Mechanisms and function of substrate recruitment by F-box proteins
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TLDR
The evolution of substrate recruitment by F-box proteins, the dysregulation of substrates in disease and potential avenues for F- box protein-directed disease therapies are focused on.Abstract:
S phase kinase-associated protein 1 (SKP1)-cullin 1 (CUL1)-F-box protein (SCF) ubiquitin ligase complexes use a family of F-box proteins as substrate adaptors to mediate the degradation of a large number of regulatory proteins involved in diverse processes The dysregulation of SCF complexes and their substrates contributes to multiple pathologies In the 14 years since the identification and annotation of the F-box protein family, the continued identification and characterization of novel substrates has greatly expanded our knowledge of the regulation of substrate targeting and the roles of F-box proteins in biological processes Here, we focus on the evolution of our understanding of substrate recruitment by F-box proteins, the dysregulation of substrate recruitment in disease and potential avenues for F-box protein-directed disease therapiesread more
Citations
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Receptor-like cytoplasmic kinases as downstream effectors of RAC/ROP GTPases in the interaction of Arabidopsis and barley with powdery mildew fungi
TL;DR: The RAC/ROP GTPase HvRACB is a susceptibility factor in the pathosystem barley – barley powdery mildew fungus and the function of the predicted Arabidopsis thaliana orthologue of HvRBK1, AtRLCK VI_A3, was investigated in the interaction ofArabidopsis with its adapted powdery Mildew fungus Erysiphe cruciferarum.
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Regulation of Iron Homeostasis by SPAK-dependent Modulation of FBXL5 Stability
TL;DR: The identification of the STE20/SPS1-related proline-alanine-rich protein kinase (SPAK) as a novel regulator of FBXL5 stability is reported, finding that SPAK, a kinase previously implicated in osmotic stress regulation, regulates intracellular iron homeostasis through its physical association withFBXL5.
Dissertation
The non-Wnt functions of APC : unravelling the link between APC and apoptosis
TL;DR: This document breaches copyright and should be removed from the public portal immediately.
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NDPK-B is Degraded by Ubiquitin Proteasome Pathway in HeLa cells
TL;DR: Results fully prove that NDPK-B is degraded by the ubiquitin proteasome pathway in HeLa cells.
Journal ArticleDOI
Disorder in the human Skp1 structure is the key to its adaptability to bind many different proteins in the SCF complex assembly.
TL;DR: The solution structure of the full-length Skp1 protein determined by NMR spectroscopy for the first time is reported and a rationale for how the protein can adapt itself, bind, and get functionally associated with other proteins in the SCF complex by utilising its flexibility and conformational sub-states is provided.
References
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TL;DR: This review discusses recent information on functions and mechanisms of the ubiquitin system and focuses on what the authors know, and would like to know, about the mode of action of ubi...
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TL;DR: These findings greatly expand the role of activated NOTCH1 in the molecular pathogenesis of human T-ALL and provide a strong rationale for targeted therapies that interfere with NOTCH signaling.
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The Mutational Landscape of Head and Neck Squamous Cell Carcinoma
Nicolas Stransky,Ann Marie Egloff,Aaron D. Tward,Aaron D. Tward,Aaron D. Tward,Aleksandar Kostic,Aleksandar Kostic,Kristian Cibulskis,Andrey Sivachenko,Gregory Kryukov,Gregory Kryukov,Michael S. Lawrence,Carrie Sougnez,Aaron McKenna,Erica Shefler,Alex H. Ramos,Petar Stojanov,Scott L. Carter,Douglas Voet,Maria L. Cortes,Daniel Auclair,Michael F. Berger,Gordon Saksena,Candace Guiducci,Robert C. Onofrio,Melissa Parkin,Marjorie Romkes,Joel L. Weissfeld,Raja R. Seethala,Lin Wang,Claudia Rangel-Escareño,Juan Carlos Fernández-López,Alfredo Hidalgo-Miranda,Jorge Melendez-Zajgla,Wendy Winckler,Kristin Ardlie,Stacey Gabriel,Matthew Meyerson,Eric S. Lander,Eric S. Lander,Eric S. Lander,Gad Getz,Todd R. Golub,Levi A. Garraway,Jennifer R. Grandis +44 more
TL;DR: In this article, the authors analyzed whole-exome sequencing data from 74 tumor-normal pairs and found that at least 30% of cases harbored mutations in genes that regulate squamous differentiation (for example, NOTCH1, IRF6, and TP63), implicating its dysregulation as a major driver of HNSCC carcinogenesis.
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