Senescence-associated reprogramming induced by interleukin-1 impairs response to EGFR neutralization
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1689-1392
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
-
online resource.
- Bibliographic citation
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Senescence-associated reprogramming induced by interleukin-1 impairs response to EGFR neutralization ; volume:27 ; number:1 ; day:2 ; month:3 ; year:2022 ; pages:1-17 ; date:12.2022
Cellular & molecular biology letters ; 27, Heft 1 (2.3.2022), 1-17, 12.2022
- Creator
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Romaniello, Donatella
Gelfo, Valerio
Pagano, Federica
Ferlizza, Enea
Sgarzi, Michela
Mazzeschi, Martina
Morselli, Alessandra
Miano, Carmen
D’Uva, Gabriele
Lauriola, Mattia
- Contributor
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SpringerLink (Online service)
- DOI
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10.1186/s11658-022-00319-7
- URN
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urn:nbn:de:101:1-2022052920122514286809
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:30 AM CEST
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
- Romaniello, Donatella
- Gelfo, Valerio
- Pagano, Federica
- Ferlizza, Enea
- Sgarzi, Michela
- Mazzeschi, Martina
- Morselli, Alessandra
- Miano, Carmen
- D’Uva, Gabriele
- Lauriola, Mattia
- SpringerLink (Online service)
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METTL3-mediated chromatin contacts promote stress granule phase separation through metabolic reprogramming during senescence
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Interplay of ARID1A and EGFR signaling in controlling acinar cell reprogramming in the pancreas
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Reprogramming of mRNA translation in cellular senescence
Paracrine cellular senescence exacerbates biliary injury and impairs regeneration
Retraction Note: Senescence impairs direct conversion of human somatic cells to neurons
A destabilizing Y891D mutation in activated EGFR impairs sensitivity to kinase inhibition
Senescence of donor cells impairs fat graft regeneration by suppressing adipogenesis and increasing expression of senescence-associated secretory phenotype factors
METTL3-mediated chromatin contacts promote stress granule phase separation through metabolic reprogramming during senescence
Chemotherapy‐Induced Senescence Reprogramming Promotes Nasopharyngeal Carcinoma Metastasis by circRNA‐Mediated PKR Activation
Targeting aurora kinases limits tumour growth through DNA damage‐mediated senescence and blockade of NF‐κB impairs this drug‐induced senescence
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The Neutralization of Egypt.
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