Soluble Alpha-APP (sAPPalpha) Regulates CDK5 Expression and Activity in Neurons

Hartl, D.; Klatt, S.; Roch, M.; Konthur, Z.; Klose, J.; Willnow, T. E.; Rohe, M.

doi:ARTN e65920DOI 10.1371/journal.pone.0065920

アイテム詳細

登録内容を編集ファイル形式で保存

一時保存へ追加

タグ情報を表示リリース履歴を表示詳細要約

公開

学術論文

Soluble Alpha-APP (sAPPalpha) Regulates CDK5 Expression and Activity in Neurons

MPS-Authors

/persons/resource/persons50383

Klatt, S.
Zoltán Konthur, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

/persons/resource/persons50390

Konthur, Z.
Zoltán Konthur, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;
Max Planck Institute of Colloids and Interfaces ;

External Resource

There are no locators available

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

フルテキスト (公開)

Hartl.pdf
(出版社版), 4MB

付随資料 (公開)

There is no public supplementary material available

引用

Hartl, D., Klatt, S., Roch, M., Konthur, Z., Klose, J., Willnow, T. E., & Rohe, M. (2013). Soluble Alpha-APP (sAPPalpha) Regulates CDK5 Expression and Activity in Neurons. PLoS One, 8(6). doi:ARTN e65920DOI 10.1371/journal.pone.0065920.

引用: https://hdl.handle.net/11858/00-001M-0000-0018-DE65-4

要旨

A growing body of evidence suggests a role for soluble alpha-amyloid precursor protein (sAPPalpha) in pathomechanisms of Alzheimer disease (AD). This cleavage product of APP was identified to have neurotrophic properties. However, it remained enigmatic what proteins, targeted by sAPPalpha, might be involved in such neuroprotective actions. Here, we used high-resolution two-dimensional polyacrylamide gel electrophoresis to analyze proteome changes downstream of sAPPalpha in neurons. We present evidence that sAPPalpha regulates expression and activity of CDK5, a kinase that plays an important role in AD pathology. We also identified the cytoprotective chaperone ORP150 to be induced by sAPPalpha as part of this protective response. Finally, we present functional evidence that the sAPPalpha receptor SORLA is essential to mediate such molecular functions of sAPPalpha in neurons.