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    Mapk10 mitogen-activated protein kinase 10 [ Mus musculus (house mouse) ]

    Gene ID: 26414, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Arrestin-3-assisted activation of JNK3 mediates dopaminergic behavioral sensitization.

    Arrestin-3-assisted activation of JNK3 mediates dopaminergic behavioral sensitization.
    Ahmed MR, Zheng C, Dunning JL, Ahmed MS, Ge C, Pair FS, Gurevich VV, Gurevich EV., Free PMC Article

    08/16/2024
    Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis.

    Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis.
    Priego M, Noriega L, Kalinin S, Hoffman LM, Feinstein DL, Morfini G., Free PMC Article

    10/4/2023
    Time series RNA-seq analysis identifies MAPK10 as a critical gene in diabetes mellitus-induced atrial fibrillation in mice.

    Time series RNA-seq analysis identifies MAPK10 as a critical gene in diabetes mellitus-induced atrial fibrillation in mice.
    Liu F, Deng Y, Zhao Y, Li Z, Gao J, Zhang Y, Yang X, Liu Y, Xia Y.

    06/18/2022
    JNK3 deficiency leads to upregulation of growth factors such as Vegfa, Pdgfb, Pgf, Hbegf and Tgfb3 in ischemic muscle by activation of the transcription factors Egr1/Creb1.

    Neural JNK3 regulates blood flow recovery after hindlimb ischemia in mice via an Egr1/Creb1 axis.
    Kant S, Craige SM, Chen K, Reif MM, Learnard H, Kelly M, Caliz AD, Tran KV, Ramo K, Peters OM, Freeman M, Davis RJ, Keaney JF Jr., Free PMC Article

    01/11/2020
    JNK isoforms are involved in the adult neurogenesis control.

    JNK Isoforms Are Involved in the Control of Adult Hippocampal Neurogenesis in Mice, Both in Physiological Conditions and in an Experimental Model of Temporal Lobe Epilepsy.
    Castro-Torres RD, Landa J, Rabaza M, Busquets O, Olloquequi J, Ettcheto M, Beas-Zarate C, Folch J, Camins A, Auladell C, Verdaguer E.

    12/21/2019
    Together these data indicate that ONA induces APP expression and that gamma-secretase cleavage of APP releases AICD, which upregulates JNK3 leading to RGC death. This pathway may be a novel target for neuronal protection in optic neuropathies and other forms of neurotrauma.

    APP upregulation contributes to retinal ganglion cell degeneration via JNK3.
    Liu C, Zhang CW, Zhou Y, Wong WQ, Lee LC, Ong WY, Yoon SO, Hong W, Fu XY, Soong TW, Koo EH, Stanton LW, Lim KL, Xiao ZC, Dawe GS., Free PMC Article

    09/14/2019
    JNK1 and/or JNK3 are promising targets for the prevention of cell death and inflammation during epileptogenesis.

    Neuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms.
    de Lemos L, Junyent F, Camins A, Castro-Torres RD, Folch J, Olloquequi J, Beas-Zarate C, Verdaguer E, Auladell C.

    02/9/2019
    Conversely, treatment with LY294002 (a selective inhibitor of Akt1) reversed the effects of quercetin. In conclusion, these findings highlight the important role of quercetin in protecting against cognitive deficits and inhibiting neuronal apoptosis via the Akt signaling pathway. We believe that quercetin might prove to be a useful therapeutic component in treating cerebral I/R diseases in the near future.

    Quercetin ameliorates ischemia/reperfusion-induced cognitive deficits by inhibiting ASK1/JNK3/caspase-3 by enhancing the Akt signaling pathway.
    Pei B, Yang M, Qi X, Shen X, Chen X, Zhang F.

    05/27/2017
    JNK3 therefore provides a mechanism that contributes to homeostatic regulation of energy balance in response to metabolic stress.

    Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress.
    Vernia S, Morel C, Madara JC, Cavanagh-Kyros J, Barrett T, Chase K, Kennedy NJ, Jung DY, Kim JK, Aronin N, Flavell RA, Lowell BB, Davis RJ., Free PMC Article

    12/17/2016
    Genetic inhibition of JNK pathway in vivo by Jnk3 knockout results in amelioration of spinal muscular atrophy phenotype

    Genetic inhibition of JNK3 ameliorates spinal muscular atrophy.
    Genabai NK, Ahmad S, Zhang Z, Jiang X, Gabaldon CA, Gangwani L., Free PMC Article

    08/27/2016
    Rotenone induces dopamine neuron death through a series of sequential events including microtubule destabilization, JNK3 activation, VMAT2 inhibition, accumulation of cytosolic dopamine, and generation of ROS.

    JNK inhibition of VMAT2 contributes to rotenone-induced oxidative stress and dopamine neuron death.
    Choi WS, Kim HW, Xia Z., Free PMC Article

    03/28/2015
    the data on anxiety, exploration and learning indicate that JNK1 ko mice displayed a stronger explorative behaviour and that knockout of JNK2 or JNK3

    Knockout of c-Jun N-terminal kinases 1, 2 or 3 isoforms induces behavioural changes.
    Reinecke K, Herdegen T, Eminel S, Aldenhoff JB, Schiffelholz T.

    09/21/2013
    JNK3 signaling is a major early pathway triggering retinal ganglion cell (RGC) death after axonal injury and may directly link axon injury to transcriptional activity that controls RGC death.

    JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.
    Fernandes KA, Harder JM, Fornarola LB, Freeman RS, Clark AF, Pang IH, John SW, Libby RT., Free PMC Article

    01/26/2013
    Deletion of JNK3 from Alzheimer (AD) mice results in a dramatic reduction in Abeta42 levels, overall plaque loads, and increased neuronal number and improved cognition, revealing AD as a metabolic disease under tight control by JNK3.

    JNK3 perpetuates metabolic stress induced by Aβ peptides.
    Yoon SO, Park DJ, Ryu JC, Ozer HG, Tep C, Shin YJ, Lim TH, Pastorino L, Kunwar AJ, Walton JC, Nagahara AH, Lu KP, Nelson RJ, Tuszynski MH, Huang K., Free PMC Article

    12/8/2012
    Mice deficient for neuron-specific isoform JNK3 have altered behavioural rhythms, with longer free-running period and compromised phase shifts to light.

    JNK regulates the photic response of the mammalian circadian clock.
    Yoshitane H, Honma S, Imamura K, Nakajima H, Nishide SY, Ono D, Kiyota H, Shinozaki N, Matsuki H, Wada N, Doi H, Hamada T, Honma K, Fukada Y., Free PMC Article

    09/1/2012
    Overall, our results show the transcriptional regulation of the MAPK pathway and the essential role of JNK in Japanese Encephalitis Virus-induced apoptosis in neuroblastoma cells.

    Transcriptional regulation and activation of the mitogen-activated protein kinase pathway after Japanese encephalitis virus infection in neuroblastoma cells.
    Gupta N, Bhaskar AS, Lakshmana Rao PV.

    08/20/2011
    This study indicated that the activation of PI3K/AKT pathway in hippocampus because of the increase in pik3cb transcription and that this mechanism is specifically related to the lack of Jnk3.

    Gene expression profile in JNK3 null mice: a novel specific activation of the PI3K/AKT pathway.
    Junyent F, de Lemos L, Verdaguer E, Folch J, Ferrer I, Ortuño-Sahagún D, Beas-Zárate C, Romero R, Pallàs M, Auladell C, Camins A.

    05/28/2011
    JNK2 and JNK3 are critically involved in stress-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavioral task.

    Hippocampal c-Jun-N-terminal kinases serve as negative regulators of associative learning.
    Sherrin T, Blank T, Hippel C, Rayner M, Davis RJ, Todorovic C., Free PMC Article

    10/30/2010
    Results demonstrate that p75NTR-mediated activation of JNK3 is required for up-regulation of TACE, which promotes receptor proteolysis, leading to prolonged activation of JNK3 and subsequent apoptosis in sympathetic neurons.

    p75 neurotrophin receptor-mediated apoptosis in sympathetic neurons involves a biphasic activation of JNK and up-regulation of tumor necrosis factor-alpha-converting enzyme/ADAM17.
    Kenchappa RS, Tep C, Korade Z, Urra S, Bronfman FC, Yoon SO, Carter BD., Free PMC Article

    08/30/2010
    Data show that neuritogenesis is delayed by lack of JNK2 and JNK3, but not JNK1.

    Distinct roles of c-Jun N-terminal kinase isoforms in neurite initiation and elongation during axonal regeneration.
    Barnat M, Enslen H, Propst F, Davis RJ, Soares S, Nothias F., Free PMC Article

    08/30/2010
    The activation of SAPK/JNK in basket cell "pinceaux" may be a consequence of altered functionality of Purkinje cells and may represent an attempt of basket cells of synaptic remodeling.

    Beta-amyloid overload does not directly correlate with SAPK/JNK activation and tau protein phosphorylation in the cerebellar cortex of Ts65Dn mice.
    Lomoio S, Scherini E, Necchi D.

    01/21/2010
    data identify JNK3 as a critical mediator of pathogenic Htt (polyQ-Htt)toxicity and provide a molecular basis for polyQ-Htt-induced inhibition of fast axonal transport.

    Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin.
    Morfini GA, You YM, Pollema SL, Kaminska A, Liu K, Yoshioka K, Björkblom B, Coffey ET, Bagnato C, Han D, Huang CF, Banker G, Pigino G, Brady ST., Free PMC Article

    01/21/2010
    JNK2/3 double deficiency blocks death due to retinoblastoma loss in both the PNS and CNS and In the medulla region of the hindbrain in the CNS, JNK2/3 deficiency blocks p53 activation.

    Required roles of Bax and JNKs in central and peripheral nervous system death of retinoblastoma-deficient mice.
    Keramaris E, Ruzhynsky VA, Callaghan SM, Wong E, Davis RJ, Flavell R, Slack RS, Park DS.

    01/21/2010
    Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling

    JNK3 signaling pathway activates ceramide synthase leading to mitochondrial dysfunction.
    Yu J, Novgorodov SA, Chudakova D, Zhu H, Bielawska A, Bielawski J, Obeid LM, Kindy MS, Gudz TI.

    01/21/2010
    MyD88-5 is distinct from other MyD88s in that MyD88-5 is preferentially expressed in neurons, colocalizes in part with mitochondria and JNK3, and regulates neuronal death.

    MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival.
    Kim Y, Zhou P, Qian L, Chuang JZ, Lee J, Li C, Iadecola C, Nathan C, Ding A., Free PMC Article

    01/21/2010
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