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A RAB35-p85/PI3K axis controls oscillatory apical protrusions required for efficient chemotactic migration.
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The authors propose that Rab35-GTP is a critical regulator of autophagy through recruiting autophagy receptor NDP52.
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The results provide evidence that MICAL1 plays an essential role in the activation of ROS/Akt signaling and cell invasive phenotype and identify a novel link between RAB35 and MICAL1 in regulating breast cancer cell invasion.
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The involvement of Rab35 in diverse and apparently unrelated cellular functions can be explained by the central role of this GTPase in regulating phosphoinositides and F-actin, both on endosomes and at the plasma membrane[review].
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Data suggest that Rab35, interacting with TBC1D10A, functions in vascular endothelial cells as a negative regulator of histamine-evoked, Ca2+-dependent Weibel-Palade body exocytosis, most likely acting through the downstream effectors ACAP2 and Arf6. (Rab35 = rab GTP-binding protein 53; TBC1D10A = TBC1 domain family member 10A; ACAP2 = centaurin beta2; Arf6 = ADP-ribosylation factor 6)
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Short-term EGF stimulation if of lung tumor cells can increase the interaction between RUSC2 and GIT2, prolonged stimulation leads to a decrease of their interaction through activating Rab35.
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Here the authors report that EspG interacts specifically with the small GTPases ARF6 and Rab35 during infection.
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Authors propose that the precise spatial and temporal activation of Rab35 acts as a major switch for OCRL recruitment on newborn endosomes, post-scission PtdIns(4,5)P2 hydrolysis, and subsequent endosomal trafficking.
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Rab35 serves as a clathrin-mediated endocytosis detector. Loss of Rab35 input leads to elevated Arf6-GTP and shifts the sorting of clathrin-independent endocytosis cargo proteins to lysosomes.
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the activation-inactivation cycles of Rab35 and ARF6 are required for the uptake of zymosan and that ACAP2 is an important component that links Rab35/ARF6 signaling during phagocytosis of zymosan.
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Two somatic RAB35 mutations found in human tumors generate alleles that constitutively activate PI3K/AKT signaling, suppress apoptosis, and transform cells in a PI3K-dependent manner.
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mutual regulation with arf6 of cell adhesion and migration
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Rab35 acts as a downstream target of Dvl2 and mediates cell migration.
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Activated ARF6 reduces Rab35 loading into the endocytic pathway.
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whereas connecdenn 1 and 2 activate Rab35 for endosomal trafficking, connecdenn 3 uniquely activates Rab35 for its role in actin regulation
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analysis of DENND1B-S complexed with its substrate Rab35
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the phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) 5-phosphatase OCRL, which is mutated in Lowe syndrome patients, is an effector of the Rab35 GTPase in cytokinesis abscission
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A Small Ras-like GTPase protein Ray was indicated to modulate p53 transcriptional activity of PRPK.
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localized to the plasma membrane and endocytic compartments and controls a fast endocytic recycling pathway; plays an essential role during the terminal steps of cytokinesis
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EPI64C and Rab35 regulate a recycling pathway in T cells and contribute to immunological synapse formation, most likely by participating in TCR transport to the immunological synapse