m6A-centered Disease Response Information
General Information of the Disease (ID: M6ADIS0037)
Name |
Gangrene or necrosis of lung
|
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ICD |
ICD-11: CA43
|
Full List of Target Gene(s) of This m6A-centered Disease Response
Interleukin-1 beta (IL1B)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, Interleukin-1 beta (IL1B) and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, Interleukin-1 beta (IL1B) and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Mitogen-activated protein kinase 14 (p38/MAPK14)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated Mitogen-activated protein kinase 14 (p38/MAPK14), ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated Mitogen-activated protein kinase 14 (p38/MAPK14), ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Mitogen-activated protein kinase 3 (ERK1/MAPK3)
In total 1 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 3 (ERK1/MAPK3), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
RAC-alpha serine/threonine-protein kinase (AKT1)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, RAC-alpha serine/threonine-protein kinase (AKT1), and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, RAC-alpha serine/threonine-protein kinase (AKT1), and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Transcription factor p65 (RELA)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited Transcription factor p65 (RELA), IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited Transcription factor p65 (RELA), IL-1-beta and TNF-alpha secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Tumor necrosis factor (TNF/TNF-alpha)
In total 2 item(s) under this target gene | ||||
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and Tumor necrosis factor (TNF/TNF-alpha) secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | YTH domain-containing family protein 3 (YTHDF3) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
Response Summary | N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and Tumor necrosis factor (TNF/TNF-alpha) secretion. | |||
Responsed Disease | Gangrene or necrosis of lung [ICD-11: CA43] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Apoptosis | hsa04210 | |||
Cell Process | Biological regulation | |||
Cell apoptosis | ||||
In-vitro Model | BEAS-2B | Normal | Homo sapiens | CVCL_0168 |
In-vivo Model | After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1. | |||
References