 1:05:16 135.
    Ferroptosis
  • 1:05:17 136.
    Slide 5
  • 1:05:17 137.
    Risk factor of COPD
  • 1:05:18 138.
    Slide 5
  • 1:06:09 139.
    Ferroptosis
  • 1:06:55 140.
    Slide 5
  • 1:06:56 141.
    Risk factor of COPD
  • 1:08:58 142.
    Slide 5
  • 1:08:59 143.
    Ferroptosis
  • 1:08:59 144.
    COPD therapy
  • 1:09:00 145.
    N6-Methyladenosine (m6A)
  • 1:09:01 146.
    circRNA
  • 1:09:06 147.
    ** after 20230821 rehearsal.pptx
  • 1:09:22 148.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 1:10:33 149.
    ** after 20230821 rehearsal.pptx
  • 1:10:42 150.
    circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
  • 1:15:23 151.
    ** after 20230821 rehearsal.pptx
  • Index
  • Notes
  • Comment
  • Fullscreen
20230821 lab meeting_照穎
Duration: 1:15:33, Browse: 128, Last Updated: 2023-08-21
    • 00:00 1.
      index 1
    • 00:11 2.
      N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
    • 00:17 3.
      ** after 20230821 rehearsal.pptx
    • 00:25 4.
      index 4
    • 00:31 5.
      N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
    • 00:32 6.
      Chronic obstructive pulmonary disease was ranked as the third leading cause of death
    • 00:35 7.
      ** after 20230821 rehearsal.pptx
    • 00:40 8.
      index 8
    • 01:06 9.
      Chronic obstructive pulmonary disease was ranked as the third leading cause of death
    • 01:13 10.
      N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
    • 03:48 11.
      Chronic obstructive pulmonary disease was ranked as the third leading cause of death
    • 04:50 12.
      Classification of severity in COPD
    • 05:25 13.
      Risk factor of COPD
    • 05:48 14.
      Slide 5
    • 06:23 15.
      Ferroptosis
    • 07:14 16.
      COPD therapy
    • 07:55 17.
      N6-Methyladenosine (m6A)
    • 09:24 18.
      circRNA
    • 10:26 19.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 10:46 20.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 10:53 21.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 10:54 22.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 10:56 23.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 10:57 24.
      circRNA
    • 10:57 25.
      N6-Methyladenosine (m6A)
    • 10:58 26.
      COPD therapy
    • 10:58 27.
      Ferroptosis
    • 10:59 28.
      Slide 5
    • 11:00 29.
      Ferroptosis
    • 11:03 30.
      COPD therapy
    • 11:05 31.
      Ferroptosis
    • 11:05 32.
      Slide 5
    • 11:05 33.
      Risk factor of COPD
    • 11:06 34.
      Classification of severity in COPD
    • 11:06 35.
      Chronic obstructive pulmonary disease was ranked as the third leading cause of death
    • 11:06 36.
      N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
    • 11:13 37.
      Iron overload is involved in experimental COPD due to excessive lipid peroxidation.
    • 11:26 38.
      N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2
    • 11:59 39.
      Chronic obstructive pulmonary disease was ranked as the third leading cause of death
    • 12:00 40.
      Classification of severity in COPD
    • 14:20 41.
      Risk factor of COPD
    • 14:22 42.
      Slide 5
    • 14:23 43.
      Ferroptosis
    • 15:01 44.
      COPD therapy
    • 15:02 45.
      N6-Methyladenosine (m6A)
    • 15:03 46.
      circRNA
    • 15:08 47.
      N6-Methyladenosine (m6A)
    • 17:17 48.
      circRNA
    • 17:19 49.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 17:20 50.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 18:09 51.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 18:31 52.
      Slide 13
    • 18:46 53.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 18:46 54.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 19:10 55.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 19:10 56.
      circRNA
    • 19:11 57.
      N6-Methyladenosine (m6A)
    • 19:12 58.
      COPD therapy
    • 19:13 59.
      Ferroptosis
    • 19:20 60.
      COPD therapy
    • 19:20 61.
      N6-Methyladenosine (m6A)
    • 19:22 62.
      circRNA
    • 19:25 63.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 19:25 64.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 21:23 65.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 21:23 66.
      Slide 13
    • 21:24 67.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 21:45 68.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 22:43 69.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 22:47 70.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 23:31 71.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 23:49 72.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 24:11 73.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 25:04 74.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 25:32 75.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 26:20 76.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 26:23 77.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 26:27 78.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 26:28 79.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 26:49 80.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 26:55 81.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 29:00 82.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 29:22 83.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 30:28 84.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 31:13 85.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 32:18 86.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 32:24 87.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 32:26 88.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 38:39 89.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 38:42 90.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 39:48 91.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 40:12 92.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 40:17 93.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 45:10 94.
      ** after 20230821 rehearsal.pptx
    • 45:31 95.
      EMSA
    • 47:38 96.
      ** after 20230821 rehearsal.pptx
    • 47:48 97.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 57:53 98.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 58:52 99.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 59:15 100.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 59:18 101.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 59:30 102.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:00:11 103.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 1:00:14 104.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:01:05 105.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:02:10 106.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:02:32 107.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:02:44 108.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:03:08 109.
      Slide 28
    • 1:04:04 110.
      Slide 29
    • 1:04:19 111.
      Slide 30
    • 1:05:03 112.
      Slide 29
    • 1:05:03 113.
      Slide 28
    • 1:05:04 114.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:05:04 115.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:05:05 116.
      Downregulated circSAV1 reduces emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:05:05 117.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:05:06 118.
      DFO ameliorated emphysema and airway remodeling through inhibiting ferroptosis in experimental COPD.
    • 1:05:07 119.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 1:05:07 120.
      In BEAS-2B cells, circSAV1 triggered ferroptosis via IREB2.
    • 1:05:08 121.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 1:05:08 122.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 1:05:09 123.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 1:05:10 124.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 1:05:10 125.
      circSAV1 enhanced free iron and triggered ferroptosis in CSE-treated BEAS-2B cells.
    • 1:05:11 126.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 1:05:12 127.
      circSAV1 was elevated in lung tissue of smokers and COPD smokers, and related to COPD progression.
    • 1:05:13 128.
      Slide 13
    • 1:05:14 129.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 1:05:14 130.
      Ferroptosis, an iron homeostasis disorder, related to COPD progression.
    • 1:05:15 131.
      Whether COPD progression was associated with ferroptosis?Which circRNA could be a biomarker in this mechanism?
    • 1:05:15 132.
      circRNA
    • 1:05:15 133.
      N6-Methyladenosine (m6A)
    • 1:05:16 134.
      COPD therapy
    • 1:05:16 135.
      Ferroptosis
    • 1:05:17 136.
      Slide 5
    • 1:05:17 137.
      Risk factor of COPD
    • 1:05:18 138.
      Slide 5
    • 1:06:09 139.
      Ferroptosis
    • 1:06:55 140.
      Slide 5
    • 1:06:56 141.
      Risk factor of COPD
    • 1:08:58 142.
      Slide 5
    • 1:08:59 143.
      Ferroptosis
    • 1:08:59 144.
      COPD therapy
    • 1:09:00 145.
      N6-Methyladenosine (m6A)
    • 1:09:01 146.
      circRNA
    • 1:09:06 147.
      ** after 20230821 rehearsal.pptx
    • 1:09:22 148.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 1:10:33 149.
      ** after 20230821 rehearsal.pptx
    • 1:10:42 150.
      circSAV1 interacted with YTHDF1 via its m6A motif, which contributed to IREB2 mRNA translation.
    • 1:15:23 151.
      ** after 20230821 rehearsal.pptx
    Location
    Folder name
    2023
    Author
    周楷軒
    Branch
    賴亮全教授
    Created
    2023-08-21 15:29:53
    Last Updated
    2023-08-21 16:03:53
    Duration
    1:15:33