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Biology subjects

Karaca, S.

Publications and source records attributed to Karaca, S..

2 recordsLinked to original sources

Transient deSUMOylation of IRF2BP proteins controls early transcription in EGFR signaling

Molecular switches are essential modules in signaling networks and transcriptional reprogramming. Here, we describe a role for small ubiquitin-related-modifier SUMO as a molecular switch in epidermal growth factor receptor (EGFR) signaling. Using quantitative mass spectrometry, we compared the endogenous SUMO-proteomes of Hela cells before and after EGF-stimulation. Thereby, we identified a small group of transcriptional co-regulators including IRF2BP1, IRF2BP2 and IRF2BPL as novel players in EGFR signaling. Comparison of cells expressing wildtype or SUMOylation deficient IRF2BP1 indicated that transient deSUMOylation of IRF2BP1 is important for appropriate expression of immediate early genes including Dual specificity phosphatase 1 (DUSP1, MKP-1), an important feedback regulator of EGFR signaling. We find that IRF2BP1 is a SUMO-dependent repressor, whose transient deSUMOylation on the DUSP1 promotor allows - and whose timely reSUMOylation restricts - DUSP1 expression. Our work thus provides a paradigm how comparative SUMO proteome analyses serve to reveal novel regulators in signal transduction and transcription.

molecular biology↗

Physiological and pathophysiological homeostasis of astroglial channel proteins by Nedd4-2

Nedd4-2 is an E3 ubiquitin ligase, missense mutation of which is related to familial epilepsy, indicating its critical role in regulating neuronal network activity. However, Nedd4-2 substrates involved in neuronal network function have yet to be identified. Using mouse lines lacking Nedd4-1 and Nedd4-2, we identified astrocytic channel proteins inwardly rectifying K+ channel 4.1 (Kir4.1) and Connexin43 as Nedd4-2 substrates. We found that the expression of Kir4.1 and Connexin43 is increased upon conditional deletion of Nedd4-2 in astrocytes, leading to an elevation of astrocytic membrane ion permeability and gap junction activity, with a consequent reduction of {gamma}-oscillatory neuronal network activity. Interestingly, our biochemical data demonstrate that missense mutations found in familial epileptic patients produce gain-of-function of Nedd4-2 gene product. Our data reveal a process of coordinated astrocytic ion channel proteostasis that controls astrocyte function and astrocyte-dependent neuronal network activity, and elucidate a potential mechanism by which aberrant Nedd4-2 function leads to epilepsy.\n\nCONDENSED TITLEUbiquitination of Astrocytic Channels by Nedd4-2\n\nSUMMARYUbiquitination is a key regulatory machinery for protein expression. Our present work provides evidence that astrocytic ion channel proteostasis coordinated by an E3 ubiquitin ligase Nedd4-2 is of particular importance for the maintenance of neuronal network activity.

neuroscience↗