BH3-only proteins are dispensable for apoptosis induced by pharmacological inhibition of both MCL-1 and BCL-XL
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1476-5403
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
-
BH3-only proteins are dispensable for apoptosis induced by pharmacological inhibition of both MCL-1 and BCL-XL ; day:5 ; month:9 ; year:2018 ; pages:1-11
Cell death and differentiation ; (5.9.2018), 1-11
- Creator
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Greaves, Georgia
- Contributor
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Milani, Mateus
Butterworth, Michael
Carter, Rachel J.
Byrne, Dominic P.
Eyers, Patrick A.
Luo, Xu
Cohen, Gerald M.
Varadarajan, Shankar
SpringerLink (Online service)
- DOI
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10.1038/s41418-018-0183-7
- URN
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urn:nbn:de:101:1-2018112002145611231383
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:50 AM CEST
Data provider
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Associated
- Greaves, Georgia
- Milani, Mateus
- Butterworth, Michael
- Carter, Rachel J.
- Byrne, Dominic P.
- Eyers, Patrick A.
- Luo, Xu
- Cohen, Gerald M.
- Varadarajan, Shankar
- SpringerLink (Online service)
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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
Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1
The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition
A direct comparison of selective BH3-mimetics reveals BCL-XL, BCL-2 and MCL-1 as promising therapeutic targets in neuroblastoma
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
MCL-1, BCL-xL and Casp-3 as key regulators in thymus homeostasis and thymic epithelial tumors
Regulation of Bcl-xL activity in apoptosis
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Lipoic acid decreases Mcl-1, Bcl-xL and up regulates Bim on ovarian carcinoma cells leading to cell death
Delayed apoptosis by neutrophils from COPD patients is associated with altered bak, bcl-xl, and mcl-1 mRNA expression
Targeting antiapoptotic proteins Bcl-xL and Mcl-1 in cholangiocarcinoma
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
Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1
The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition
A direct comparison of selective BH3-mimetics reveals BCL-XL, BCL-2 and MCL-1 as promising therapeutic targets in neuroblastoma
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
MCL-1, BCL-xL and Casp-3 as key regulators in thymus homeostasis and thymic epithelial tumors
Regulation of Bcl-xL activity in apoptosis
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Lipoic acid decreases Mcl-1, Bcl-xL and up regulates Bim on ovarian carcinoma cells leading to cell death
Delayed apoptosis by neutrophils from COPD patients is associated with altered bak, bcl-xl, and mcl-1 mRNA expression
Targeting antiapoptotic proteins Bcl-xL and Mcl-1 in cholangiocarcinoma
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
Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1
The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition
A direct comparison of selective BH3-mimetics reveals BCL-XL, BCL-2 and MCL-1 as promising therapeutic targets in neuroblastoma
Dual inhibition of anti-apoptotic proteins BCL-XL and MCL-1 enhances cytotoxicity of Nasopharyngeal carcinoma cells
MCL-1, BCL-xL and Casp-3 as key regulators in thymus homeostasis and thymic epithelial tumors
Regulation of Bcl-xL activity in apoptosis
Photodynamic therapy combined with Bcl-2/Bcl-xL inhibition increases the Noxa/Mcl-1 ratio independent of usp9X and synergistically enhances apoptosis in glioblastoma
Lipoic acid decreases Mcl-1, Bcl-xL and up regulates Bim on ovarian carcinoma cells leading to cell death