Tao Zhang's research while affiliated with Fujian Medical University and other places
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Publications (15)
Alzheimer’s disease (AD) is the most prevalent form of dementia in the elderly and represents a major clinical challenge in the ageing society. Neuropathological hallmarks of AD include neurofibrillary tangles composed of hyperphosphorylated tau, senile plaques derived from the deposition of amyloid-β (Aβ) peptides, brain atrophy induced by neurona...
Breast cancer is one of the major malignancies in women, and most related deaths are due to recurrence, drug resistance, and metastasis. The expression of the mouse double minute 2 (MDM2) oncogene is upregulated in breast cancer; however, its regulatory mechanism has yet to be fully elucidated. Herein, we identified the tumor suppressor death-assoc...
Death-associated protein kinase 1 (DAPK1) is a stress-responsive calcium/calmodulin (CaM)-regulated serine/threonine protein kinase that is actively involved in stress-induced cell death. The dysregulation of DAPK1 has been established in various neurological disorders such as epilepsy, Alzheimer’s disease (AD), and Parkinson’s disease (PD). Recent...
Aims
The autophagy‐lysosomal pathway is important for maintaining cellular proteostasis, while dysfunction of this pathway has been suggested to drive the aberrant intraneuronal accumulation of tau protein, leading to synaptic damage and cognitive impairment. Previous studies have demonstrated that the activation of transient receptor potential van...
Death-associated protein kinase 1 (DAPK1), a Ca2+/calmodulin-dependent serine/threonine kinase, mediates various neuronal functions, including cell death. Abnormal upregulation of DAPK1 is observed in human patients with neurological diseases, such as Alzheimer’s disease (AD) and epilepsy. Ablation of DAPK1 expression and suppression of DAPK1 activ...
Background
Intracellular accumulation of the microtubule-associated protein tau and its hyperphosphorylated forms is a key neuropathological feature of Alzheimer’s disease (AD). Melatonin has been shown to prevent tau hyperphosphorylation in cellular and animal models. However, the molecular mechanisms by which melatonin attenuates tau hyperphospho...
Dysregulation of microRNAs has been implicated in diverse diseases, including Alzheimer's disease (AD). MiR-191-5p in plasma/serum has been identified as a novel and promising noninvasive diagnostic biomarker for AD. However, whether miR-191-5p is involved in AD pathogenesis is largely unknown, and its levels in human AD brains are undetermined. He...
The neuropathology of Alzheimer’s disease (AD) is characterized by intracellular aggregation of hyperphosphorylated tau and extracellular accumulation of beta-amyloid (Aβ). Death-associated protein kinase 1 (DAPK1), as a novel therapeutic target, shows promise for the treatment of human AD, but the regulatory mechanisms of DAPK1 expression in AD re...
Glutamate excitotoxicity induces neuronal cell death during epileptic seizures. Death-associated protein kinase 1 (DAPK1) expression is highly increased in the brains of epilepsy patients; however, the underlying mechanisms by which DAPK1 influences neuronal injury and its therapeutic effect on glutamate excitotoxicity have not been determined. We...
The aggregation of amyloid-β (Aβ) peptides into oligomers and fibrils is a key pathological feature of Alzheimer's disease (AD). An increasing amount of evidence suggests that oligomeric Aβ might be the major culprit responsible for various neuropathological changes in AD. Death-associated protein kinase 1 (DAPK1) is abnormally elevated in brains o...
Epilepsy is a chronic encephalopathy and one of the most common neurological disorders. Death-associated protein kinase 1 (DAPK1) expression has been shown to be upregulated in the brains of human epilepsy patients compared with those of normal subjects. However, little is known about the impact of DAPK1 on epileptic seizure conditions. In this stu...
Background
Death‐associated protein kinase 1 (DAPK1) is a serine/threonine kinase that plays an important role in regulating neuronal function and is genetically linked to Alzheimer’s disease (AD). We previously showed that DAPK1 expression is markedly increased in 75% of human AD brains. Moreover, we found that DAPK1 promotes tau protein accumulat...
Neurodegenerative diseases are the second most common cause of death and characterized by progressive impairments in movement or mental functioning in the central or peripheral nervous system. The prevention of neurodegenerative disorders has become an emerging public health challenge for our society. Melatonin, a pineal hormone, has various physio...
Death‐associated protein kinase 1 (DAPK1) is upregulated in the brains of human Alzheimer’s disease (AD) patients compared with normal subjects, and aberrant DAPK1 regulation is implicated in the development of AD. However, little is known about whether and how DAPK1 function is regulated in AD. Here, we identified melatonin as a critical regulator...
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive dysfunction and behavioral impairment. In China, the number of AD patients is growing rapidly, which poses a considerable burden on society and families. In recent years, through the advancement of genome-wide association studies, second-generation gene s...
Citations
... As a crucial regulator of cellular autophagy, DAPK1 has been shown to be extensively involved in the pathological processes of neuronal injury [29][30][31][32] . Research by Youn DH et al. found that DAPK1-mediated autophagy and mitochondrial dysfunction-related mitophagy may play an important role in the pathogenesis of delayed cerebral ischemia [33] . ...
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... The high abundance of proteins for RNA metabolism and chromatin regulation (~14%) implicates that DAPK1 may exert a widespread effect on gene transcription and translation. In support of this, our recent RNA-transcriptomic analysis demonstrated that DAPK1 affects global gene expression in mouse brain likely through regulating DNA transcription-related pathways [25]. ...
... The inhibition of Aβ1-42-induced microglial cell injury was due to the inactivation of the MAPK signaling pathway, in which Map3k12 was targeted by miR-191-5p. Moreover, miR-191-5p reduced tau phosphorylation and enhanced neurite outgrowth in vitro (Wang et al., 2022a). This study also found that miR-191-5p reduced the levels of phosphorylated amyloid precursor protein (APP) and the generation of Aβ. ...
... In general, miRNAs act in mammals by not fully binding to target genes, thereby inhibiting their translation [31][32][33]. However, our research ndings demonstrated that miR-4763-3p also in uences the transcription of ATP11A, which provoked our curiosity. ...
... Substantial evidence indicates that DAPK1 is involved in apoptosis, autophagy, necrosis, and anoikis-like cell death [4,[6][7][8]. Both DAPK1 knockout (DAPK1-KO) and the inhibition of DAPK1 function protects neurons against neuronal damage, whereas DAPK1 overexpression induces cell death [9][10][11][12]. In addition, DAPK1 may be involved in neurogenesis and other neuronal functions, such as synaptic transmission and plasticity, as well as cognition [5,6,[13][14][15][16]. ...
... Our study has identified a potential regulatory axis, mmu_ circ_0013163/miR-504-3p/Smurf1, which might contribute to the pathological development of morphine addiction (Fig. S18). The miR-504-3p was reported to alleviate taurelated pathologies by targeting the p39, an activator of tau kinase cyclin-dependent kinase 5 (CDK5) [68]. The downstream target of miR-504-3p was predicted to be Smurf1, which has been validated to be significantly up-regulated in the morphine group (Fig. 3D). ...
... We have already seen that glyphosate suppresses melatonin synthesis, and that melatonin plays a critical role in suppressing DAPK1 activity [39,87]. DAPK1 is a potent modulator of PIN1 activity and their molecular interactions are significantly implicated in the development of tau-associated pathology [104], in the amyloid β-related pathology of Alzheimer's disease (AD) [152] and in the disablement of neuronal network restoration following neural traumas [153]. Therefore, as DAPK1 directly inhibits PIN1 function [86], it is important to revisit DAPK1 regulatory aspects of activation and/or deactivation that relate to the DAPK1 tertiary structure. ...
... Substantial evidence indicates that DAPK1 is involved in apoptosis, autophagy, necrosis, and anoikis-like cell death [4,[6][7][8]. Both DAPK1 knockout (DAPK1-KO) and the inhibition of DAPK1 function protects neurons against neuronal damage, whereas DAPK1 overexpression induces cell death [9][10][11][12]. In addition, DAPK1 may be involved in neurogenesis and other neuronal functions, such as synaptic transmission and plasticity, as well as cognition [5,6,[13][14][15][16]. ...
... A novel DAPK1 inhibitor should be able to stop the degeneration of synaptic transmission and the alteration of synaptic plasticity. Plenty of evidence suggest that DAPK1 is a crucial target in AD (Chen et al., 2020;You et al., 2017; and a novel target-specific DAPK1 inhibitor can be designed using computational methods for treating and managing AD symptoms. ...
... Serotonin then undergoes acetylation by serotonin N-acetyltransferase (SNAT or AANAT, the acronym for arylalkylamine N-acetyltransferase-the rate-limiting enzyme), converting into N-acetylserotonin. Finally, melatonin is produced through the methylation of N-acetylserotonin by N-acetylserotonin O-methyltransferase (ASMT, previously identified as hydroxyindole-O-methyltransferase or HIOMT) [2,[10][11][12][13]. The melatonin synthesis pathway is schematized in Figure 2. ...
Reference: Melatonin and Vascular Function
