| Excitotoxicity induces Kidins220 and GluN1 traffic to the Golgi apparatus before Kidins220 is degraded by the protease calpain. Excitotoxicity also triggers an early activation of Rap1-GTPase followed by its inactivation. Kidins220 excitotoxic endocytosis and subsequent calpain-mediated downregulation governs inactivation of Rap1 that is associated to decreases in ERK activity preceding neuronal death. | Excitotoxic targeting of Kidins220 to the Golgi apparatus precedes calpain cleavage of Rap1-activation complexes.
López-Menéndez C, Simón-García A, Gamir-Morralla A, Pose-Utrilla J, Luján R, Mochizuki N, Díaz-Guerra M, Iglesias T., Free PMC Article | 07/11/2020 |
| This work reveals a crucial physiological role of KIDINS220 in development and provides insight into how perturbation of the complex interplay of KIDINS220 isoforms and their relative expression can affect neuron control and human metabolism. Altogether, we here show that de novo protein-truncating KIDINS220 variants cause a new syndrome, SINO. This is the first report of KIDINS220 variants causing a human disease. | Heterozygous KIDINS220/ARMS nonsense variants cause spastic paraplegia, intellectual disability, nystagmus, and obesity.
Josifova DJ, Monroe GR, Tessadori F, de Graaff E, van der Zwaag B, Mehta SG, DDD Study, Harakalova M, Duran KJ, Savelberg SM, Nijman IJ, Jungbluth H, Hoogenraad CC, Bakkers J, Knoers NV, Firth HV, Beales PL, van Haaften G, van Haelst MM. | 09/30/2017 |
| overexpression of ARMS blocked NGF-mediated secretion, without affecting basal secretion, a decrease in ARMS resulted in potentiation. Similar effects were observed with synembryn-B, a protein that interacts directly with ARMS. Downstream of ARMS and synembryn-B are Galphaq and Trio proteins, which modulate the activity of Rac1 in response to NGF | ARMS/Kidins220 and synembryn-B levels regulate NGF-mediated secretion.
López-Benito S, Lillo C, Hernández-Hernández Á, Chao MV, Arévalo JC. | 08/5/2017 |
| the existence of novel Kidins220/ARMS splice isoforms with unique properties | Novel Kidins220/ARMS Splice Isoforms: Potential Specific Regulators of Neuronal and Cardiovascular Development.
Schmieg N, Thomas C, Yabe A, Lynch DS, Iglesias T, Chakravarty P, Schiavo G., Free PMC Article | 04/30/2016 |
| a novel partner of Kidins220/ARMS | Kidins220/ARMS interacts with Pdzrn3, a protein containing multiple binding domains.
Andreazzoli M, Gestri G, Landi E, D'Orsi B, Barilari M, Iervolino A, Vitiello M, Wilson SW, Dente L. | 11/24/2012 |
| findings show that Kidins220/ARMS is a novel component of the uropod involved in the regulation of T-cell motility, an essential process for the immune response | The neuronal protein Kidins220/ARMS associates with ICAM-3 and other uropod components and regulates T-cell motility.
Jean-Mairet RM, López-Menéndez C, Sánchez-Ruiloba L, Sacristán S, Rodríguez-Martínez M, Riol-Blanco L, Sánchez-Mateos P, Sánchez-Madrid F, Rodríguez-Fernández JL, Campanero MR, Iglesias T. | 06/4/2011 |
| A decrease in ARMS/Kidins220 levels suppressed GABAergic neurotransmission; overexpression of ARMS/Kidins220 produced an increase in GABAergic neurotransmission in hippocampal neurons; ARMS/Kidins220 regulates GABAergic neurotransmission presynaptically. | Regulation of inhibitory neurotransmission by the scaffolding protein ankyrin repeat-rich membrane spanning/kinase D-interacting substrate of 220 kDa.
Sutachan JJ, Chao MV, Ninan I. | 03/5/2011 |
| the levels of ARMS/Kidins220 can be regulated by neuronal activity and calpain action to influence synaptic function. | The ankyrin repeat-rich membrane spanning (ARMS)/Kidins220 scaffold protein is regulated by activity-dependent calpain proteolysis and modulates synaptic plasticity.
Wu SH, Arévalo JC, Neubrand VE, Zhang H, Arancio O, Chao MV., Free PMC Article | 01/29/2011 |
| The direct interaction between ARMS/Kidins220 and Sept5 suggests a possible role of ARMS/Kidins220 as a functional link between neurotrophin receptors and septins to mediate neurotrophin-induced intracellular signaling events. | Ankyrin repeat-rich membrane spanning/Kidins220 protein interacts with mammalian Septin 5.
Park HJ, Park HW, Lee SJ, Arevalo JC, Park YS, Lee SP, Paik KS, Chao MV, Chang MS. | 01/1/2011 |
| Kidins220 regulates Rac1-dependent neurite outgrowth by direct interaction with the Trio. | Kidins220/ARMS regulates Rac1-dependent neurite outgrowth by direct interaction with the RhoGEF Trio.
Neubrand VE, Thomas C, Schmidt S, Debant A, Schiavo G. | 09/6/2010 |
| Kidins220/ARMS participation in neuronal life and death pathways. | Kidins220/ARMS downregulation by excitotoxic activation of NMDARs reveals its involvement in neuronal survival and death pathways.
López-Menéndez C, Gascón S, Sobrado M, Vidaurre OG, Higuero AM, Rodríguez-Peña A, Iglesias T, Díaz-Guerra M. | 01/21/2010 |
| Kidins220/ARMS-positive carriers undergo a kinesin-1-dependent transport linked to neurotrophin action. | Kidins220/ARMS is transported by a kinesin-1-based mechanism likely to be involved in neuronal differentiation.
Bracale A, Cesca F, Neubrand VE, Newsome TP, Way M, Schiavo G., Free PMC Article | 01/21/2010 |
| Lipid raft disruption triggers protein kinase C and Src-dependent protein kinase D activation and Kidins220 phosphorylation in neuronal cells | Lipid raft disruption triggers protein kinase C and Src-dependent protein kinase D activation and Kidins220 phosphorylation in neuronal cells.
Cabrera-Poch N, Sánchez-Ruiloba L, Rodríguez-Martínez M, Iglesias T. | 01/21/2010 |
| Altogether, our findings suggest that ARMS may play an important role in regulating postsynaptic signal transduction through the syntrophin-mediated localization of receptor tyrosine kinases such as EphA4. | {alpha}-Syntrophin regulates ARMS localization at the neuromuscular junction and enhances EphA4 signaling in an ARMS-dependent manner.
Luo S, Chen Y, Lai KO, Arévalo JC, Froehner SC, Adams ME, Chao MV, Ip NY., Free PMC Article | 01/21/2010 |