Search results for "Small GTPase"

showing 7 items of 7 documents

RPGR protein complex regulates proteasome activity and mediates store-operated calcium entry

2018

Ciliopathies are a group of genetically heterogeneous disorders, characterized by defects in cilia genesis or maintenance. Mutations in the RPGR gene and its interacting partners, RPGRIP1 and RPGRIP1L, cause ciliopathies, but the function of their proteins remains unclear. Here we show that knockdown (KD) of RPGR, RPGRIP1 or RPGRIP1L in hTERT-RPE1 cells results in abnormal actin cytoskeleton organization. The actin cytoskeleton rearrangement is regulated by the small GTPase RhoA via the planar cell polarity (PCP) pathway. RhoA activity was upregulated in the absence of RPGR, RPGRIP1 or RPGRIP1L proteins. In RPGR, RPGRIP1 or RPGRIP1L KD cells, we observed increased levels of DVl2 and DVl3 pr…

0301 basic medicineRMRHOAactin cytoskeletonbiologyChemistryEndoplasmic reticulumCiliumSTIM1RPGR complex030105 genetics & heredityActin cytoskeletonStore-operated calcium entryActin cytoskeleton organizationeye diseasesCell biology03 medical and health sciencesendoplasmic reticulum030104 developmental biologyciliopathyOncologybiology.proteinSmall GTPasestore-operated Ca2+ entryResearch PaperOncotarget
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Inhibitors of Rho-kinase modulate amyloid-β (Aβ) secretion but lack selectivity for Aβ42

2005

Certain non-steroidal anti-inflammatory drugs (NSAIDs) preferentially inhibit production of the amyloidogenic Abeta42 peptide, presumably by direct modulation of gamma-secretase activity. A recent report indicated that NSAIDs could reduce Abeta42 by inhibition of the small GTPase Rho, and a single inhibitor of Rho kinase (ROCK) mimicked the effects of Abeta42-lowering NSAIDs. To investigate whether Abeta42 reduction is a common property of ROCK inhibitors, we tested commercially available compounds in cell lines that were previously used to demonstrate the Abeta42-lowering activity of NSAIDs. Surprisingly, we found that two ROCK inhibitors reduced total Abeta secretion in a dose-dependent m…

Cell SurvivalMutantPeptideCHO CellsProtein Serine-Threonine KinasesPharmacologyBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesSecretionSmall GTPaseEnzyme InhibitorsRho-associated protein kinasechemistry.chemical_classificationrho-Associated KinasesAmyloid beta-PeptidesbiologyAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsIn vitro toxicologyProtein-Tyrosine KinasesPeptide Fragmentsnervous system diseasesBiochemistrychemistrybiology.proteinAmyloid Precursor Protein SecretasesSelectivityProtein Processing Post-TranslationalJournal of Neurochemistry
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Unjamming overcomes kinetic and proliferation arrest in terminally differentiated cells and promotes collective motility of carcinoma.

2019

During wound repair, branching morphogenesis and carcinoma dissemination, cellular rearrangements are fostered by a solid-to-liquid transition, known as unjamming. The biomolecular machinery behind unjamming and its pathophysiological relevance remain, however, unclear. Here, we study unjamming in a variety of normal and tumorigenic epithelial two-dimensional (2D) and 3D collectives. Biologically, the increased level of the small GTPase RAB5A sparks unjamming by promoting non-clathrin-dependent internalization of epidermal growth factor receptor that leads to hyperactivation of the kinase ERK1/2 and phosphorylation of the actin nucleator WAVE2. This cascade triggers collective motility effe…

EndosomeCellular differentiationmedia_common.quotation_subjectMotility02 engineering and technologySettore MED/08 - Anatomia Patologica010402 general chemistry01 natural sciencesExtracellular matrixCell MovementCell Line TumorHumansGeneral Materials ScienceSmall GTPaseEpidermal growth factor receptorInternalizationActinmedia_commonCell Proliferationrab5 GTP-Binding ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyChemistryMechanical EngineeringCell DifferentiationGeneral Chemistry021001 nanoscience & nanotechnologyCondensed Matter Physics0104 chemical sciencesCell biologyErbB ReceptorsKineticscarcinoma differentiated neoplastic cellsMechanics of Materialsbiology.protein0210 nano-technologyNature materials
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miR-124-regulated RhoG reduces neuronal process complexity via ELMO/Dock180/Rac1 and Cdc42 signalling

2012

The small GTPase RhoG plays a central role in actin remodelling during diverse biological processes such as neurite outgrowth, cell migration, phagocytosis of apoptotic cells, and the invasion of pathogenic bacteria. Although it is known that RhoG stimulates neurite outgrowth in the rat pheochromocytoma PC12 cell line, neither the physiological function nor the regulation of this GTPase in neuronal differentiation is clear. Here, we identify RhoG as an inhibitor of neuronal process complexity, which is regulated by the microRNA miR-124. We find that RhoG inhibits dendritic branching in hippocampal neurons in vitro and in vivo. RhoG also inhibits axonal branching, acting via an ELMO/Dock180/…

General Immunology and MicrobiologyNeuriteDock180General NeuroscienceCell migrationRAC1CDC42GTPaseBiologyGeneral Biochemistry Genetics and Molecular BiologyCell biologynervous systemSmall GTPaseRhoGMolecular BiologyThe EMBO Journal
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Dissecting the different biological effects of oncogenic Ras isoforms in cancer cell lines: Could stimulation of oxidative stress be the one more wea…

2012

Abstract Ras proteins are small GTPase functioning as molecular switches that, in response to particular extracellular signalling, as growth factors, activate a diverse array of intracellular effector cascades regulating cell proliferation, differentiation and apoptosis. Human tumours frequently express Ras proteins (Ha-, Ki-, N-Ras) activated by point mutations which contribute to malignant phenotype, including invasiveness and angiogenesis. Despite the common signalling pathways leading to similar cellular responses, studies clearly demonstrate unique roles of the Ras family members in normal and pathological conditions and the lack of functional redundancy seems to be explainable, at lea…

MAPK/ERK pathwayEffectorAnti-apoptotic Ras signalling cascadeCancer cellmedicineSmall GTPaseGeneral MedicineBiologyCell adhesionmedicine.disease_causeOxidative stressIntracellularCell biologyMedical Hypotheses
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Transcriptional activation of the small GTPase gene rhoB by genotoxic stress is regulated via a CCAAT element

2001

The gene encoding the Ras-related GTPase RhoB-specific is immediate-early inducible by genotoxic treatments. Regulation of transcriptional activation of rhoB is still unclear. Here we show that cells lacking either p53 or c-Fos are not different from wild-type cells with respect to the level of rhoB induction upon UV irradiation, indicating that these transcription factors are not crucial for stimulation of rhoB mRNA expression. Extracts from UV-irradiated and non-irradiated cells revealed similar DNA-binding activities to a 0.17 kb rhoB promoter fragment harboring the functional element(s) necessary for stimulation of rhoB by UV light. By means of immunoprecipitation we found that an ATF-2…

Transcriptional ActivationImmunoprecipitationUltraviolet RaysRHOBMolecular Sequence DataCAAT boxOligonucleotidesBiologyResponse ElementsArticlechemistry.chemical_compoundMiceRhoB GTP-Binding ProteinGeneticsAnimalsSmall GTPaseRNA MessengerPromoter Regions GeneticrhoB GTP-Binding ProteinTranscription factorBinding SitesCcaat-enhancer-binding proteinsBase Sequence3T3 CellsDNAMolecular biologyMethyl methanesulfonatechemistryCCAAT-Binding FactorMutationCCAAT-Enhancer-Binding ProteinsProtein BindingTranscription Factors
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Focus on the Small GTPase Rab1: A Key Player in the Pathogenesis of Parkinson’s Disease

2021

Parkinson’s disease (PD) is the second most frequent neurodegenerative disease. It is characterized by the loss of dopaminergic neurons in the substantia nigra and the formation of large aggregates in the survival neurons called Lewy bodies, which mainly contain α-synuclein (α-syn). The cause of cell death is not known but could be due to mitochondrial dysfunction, protein homeostasis failure, and alterations in the secretory/endolysosomal/autophagic pathways. Survival nigral neurons overexpress the small GTPase Rab1. This protein is considered a housekeeping Rab that is necessary to support the secretory pathway, the maintenance of the Golgi complex structure, and the regulation of macroau…

autophagyParkinson's diseaseQH301-705.5Substantia nigraReviewBiologyCatalysisInorganic Chemistryα-synucleinmedicineAnimalsHumansSmall GTPaseBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopySecretory pathwayRab1GTPasesOrganic ChemistryNeurodegenerationDopaminergicRAB1Parkinson DiseaseLRRK2General Medicinemedicine.diseaseLRRK2Computer Science Applicationssecretory pathwayrab1 GTP-Binding ProteinsChemistrynervous systemParkinson’s diseaseNeuroscienceGolgi fragmentationInternational Journal of Molecular Sciences
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