Retraction Note to: Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1471-2202
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Retraction Note to: Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death ; volume:18 ; number:1 ; day:9 ; month:5 ; year:2017 ; pages:1 ; date:12.2017
BMC neuroscience ; 18, Heft 1 (9.5.2017), 1, 12.2017
- Classification
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Biowissenschaften, Biologie
- Keyword
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Hirnkrankheit
Neuropsychiatrie
Nervenkrankheit
- Creator
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Kim, Hyung-Wook
- Contributor
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Chang, Yunyoung C.
Chen, Mei
Rapoport, Stanley I.
Rao, Jagadeesh S.
SpringerLink (Online service)
- DOI
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10.1186/s12868-017-0359-y
- URN
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urn:nbn:de:1111-201705142284
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:20 AM CEST
Data provider
This object is provided by:
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Kim, Hyung-Wook
- Chang, Yunyoung C.
- Chen, Mei
- Rapoport, Stanley I.
- Rao, Jagadeesh S.
- SpringerLink (Online service)
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Levels of pro-apoptotic regulator Bad and anti-apoptotic regulator Bcl-xL determine the type of the apoptotic logic gate
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The N-terminus and alpha-5, alpha-6 helices of the pro-apoptotic protein Bax, modulate functional interactions with the anti-apoptotic protein Bcl-xL
Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death
Regulation of pro-apoptotic and anti-apoptotic factors in obesity-related esophageal adenocarcinoma
Functional analysis of novel pro-apoptotic factor CLTAP
Levels of pro-apoptotic regulator Bad and anti-apoptotic regulator Bcl-xL determine the type of the apoptotic logic gate
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c-Myc dependent expression of pro-apoptotic Bim renders HER2-overexpressing breast cancer cells dependent on anti-apoptotic Mcl-1
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