path(MESH:"Mitochondrial Diseases")

Entity

Name

Mitochondrial Diseases

Namespace

MeSH

Namespace Version

20181007

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Mechanistic knowledge surrounding heme

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065