DAPK1-ERK signal mediates oxygen glucose deprivation reperfusion induced apoptosis in mouse N2a cells

Xiong, Wei; Wu, Yan; Xian, Wenjing; Song, Limin; Hu, Lisha; Pan, Shangwen; Liu, Min; Yao, Shanglong; Pei, Lei; Shang, You

doi:10.1016/j.jns.2018.01.003

Cited by 31 publications

(25 citation statements)

References 39 publications

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“…Plausibly, potentiation of exGluN2B Ca 2+ currents by DAPK1 could result in greater Ca 2+ release from ER stores, thus promoting SOCE and spine loss in HD. Second, ERK can be sequestered in the cytosol by DAPK1 (Chen et al, 2005;Xiong et al, 2018), which may prevent its activation and subsequent activity toward the CREB-kinase ribosomal s6 kinase (Chen et al, 2005;Roskoski, 2012). DAPK1 lowering may thus release ERK to indirectly promote CREB phosphorylation and another pro-survival signaling.…”

Section: Discussionmentioning

confidence: 99%

DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

Schmidt

Caron

Aly

et al. 2020

Front. Cell. Neurosci.

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Huntington disease (HD) is a devastating neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. Disrupted cortico-striatal transmission is an early event that contributes to neuronal spine and synapse dysfunction primarily in striatal medium spiny neurons, the most vulnerable cell type in the disease, but also in neurons of other brain regions including the cortex. Although striatal and cortical neurons eventually degenerate, these synaptic and circuit changes may underlie some of the earliest motor, cognitive, and psychiatric symptoms. Moreover, synaptic dysfunction and spine loss are hypothesized to be therapeutically reversible before neuronal death occurs, and restoration of normal synaptic function may delay neurodegeneration. One of the earliest synaptic alterations to occur in HD mouse models is enhanced striatal extrasynaptic NMDA receptor expression and activity. This activity is mediated primarily through GluN2B subunitcontaining receptors and is associated with increased activation of cell death pathways, inhibition of survival signaling, and greater susceptibility to excitotoxicity. Abbreviations: AHA, azidohomoalanine; AP5, amino-5-phosphonovaleric acid; a competitive NMDA receptor antagonist; BACHD, Transgenic mouse model of Huntington disease containing the full-length human mutant huntingtin gene with 97 mixed CAA-CAG repeats; BDNF, brain-derived neurotrophic factor; C6R, Transgenic mouse model expressing full-length human mutant huntingtin bearing a point mutation at the D586 caspase cleavage site; CaMKII, calcium/calmodulindependent protein kinase II; CB, cerebellum; CK2, casein kinase 2; COS-7, fibroblast-like cell line derived from monkey kidney tissue; CREB, cAMP response element-binding protein; CS, cortico-striatal; CTX, cortex; cortical; DAPK1, death-associated protein kinase 1; DARPP32, dopamine-and cAMP-regulated neuronal phosphoprotein; DIV, day-in vitro; DKI, DAPK1 inhibitor; also referred to as TC

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Section: Discussionmentioning

confidence: 99%

DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

Schmidt

Caron

Aly

et al. 2020

Front. Cell. Neurosci.

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“…DAPK1-ERK1/2 signals also regulate neuronal apoptosis following ischemia-reperfusion [ 88 ]. In the report, ischemia-reperfusion led to activation of DAPK1 and ERK1/2.…”

Section: Cross-talk Between Dapks and Erk Signalingmentioning

confidence: 99%

“…These results reveal the potential mechanism of the DAPK1-ERK1/2 signal in the contribution to neuronal apoptosis in response to ischemia-reperfusion. Prevention of this signal pathway might become a promising therapeutic target against stroke [ 88 ].…”

Section: Cross-talk Between Dapks and Erk Signalingmentioning

confidence: 99%

Novel Functions of Death-Associated Protein Kinases through Mitogen-Activated Protein Kinase-Related Signals

Elbadawy

Usui

Yamawaki

et al. 2018

IJMS

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Death associated protein kinase (DAPK) is a calcium/calmodulin-regulated serine/threonine kinase; its main function is to regulate cell death. DAPK family proteins consist of DAPK1, DAPK2, DAPK3, DAPK-related apoptosis-inducing protein kinases (DRAK)-1 and DRAK-2. In this review, we discuss the roles and regulatory mechanisms of DAPK family members and their relevance to diseases. Furthermore, a special focus is given to several reports describing cross-talks between DAPKs and mitogen-activated protein kinases (MAPK) family members in various pathologies. We also discuss small molecule inhibitors of DAPKs and their potential as therapeutic targets against human diseases.

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“…DAPK1 is a kinase that plays an important role in various neuronal injury models (Xu et al, 2018). It has been found that it is implicated in the molecular response to ischemic brain injury and apoptosis‐mediated cell death in neurons (Pelled et al, 2002; Xiong et al, 2018; Yamamoto et al, 2002, 1999). It is considered as a strong positive regulator of neuronal apoptosis in vitro and in vivo (Pelled et al, 2002; Yamamoto et al, 2002).…”

Section: Dapk1 and Diseasesmentioning

confidence: 99%

Role of DAPK1 in neuronal cell death, survival and diseases in the nervous system

Alsaadi

2019

Intl J of Devlp Neuroscience

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DAPK (death‐associated protein kinase) is a calcium/calmodulin (Ca2+/CaM) regulated serine/threonine kinase. Structurally, it assumes a multi‐domain structure and participates in various apoptotic systems which imply that it may interact with a wide range of intracellular components to exert its action. DAPK plays vital roles in pro‐apoptotic, apoptotic and autophagic pathways. In addition, it plays important roles in many diseases such as cancer, Alzheimer's disease, cerebral ischemia and epilepsy. Although a novel protein, DAPK's various cellular signal transduction pathways proves that it can be a target for a potential future therapeutic effects. Specific role of DAPK in the development and maintenance of the nervous system needs to be further investigated as it is involved in neurodegeneration, traumatic brain injury and neuronal development or recovery from injury. This review summarizes DAPK signaling pathways in autophagy, apoptosis, and stresses the important role it might play in the nervous system.

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DAPK1-ERK signal mediates oxygen glucose deprivation reperfusion induced apoptosis in mouse N2a cells

Cited by 31 publications

References 39 publications

DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease

Novel Functions of Death-Associated Protein Kinases through Mitogen-Activated Protein Kinase-Related Signals

Role of DAPK1 in neuronal cell death, survival and diseases in the nervous system

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