The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1471-2407
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition ; volume:12 ; number:1 ; day:21 ; month:11 ; year:2012 ; pages:1-12 ; date:12.2012
BMC cancer ; 12, Heft 1 (21.11.2012), 1-12, 12.2012
- Urheber
-
Peddaboina, Chander
- Beteiligte Personen und Organisationen
-
Jupiter, Daniel
Fletcher, Steven
Yap, Jeremy L.
Rai, Arun
Tobin, Richard P.
Jiang, Weihua
Rascoe, Philip
Rogers, M Karen Newell
Smythe, W Roy
Cao, Xiaobo
SpringerLink (Online service)
- DOI
-
10.1186/1471-2407-12-541
- URN
-
urn:nbn:de:1111-20160304527
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.0078, 06:37 MEZ
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
- Peddaboina, Chander
- Jupiter, Daniel
- Fletcher, Steven
- Yap, Jeremy L.
- Rai, Arun
- Tobin, Richard P.
- Jiang, Weihua
- Rascoe, Philip
- Rogers, M Karen Newell
- Smythe, W Roy
- Cao, Xiaobo
- SpringerLink (Online service)
Ähnliche Objekte (12)
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
BH3-only proteins are dispensable for apoptosis induced by pharmacological inhibition of both MCL-1 and BCL-XL
Targeting antiapoptotic proteins Bcl-xL and Mcl-1 in cholangiocarcinoma
Calcium signals inhibition sensitizes ovarian carcinoma cells to anti-Bcl-xL strategies through Mcl-1 down-regulation
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Rolle von Bcl-2, Bcl-xl und Mcl-1 für die Apoptoseresistenz und Chemoresistenz des Pankreaskarzinoms
BCL-XL and MCL-1 are the key BCL-2 family proteins in melanoma cell survival
Bcl-xL inhibition enhances Dinaciclib-induced cell death in soft-tissue sarcomas
Transient apoptosis inhibition by Bcl-xL overexpression during hematopoietic stem cell transplantation
Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems
Inhibition of Bcl-2/Bcl-xL and c-MET causes synthetic lethality in model systems of glioblastoma
Inhibition of cyclin E1 sensitizes hepatocellular carcinoma cells to regorafenib by mcl-1 suppression
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
BH3-only proteins are dispensable for apoptosis induced by pharmacological inhibition of both MCL-1 and BCL-XL
Targeting antiapoptotic proteins Bcl-xL and Mcl-1 in cholangiocarcinoma
Calcium signals inhibition sensitizes ovarian carcinoma cells to anti-Bcl-xL strategies through Mcl-1 down-regulation
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Rolle von Bcl-2, Bcl-xl und Mcl-1 für die Apoptoseresistenz und Chemoresistenz des Pankreaskarzinoms
BCL-XL and MCL-1 are the key BCL-2 family proteins in melanoma cell survival
Bcl-xL inhibition enhances Dinaciclib-induced cell death in soft-tissue sarcomas
Transient apoptosis inhibition by Bcl-xL overexpression during hematopoietic stem cell transplantation
Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems
Inhibition of Bcl-2/Bcl-xL and c-MET causes synthetic lethality in model systems of glioblastoma
Inhibition of cyclin E1 sensitizes hepatocellular carcinoma cells to regorafenib by mcl-1 suppression
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
BH3-only proteins are dispensable for apoptosis induced by pharmacological inhibition of both MCL-1 and BCL-XL
Targeting antiapoptotic proteins Bcl-xL and Mcl-1 in cholangiocarcinoma
Calcium signals inhibition sensitizes ovarian carcinoma cells to anti-Bcl-xL strategies through Mcl-1 down-regulation
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Rolle von Bcl-2, Bcl-xl und Mcl-1 für die Apoptoseresistenz und Chemoresistenz des Pankreaskarzinoms
BCL-XL and MCL-1 are the key BCL-2 family proteins in melanoma cell survival
Bcl-xL inhibition enhances Dinaciclib-induced cell death in soft-tissue sarcomas
Transient apoptosis inhibition by Bcl-xL overexpression during hematopoietic stem cell transplantation
Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems
Inhibition of Bcl-2/Bcl-xL and c-MET causes synthetic lethality in model systems of glioblastoma