Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
about
Dysregulation of the autophagy-endolysosomal system in amyotrophic lateral sclerosis and related motor neuron diseasesInteraction of two hereditary spastic paraplegia gene products, spastin and atlastin, suggests a common pathway for axonal maintenanceHomo-oligomerization of ALS2 through its unique carboxyl-terminal regions is essential for the ALS2-associated Rab5 guanine nucleotide exchange activity and its regulatory function on endosome traffickingRin1 interacts with signal-transducing adaptor molecule (STAM) and mediates epidermal growth factor receptor trafficking and degradationCharacterization of RIN3 as a guanine nucleotide exchange factor for the Rab5 subfamily GTPase Rab31C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal traffickingGapex-5, a Rab31 guanine nucleotide exchange factor that regulates Glut4 trafficking in adipocytes.Defective relocalization of ALS2/alsin missense mutants to Rac1-induced macropinosomes accounts for loss of their cellular function and leads to disturbed amphisome formationRho guanine nucleotide exchange factors: regulators of Rho GTPase activity in development and diseaseRho family GTPases: key players in neuronal development, neuronal survival, and neurodegenerationActin-Dependent Alterations of Dendritic Spine Morphology in ShankopathiesMice deficient in the Rab5 guanine nucleotide exchange factor ALS2/alsin exhibit age-dependent neurological deficits and altered endosome traffickingAls2-deficient mice exhibit disturbances in endosome trafficking associated with motor behavioral abnormalitiesLoss of ALS2 function is insufficient to trigger motor neuron degeneration in knock-out mice but predisposes neurons to oxidative stressAmyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor traffickingRabGEF1 regulates stem cell factor/c-Kit-mediated signaling events and biological responses in mast cellsRegulation of endosomal motility and degradation by amyotrophic lateral sclerosis 2/alsin.Sequential signaling in plasma-membrane domains during macropinosome formation in macrophagesComponents of the antigen processing and presentation pathway revealed by gene expression microarray analysis following B cell antigen receptor (BCR) stimulationProtein Homeostasis in Amyotrophic Lateral Sclerosis: Therapeutic Opportunities?Establishment of extracellular signal-regulated kinase 1/2 bistability and sustained activation through Sprouty 2 and its relevance for epithelial function.Redox modifier genes and pathways in amyotrophic lateral sclerosis.Complex genetics of amyotrophic lateral sclerosis.A screen to identify cellular modulators of soluble levels of an amyotrophic lateral sclerosis (ALS)-causing mutant SOD1.Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis.The emerging role of guanine nucleotide exchange factors in ALS and other neurodegenerative diseases.Caenorhabditis elegans RME-6 is a novel regulator of RAB-5 at the clathrin-coated pitGAPex-5 mediates ubiquitination, trafficking, and degradation of epidermal growth factor receptor.Rab GTPases as regulators of endocytosis, targets of disease and therapeutic opportunities.Neuronal apoptosis induced by selective inhibition of Rac GTPase versus global suppression of Rho family GTPases is mediated by alterations in distinct mitogen-activated protein kinase signaling cascades.Alsin and SOD1(G93A) proteins regulate endosomal reactive oxygen species production by glial cells and proinflammatory pathways responsible for neurotoxicityMice deficient in the ALS2 gene exhibit lymphopenia and abnormal hematopietic function.Rab GTPases implicated in inherited and acquired disorders.Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences.Rho-linked genes and neurological disorders.Mitochondria in amyotrophic lateral sclerosis: a trigger and a target.Anti-ALS activity of alsin, the product of the ALS2 gene, and activity-dependent neurotrophic factor.Absence of alsin function leads to corticospinal motor neuron vulnerability via novel disease mechanismsAlsin and the molecular pathways of amyotrophic lateral sclerosisTransgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration.
P2860
Q21285051-EA45175F-D92E-4151-B7D9-7563A64E6856Q24295258-5F2DB880-EDAF-42ED-BC03-D9036BD80748Q24298929-97014499-3ADA-496F-BD34-C8AC6A1AC55CQ24301513-D3F99323-6FA7-46C5-B4B2-BDEC0D0CC45AQ24303566-63E7CEA9-44FB-4C73-8B23-1C207DB61E43Q24337586-C7259BA7-93F2-4600-A15A-59B5197AC8D7Q24338228-0D557A49-E5B4-458D-88DF-621BA8A6A143Q24339422-C4FC6044-5E03-41C1-BACD-8AB80D555EEFQ26853181-4702FA0F-5FAA-4718-BCA8-D612FD8B47A9Q27027490-D3E66BB1-A059-49C3-97F8-033A53F4AB7FQ28066333-2CB16F34-3C06-4AF0-A6A8-03BCE41D4386Q28505562-378CFFF5-347F-44C9-BF52-F53088506812Q28510453-9522DB1E-17BF-4200-8338-298E9510ED4AQ28511013-8AC7245A-0040-45F5-82CF-31ECA43F4F7DQ28513282-1F856559-211A-4600-AAC3-F59475219936Q28586055-A55B3633-DA18-4C57-BE7C-8A7AD6836106Q30489444-2E5B2938-89F4-4213-9265-638ED566C375Q30489942-1F53749F-0EC9-42C0-93A3-78FB6F7EA8DAQ33242003-DBD924BC-8BB1-4456-A56A-5DAF949E9DCFQ33621868-835F7EC8-0C35-40D2-98CA-E0FF16162F4CQ33725465-7345E349-50B9-4035-9FF9-2801F311E0CEQ33742737-22A6D082-F997-4FD6-9386-5C19D5FA555BQ33910597-47785F02-23B6-4A0D-BA47-55081B44DBAEQ34005076-A6AE4EA4-CDE3-492C-AB90-278B4AE173E9Q34148669-EF0B78A9-7B81-489A-8DDD-3A0FA7FDDE36Q34159126-FC0139CF-A443-4F7B-A9AB-C5491FE1C419Q34442081-2BB4868F-BDE4-4F65-A2E5-F24A9B9C4D8DQ34633785-9B528E15-9643-4B67-9194-A173BE3F79B3Q35278147-FA6D02BC-FA17-41F4-B3FA-E87E9FDC24EEQ35351477-CFB7D809-1099-4F84-A293-130E56D9AAEFQ35562672-10AA9D78-C413-44FD-A0B8-0113DC73B418Q35633071-75753361-85F6-4D77-81E7-93A9BBB759EEQ36090727-0C9DADF4-6D75-40C2-95E8-E1F5B82E0651Q36211097-B3067466-4F02-408F-B445-40D988890641Q36447580-213FFBB9-62F5-4447-8BDC-9BCD93FE0F75Q36565597-A7FD65A8-B4C5-4DC8-AF75-E27FC1C47451Q36565653-3CECE131-6151-4AEA-9A29-5AADCD5942B6Q36608848-2D1253E0-2A83-4F94-8CE9-7B124B782769Q36625827-98D777AC-4526-4877-BC44-52FCB8DF804FQ36861432-C149483E-E29F-4417-B247-8F321D7230B9
P2860
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
description
2004 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի հունիսին հրատարակված գիտական հոդված
@hy
article publié dans la revue scientifique Journal of Biological Chemistry
@fr
artículu científicu espublizáu en 2004
@ast
im Juni 2004 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2004/06/04)
@sk
vědecký článek publikovaný v roce 2004
@cs
wetenschappelijk artikel (gepubliceerd op 2004/06/04)
@nl
наукова стаття, опублікована в червні 2004
@uk
name
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@ast
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@en
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@nl
type
label
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@ast
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@en
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@nl
prefLabel
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@ast
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@en
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@nl
P2093
P2860
P3181
P356
P1476
Alsin is a Rab5 and Rac1 guanine nucleotide exchange factor
@en
P2093
Bruce F Horazdovsky
Justin D Topp
Robert D Gerard
P2860
P304
24612-24623
P3181
P356
10.1074/JBC.M313504200
P407
P50
P577
2004-03-19T00:00:00Z