Proteomic analysis of Rac1 signaling regulation by guanine nucleotide exchange factors
| Autor: | Marei, Hadir, Carpy, Alejandro, Macek, Boris, Malliri, Angeliki |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
Proteomics
rac1 GTP-Binding Protein P-Rex1 Small GTPases Tandem Affinity Purification (TAP) Cell Communication Stable Isotope Labeling by Amino acids in Cell culture (SILAC) TMOD3 Mice IQGAP1 Cell Movement Cell Line Tumor Protein Interaction Mapping Tiam1 Animals Guanine Nucleotide Exchange Factors Humans Extra Views Ingenuity Integrated Pathway Analysis (IPA) Guanine nucleotide Exchange Factors (GEFs) ras GTPase-Activating Proteins Isotope Labeling NIH 3T3 Cells Rac1 Protein Binding Signal Transduction |
| Zdroj: | Cell Cycle |
| ISSN: | 1551-4005 1538-4101 |
| Popis: | The small GTPase Rac1 is implicated in various cellular processes that are essential for normal cell function. Deregulation of Rac1 signaling has also been linked to a number of diseases, including cancer. The diversity of Rac1 functioning in cells is mainly attributed to its ability to bind to a multitude of downstream effectors following activation by Guanine nucleotide Exchange Factors (GEFs). Despite the identification of a large number of Rac1 binding partners, factors influencing downstream specificity are poorly defined, thus hindering the detailed understanding of both Rac1's normal and pathological functions. In a recent study, we demonstrated a role for 2 Rac-specific GEFs, Tiam1 and P-Rex1, in mediating Rac1 anti- versus pro-migratory effects, respectively. Importantly, via conducting a quantitative proteomic screen, we identified distinct changes in the Rac1 interactome following activation by either GEF, indicating that these opposing effects are mediated through GEF modulation of the Rac1 interactome. Here, we present the full list of identified Rac1 interactors together with functional annotation of the differentially regulated Rac1 binding partners. In light of this data, we also provide additional insights into known and novel signaling cascades that might account for the GEF-mediated Rac1-driven cellular effects. |
| Databáze: | OpenAIRE |
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