- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
1 Online-Ressource.
- Sprache
-
Englisch
- Erschienen in
-
Trans-activating mutations of the pseudokinase ERBB3 ; volume:43 ; number:29 ; day:28 ; month:5 ; year:2024 ; pages:2253-2265 ; date:7.2024
Oncogene ; 43, Heft 29 (28.5.2024), 2253-2265, 7.2024
- Urheber
-
Koivu, Marika K. A.
Chakroborty, Deepankar
Airenne, Tomi T.
Johnson, Mark S.
Kurppa, Kari J.
Elenius, Klaus
- Beteiligte Personen und Organisationen
-
SpringerLink (Online service)
- DOI
-
10.1038/s41388-024-03070-9
- URN
-
urn:nbn:de:101:1-2409292103381.695609311187
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.2025, 07:29 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Koivu, Marika K. A.
- Chakroborty, Deepankar
- Airenne, Tomi T.
- Johnson, Mark S.
- Kurppa, Kari J.
- Elenius, Klaus
- SpringerLink (Online service)
Ähnliche Objekte (12)
Activating FGFR1 Mutations in Sporadic Pheochromocytomas
Somatic activating mutations in MAP2K1 cause melorheostosis
Mechanism of activating mutations and allosteric drug inhibition of the phosphatase SHP2
Point mutations M2-trans-membrane Torpedo
E‐cadherin can limit the transforming properties of activating β‐catenin mutations
Recurrent activating mutations of PPARγ associated with luminal bladder tumors
Activating PIK3CA mutations coexist with BRAF or NRAS mutations in a limited fraction of melanomas
Intratumoral heterogeneity of EGFR-activating mutations in advanced NSCLC patients at the single-cell level
PI3K/mTOR inhibition promotes the regression of experimental vascular malformations driven by PIK3CA-activating mutations
Novel mutatıons and diverse clinical phenotypes in recombınase-activating gene 1 deficiency
PIK3CA-activating mutations and chemotherapy sensitivity in stage II–III breast cancer
Activating de novo mutations in NFE2L2 encoding NRF2 cause a multisystem disorder
Activating FGFR1 Mutations in Sporadic Pheochromocytomas
Somatic activating mutations in MAP2K1 cause melorheostosis
Mechanism of activating mutations and allosteric drug inhibition of the phosphatase SHP2
Point mutations M2-trans-membrane Torpedo
E‐cadherin can limit the transforming properties of activating β‐catenin mutations
Recurrent activating mutations of PPARγ associated with luminal bladder tumors
Activating PIK3CA mutations coexist with BRAF or NRAS mutations in a limited fraction of melanomas
Intratumoral heterogeneity of EGFR-activating mutations in advanced NSCLC patients at the single-cell level
PI3K/mTOR inhibition promotes the regression of experimental vascular malformations driven by PIK3CA-activating mutations
Novel mutatıons and diverse clinical phenotypes in recombınase-activating gene 1 deficiency
PIK3CA-activating mutations and chemotherapy sensitivity in stage II–III breast cancer
Activating de novo mutations in NFE2L2 encoding NRF2 cause a multisystem disorder
Activating FGFR1 Mutations in Sporadic Pheochromocytomas
Somatic activating mutations in MAP2K1 cause melorheostosis
Mechanism of activating mutations and allosteric drug inhibition of the phosphatase SHP2
Point mutations M2-trans-membrane Torpedo
E‐cadherin can limit the transforming properties of activating β‐catenin mutations
Recurrent activating mutations of PPARγ associated with luminal bladder tumors
Activating PIK3CA mutations coexist with BRAF or NRAS mutations in a limited fraction of melanomas
Intratumoral heterogeneity of EGFR-activating mutations in advanced NSCLC patients at the single-cell level
PI3K/mTOR inhibition promotes the regression of experimental vascular malformations driven by PIK3CA-activating mutations
Novel mutatıons and diverse clinical phenotypes in recombınase-activating gene 1 deficiency
PIK3CA-activating mutations and chemotherapy sensitivity in stage II–III breast cancer