- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- Extent
-
1 Online-Ressource.
- Language
-
Englisch
- Bibliographic citation
-
The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy ; volume:15 ; number:9 ; day:18 ; month:9 ; year:2024 ; pages:1-13 ; date:9.2024
Cell death & disease ; 15, Heft 9 (18.9.2024), 1-13, 9.2024
- Creator
-
Meng, Chen
Su, Haibi
Shu, Meiling
Shen, Feng
Lu, Yijie
Wu, Shishi
Su, Zhenghua
Yu, Mengyao
Yang, Di
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1038/s41419-024-07053-2
- URN
-
urn:nbn:de:101:1-2412012105417.333592052797
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
- 15.08.2025, 5:29 AM UTC
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Meng, Chen
- Su, Haibi
- Shu, Meiling
- Shen, Feng
- Lu, Yijie
- Wu, Shishi
- Su, Zhenghua
- Yu, Mengyao
- Yang, Di
- SpringerLink (Online service)
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m6A demethylase FTO regulate CTNNB1 to promote adipogenesis of chicken preadipocyte
Demethylase ALKBH5 suppresses invasion of gastric cancer via PKMYT1 m6A modification
Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
ADAP1 limits neonatal cardiomyocyte hypertrophy by reducing integrin cell surface expression
The biological function of m6A demethylase ALKBH5 and its role in human disease
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy
MRI based non-invasive detection of cardiomyocyte hypertrophy and cell-volume changes
Sumoylation-independent activation of calcineurin-NFAT-signaling via SUMO2 causes cardiomyocyte hypertrophy
Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure
Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation
Inhibition of cardiomyocyte hypertrophy by heterocyclic thiourylenes in vitro
Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival
m6A demethylase FTO regulate CTNNB1 to promote adipogenesis of chicken preadipocyte
Demethylase ALKBH5 suppresses invasion of gastric cancer via PKMYT1 m6A modification
Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
ADAP1 limits neonatal cardiomyocyte hypertrophy by reducing integrin cell surface expression
The biological function of m6A demethylase ALKBH5 and its role in human disease
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy
MRI based non-invasive detection of cardiomyocyte hypertrophy and cell-volume changes
Sumoylation-independent activation of calcineurin-NFAT-signaling via SUMO2 causes cardiomyocyte hypertrophy
Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure
Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation
Inhibition of cardiomyocyte hypertrophy by heterocyclic thiourylenes in vitro
Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival
m6A demethylase FTO regulate CTNNB1 to promote adipogenesis of chicken preadipocyte
Demethylase ALKBH5 suppresses invasion of gastric cancer via PKMYT1 m6A modification
Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
ADAP1 limits neonatal cardiomyocyte hypertrophy by reducing integrin cell surface expression
The biological function of m6A demethylase ALKBH5 and its role in human disease
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy
MRI based non-invasive detection of cardiomyocyte hypertrophy and cell-volume changes