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Alan Tseng

Researcher at University of Illinois at Chicago

Publications -  27
Citations -  1663

Alan Tseng is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Protein kinase B & Phosphorylation. The author has an hindex of 18, co-authored 27 publications receiving 1477 citations. Previous affiliations of Alan Tseng include Brigham and Women's Hospital & Beth Israel Deaconess Medical Center.

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SCF FBW7 regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

TL;DR: It is shown that the E3 ubiquitin ligase SCFFBW7 (a SKP1–cullin-1–F-box complex that contains FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family member, for ubiquitylation and destruction in a manner that depends on phosphorylation by glycogen synthase kinase 3.
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Phosphorylation by Akt1 promotes cytoplasmic localization of Skp2 and impairs APCCdh1-mediated Skp2 destruction

TL;DR: It is shown that the serine/threonine protein kinase Akt1, but not Akt2, directly controls Skp2 stability by a mechanism that involves degradation by the APC–Cdh1 ubiquitin ligase complex.
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Phosphorylation by Casein Kinase I promotes the turnover of the Mdm2 oncoprotein via the SCFβ-TRCP ubiquitin ligase

TL;DR: It is reported that Mdm2 is rapidly degraded after DNA damage and that phosphorylation of MDM2 by casein kinase I (CKI) at multiple sites triggers its interaction with, and subsequent ubiquitination and destruction, by SCF(beta-TRCP).
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Rictor Forms a Complex with Cullin-1 to Promote SGK1 Ubiquitination and Destruction

TL;DR: Findings indicate that the Rictor/Cullin-1 E3 ligase activity is regulated by a specific signal relay cascade and that misregulation of this mechanism may contribute to the frequent overexpression of SGK1 in various human cancers.
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Platelet-neutrophil interactions under thromboinflammatory conditions.

TL;DR: The current understanding of the regulatory mechanisms of platelet–neutrophil interactions in thromboinflammatory disease is discussed.