106 results match your criteria dapk1 mice


Cis P-tau underlies vascular contribution to cognitive impairment and dementia and can be effectively targeted by immunotherapy in mice.

Sci Transl Med 2021 Jun;13(596)

Division of Translational Therapeutics, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

Compelling evidence supports vascular contributions to cognitive impairment and dementia (VCID) including Alzheimer's disease (AD), but the underlying pathogenic mechanisms and treatments are not fully understood. Cis P-tau is an early driver of neurodegeneration resulting from traumatic brain injury, but its role in VCID remains unclear. Here, we found robust cis P-tau despite no tau tangles in patients with VCID and in mice modeling key aspects of clinical VCID, likely because of the inhibition of its isomerase Pin1 by DAPK1. Read More

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Inhibition of death-associated protein kinase 1 attenuates cis P-tau and neurodegeneration in traumatic brain injury.

Prog Neurobiol 2021 May 9:102072. Epub 2021 May 9.

Division of Translational Therapeutics, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA; Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA. Electronic address:

Traumatic brain injury (TBI) is the leading cause of mortality and disability in young people and may lead to the development of progressive neurodegeneration, such as that observed in chronic traumatic encephalopathy. We have recently found that the conformation-specific cis phosphorylated form of tau (cis P-tau) is a major early driver of neurodegeneration after TBI. However, not much is known about how cis P-tau is regulated in TBI. Read More

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Young DAPK1 knockout mice have altered presynaptic function.

J Neurophysiol 2021 May 21;125(5):1973-1981. Epub 2021 Apr 21.

Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.

The death-associated protein kinase 1 (DAPK1) has recently been shown to have a physiological function in long-term depression (LTD) of glutamatergic synapses: acute inhibition of DAPK1 blocked the LTD that is normally seen at the hippocampal CA1 synapse in young mice, and a pharmacogenetic combination approach showed that this specifically required DAPK1-mediated suppression of postsynaptic Ca/calmodulin-dependent protein kinase II binding to the NMDA-type glutamate receptor (NMDAR) subunit GluN2B during LTD stimuli. Surprisingly, we found here that genetic deletion of DAPK1 (in DAPK1 mice) did not reduce LTD. Paired pulse facilitation experiments indicated a presynaptic compensation mechanism: in contrast to wild-type mice, LTD stimuli in DAPK1 mice decreased presynaptic release probability. Read More

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miR-214 Alleviates Ischemic Stroke-Induced Neuronal Death by Targeting DAPK1 in Mice.

Front Neurosci 2021 26;15:649982. Epub 2021 Mar 26.

The Brain Cognition and Brain Disease Institute, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.

Background: Ischemic stroke induces neuronal cell death and causes brain dysfunction. Preventing neuronal cell death after stroke is key to protecting the brain from stroke damage. Nevertheless, preventative measures and treatment strategies for stroke damage are scarce. Read More

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Requirement of splicing factor hnRNP A2B1 for tumorigenesis of melanoma stem cells.

Stem Cell Res Ther 2021 Jan 28;12(1):90. Epub 2021 Jan 28.

College of Life Sciences and Laboratory for Marine Biology and Biotechnology of Pilot National Laboratory for Marine Science and Technology (Qingdao), Zhejiang University, Hangzhou, 310058, People's Republic of China.

Background: Cancer stem cells play essential roles in tumorigenesis, thus forming an important target for tumor therapy. The hnRNP family proteins are important splicing factors that have been found to be associated with tumor progression. However, the influence of hnRNPs on cancer stem cells has not been extensively explored. Read More

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January 2021

Extracellular vesicle-encapsulated microRNA-425-derived from drug-resistant cells promotes non-small-cell lung cancer progression through DAPK1-medicated PI3K/AKT pathway.

J Cell Physiol 2021 May 30;236(5):3808-3820. Epub 2020 Nov 30.

State Key Laboratory of Respiratory Disease, Department of Thoracic Surgery and Oncology, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Investigations in the area of tumor-derived extracellular vesicles (EVs) open a new horizon in developing cancer biology and its potential as cancer biomarkers. Following this prospect, we aimed to identify that the role of successfully isolated EVs from drug-resistance cells in the progression of non-small-cell lung cancer (NSCLC). P-EVs and R-EVs secreted by A549 cells and drug-resistant A549-R cells respectively were extracted and characterized. Read More

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Low DAPK1 expression correlates with poor prognosis and sunitinib resistance in clear cell renal cell carcinoma.

Aging (Albany NY) 2020 11 16;13(2):1842-1858. Epub 2020 Nov 16.

Department of Urology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

We investigated the prognostic significance of Death-Associated Protein Kinase 1 (DAPK1) and its role in sunitinib resistance in clear cell renal cell carcinoma (ccRCC). DAPK1 mRNA levels were significantly lower in tumor tissues than normal kidney tissues in TCGA-KIRC dataset (n=428). Both overall survival and disease-free survival were significantly shorter in ccRCC patients with low DAPK1 expression than those with high DAPK1 expression. Read More

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November 2020

Death-associated protein kinase 1 (DAPK1) controls CD8 T cell activation, trafficking, and antitumor activity.

FASEB J 2021 01 13;35(1):e21138. Epub 2020 Nov 13.

Department of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Appropriate migration of cytotoxic T effector cells into the tumors is crucial for their antitumor function. Despite the controversial role of PI3K-Akt in CD8 T cell mTORC1 activation, a link between Akt-mTORC1 signaling and CD8 trafficking has been demonstrated. We have recently discovered that TCR-induced calcineurin activates DAPK1, which interacts with TSC2 via its death domain and phosphorylates TSC2 via its kinase domain to mediate mTORC1 activation in CD8 T cells. Read More

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January 2021

Redox DAPK1 destabilizes Pellino1 to govern inflammation-coupling tubular damage during septic AKI.

Theranostics 2020 15;10(25):11479-11496. Epub 2020 Sep 15.

Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, Zhejiang, P.R.China.

Tubular damage initiated by inflammatory response and ischemic/hypoxic stress is a hallmark of septic acute kidney injury (AKI), albeit the molecular mechanism coupling the two events remains unclear. We investigated the intrinsic nature of tubular damage with respect to inflammatory/hypoxic stress during septic AKI. The apoptotic response of tubular cells to LPS stimuli was analyzed before and after hypoxia exposure. Read More

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Death-associated Protein Kinase 1 Mediates Ventilator-induced Lung Injury in Mice by Promoting Alveolar Epithelial Cell Apoptosis.

Anesthesiology 2020 10;133(4):905-918

Background: Alveolar epithelial cell apoptosis is implicated in the onset of ventilator-induced lung injury. Death-associated protein kinase 1 (DAPK1) is associated with cell apoptosis. The hypothesis was that DAPK1 participates in ventilator-induced lung injury through promoting alveolar epithelial cell apoptosis. Read More

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October 2020

Tumor suppressor death-associated protein kinase 1 inhibits necroptosis by p38 MAPK activation.

Cell Death Dis 2020 05 4;11(5):305. Epub 2020 May 4.

Institute of Molecular Biology, Academia Sinica, Taipei, 11529, Taiwan.

Death-associated protein kinase 1 (DAPK1, DAPk, DAPK) is known for its involvement in apoptosis and autophagy-associated cell death. Here, we identified an unexpected function of DAPK1 in suppressing necroptosis. DAPK1-deficiency renders macrophages and dendritic cells susceptible to necroptotic death. Read More

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Presynaptic Caytaxin prevents apoptosis via deactivating DAPK1 in the acute phase of cerebral ischemic stroke.

Exp Neurol 2020 07 8;329:113303. Epub 2020 Apr 8.

Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; The Institute for Brain Research (IBR), Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address:

Death-associated protein kinase 1 (DAPK1) is a key protein that mediates neuronal death in ischemic stroke. Although the substrates of DAPK1 and molecular signal in stroke have been gradually discovered, the modulation of DAPK1 itself is still unclear. Here we first reveal that Caytaxin, a brain-specific member of BCL2/adenovirus E1B -interacting protein (BNIP-2), increases and interacts with DAPK1 as early as 2 h after middle cerebral artery occlusion (MCAO) in the penumbra area of mouse brain. Read More

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LncRNA MALAT1 targeting miR-124-3p regulates DAPK1 expression contributes to cell apoptosis in Parkinson's Disease.

J Cell Biochem 2020 Apr 10. Epub 2020 Apr 10.

Department of Neurology, Tianjin First Central Hospital, Tianjin, China.

Death associated protein kinase 1 (DAPK1) was initially discovered in the progress of gamma-interferon induced programmed cell death, it is a key factor in the central nervous system, including Parkinson's disease (PD). However, the underlying mechanisms of DAPK1 in PD remain unclear and this research work aims to explore the potential mechanisms of DAPK1 in PD. In the study, we exposed SH-SY5Y cells to MPP and treated mice with MPTP to investigate the roles of DAPK1 in PD and the underlying mechanisms. Read More

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Integrated miRNA/mRNA Counter-Expression Analysis Highlights Oxidative Stress-Related Genes and as Blood Markers of Coronary Arterial Disease.

Int J Mol Sci 2020 Mar 12;21(6). Epub 2020 Mar 12.

Independent Researcher; C/S. Albert Magne 12-14, Esc-B, SobAtic, Esplugues de llobregat, 08950 Barcelona, Spain.

Our interest in the mechanisms of atherosclerosis progression (ATHp) has led to the recent identification of 13 miRNAs and 1285 mRNAs whose expression was altered during ATHp. Here, we deepen the functional relationship among these 13 miRNAs and genes associated to oxidative stress, a crucial step in the onset and progression of vascular disease. We first compiled a list of genes associated to the response to oxidative stress (Oxstress genes) by performing a reverse Gene Ontology analysis (rGO, from the GO terms to the genes) with the GO terms GO0006979, GO1902882, GO1902883 and GO1902884, which included a total of 417 unique Oxstress genes. Read More

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H19/miR-130a-3p/DAPK1 axis regulates the pathophysiology of neonatal hypoxic-ischemia encephalopathy.

Neurosci Res 2021 Feb 12;163:52-62. Epub 2020 Mar 12.

Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, 310053, China.

Perinatal hypoxic ischemia encephalopathy (HIE) is a serious disease occurring in neonate. Growing studies have already validated the pivotal function of microRNAs (miRNAs) in a variety of diseases. However, whether miR-130a-3p participated in neonatal HIE remains vague. Read More

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February 2021

Oxytocin Alleviates MPTP-Induced Neurotoxicity in Mice by Targeting MicroRNA-26a/Death-Associated Protein Kinase 1 Pathway.

J Alzheimers Dis 2020 ;74(3):883-901

Department of Pathophysiology, Key lab of a neurological disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.

Neurotoxicity is one of the major pathological changes in multiple neurological disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD), the second popular neurodegenerative disease in aged people. It is known that the AD and PD share the similar neuropathological hallmarks, such as the oxidative stress, loss of specific neurons, and aggregation of specific proteins. However, there are no effective therapeutic drugs for both AD and PD yet. Read More

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Dapk1 improves inflammation, oxidative stress and autophagy in LPS-induced acute lung injury via p38MAPK/NF-κB signaling pathway.

Mol Immunol 2020 04 8;120:13-22. Epub 2020 Feb 8.

Surgical Intensive Care Unit, China-Japan Friendship Hospital, Beijing 100029, China. Electronic address:

Objective: To investigate the impact of death-associated protein kinase 1 (Dapk1) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) via p38MAPK/NF-κB pathway.

Methods: Dapk1 and Dapk1 mice were randomized into Control, LPS, SB203580 (a p38MAPK pathway inhibitor) + LPS, and PDTC (a NF-κB pathway inhibitor) + LPS groups. Cell counts, lung wet to dry weight ratio (W/D weight ratio), as well as indicators of oxidative stress were determined followed by the detection with HE staining, ELISA, qRT-PCR, Western blotting and Immunofluorescence. Read More

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CaMKII versus DAPK1 Binding to GluN2B in Ischemic Neuronal Cell Death after Resuscitation from Cardiac Arrest.

Cell Rep 2020 01;30(1):1-8.e4

Department of Pharmacology, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA; Program in Neuroscience, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address:

DAPK1 binding to GluN2B was prominently reported to mediate ischemic cell death in vivo. DAPK1 and CaMKII bind to the same GluN2B region, and their binding is mutually exclusive. Here, we show that mutating the binding region on GluN2B (L1298A/R1300Q) protected against neuronal cell death induced by cardiac arrest followed by resuscitation. Read More

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January 2020

Prolyl oligopeptidase inhibition activates autophagy via protein phosphatase 2A.

Pharmacol Res 2020 01 20;151:104558. Epub 2019 Nov 20.

Division of Pharmacology and Pharmacotherapy/Drug Research Program, Faculty of Pharmacy, University of Helsinki, Finland. Electronic address:

Prolyl oligopeptidase (PREP) is a serine protease that has been studied particularly in the context of neurodegenerative diseases for decades but its physiological function has remained unclear. We have previously found that PREP negatively regulates beclin1-mediated macroautophagy (autophagy), and that PREP inhibition by a small-molecule inhibitor induces clearance of protein aggregates in Parkinson's disease models. Since autophagy induction has been suggested as a potential therapy for several diseases, we wanted to further characterize how PREP regulates autophagy. Read More

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January 2020

Calcium/Calmodulin-Dependent Kinase (CaMKII) Inhibition Protects Against Purkinje Cell Damage Following CA/CPR in Mice.

Mol Neurobiol 2020 Jan 13;57(1):150-158. Epub 2019 Sep 13.

Neuronal Injury Program, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.

Ischemic brain damage is triggered by glutamate excitotoxicity resulting in neuronal cell death. Previous research has demonstrated that N-methly-D-aspartate (NMDA) receptor activation triggers downstream calcium-dependent signaling pathways, specifically Ca/calmodulin-dependent protein kinase II (CaMKII). Inhibiting CaMKII is protective against hippocampal ischemic injury, but there is little known about its role in the cerebellum. Read More

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January 2020

Metformin reduces fibrosis factors in insulin resistant and hypertrophied adipocyte via integrin/ERK, collagen VI, apoptosis, and necrosis reduction.

Life Sci 2019 Sep 23;233:116682. Epub 2019 Jul 23.

Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, IR, Iran. Electronic address:

Aims: Fibrosis as the hallmark of adipose tissue dysfunction which is associated with insulin resistance and type 2 diabetes, results from deposition of excess extra cellular matrix components like collagen and increased cell death. Here we investigated the effect of antidiabetic drug, Metformin, on the factors that play role in fibrosis such as; integrin/ERK pathway, collagen VI, MMP2, MMP9, apoptosis markers including DAPK1, DAPK3, DAP, SIVA, necrosis markers including RIPK1, RIPK3, and MLKL in insulin resistant and hypertrophied adipocytes.

Methods: 3T3-L1 adipocytes after differentiation to insulin resistant and hypertrophied cells, treated with Metformin, and the gene expression of aforementioned factors assayed by real time PCR. Read More

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September 2019

The lncRNA DAPK-IT1 regulates cholesterol metabolism and inflammatory response in macrophages and promotes atherogenesis.

Biochem Biophys Res Commun 2019 09 9;516(4):1234-1241. Epub 2019 Jul 9.

Department of Neurosurgery, General Hospital of TISCO, Shanxi Medical University, Taiyuan, China.

Atherosclerosis is the leading cause of cardiovascular disease (CVD) and the leading reason behind mortality and morbidity in Western countries. The role of long noncoding RNAs (lncRNAs) in CVD is still unexplored with inadequate research on the involvement of lncRNAs in atherogenesis. We found the lncRNA DAPK1-IT1 and lipoprotein lipase (LPL) to be up-regulated in THP-1 macrophage-derived foam cells. Read More

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September 2019

Inhibition of miR-34a-5p can rescue disruption of the p53-DAPK axis to suppress progression of clear cell renal cell carcinoma.

Mol Oncol 2019 10 24;13(10):2079-2097. Epub 2019 Aug 24.

Department of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.

DAPK, a transcriptional target of the p53 protein, has long been characterized as a tumor suppressor that acts as a negative regulator in multiple cellular processes. However, increasing studies have suggested that the role of DAPK may vary depending on cell type and cellular context. Thus far, the expression and function of DAPK in clear cell renal cell carcinoma (ccRCC) remain ambiguous. Read More

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October 2019

New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD.

Autophagy 2020 01 9;16(1):38-51. Epub 2019 Jul 9.

M2iSH, UMR 1071 Inserm, INRA USC 2018, CRNH, University of Clermont Auvergne, Clermont-Ferrand, France.

One of the most significant challenges of inflammatory bowel disease (IBD) research is to understand how alterations in the symbiotic relationship between the genetic composition of the host and the intestinal microbiota, under impact of specific environmental factors, lead to chronic intestinal inflammation. Genome-wide association studies, followed by functional studies, have identified a role for numerous autophagy genes in IBD, especially in Crohn disease. Studies using and models, in addition to human clinical studies have revealed that autophagy is pivotal for intestinal homeostasis maintenance, gut ecology regulation, appropriate intestinal immune responses and anti-microbial protection. Read More

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January 2020

SerThr-PhosphoProteome of Brain from Aged PINK1-KO+A53T-SNCA Mice Reveals pT1928-MAP1B and pS3781-ANK2 Deficits, as Hub between Autophagy and Synapse Changes.

Int J Mol Sci 2019 Jul 4;20(13). Epub 2019 Jul 4.

Experimental Neurology, Goethe University Medical Faculty, 60590 Frankfurt am Main, Germany.

Hereditary Parkinson's disease (PD) can be triggered by an autosomal dominant overdose of alpha-Synuclein (SNCA) as stressor or the autosomal recessive deficiency of PINK1 Serine/Threonine-phosphorylation activity as stress-response. We demonstrated the combination of PINK1-knockout with overexpression of SNCA in double mutant (DM) mice to exacerbate locomotor deficits and to reduce lifespan. To survey posttranslational modifications of proteins underlying the pathology, brain hemispheres of old DM mice underwent quantitative label-free global proteomic mass spectrometry, focused on Ser/Thr-phosphorylations. Read More

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Activation of death-associated protein kinase 1 promotes neutrophil apoptosis to accelerate inflammatory resolution in acute respiratory distress syndrome.

Lab Invest 2019 07 25;99(8):1143-1156. Epub 2019 Mar 25.

Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Acute respiratory distress syndrome (ARDS) is a uniform progression of overwhelming inflammation in lung tissue with extensive infiltration of inflammatory cells. Neutrophil apoptosis is thought to be a significant process in the control of the resolution phase of inflammation. It has been proved that 5-Aza-2'-deoxycytidine (Aza) can inhibit cancer by activating death-associated protein kinase 1 (DAPK1) to promote apoptosis. Read More

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MicroRNA-26a/Death-Associated Protein Kinase 1 Signaling Induces Synucleinopathy and Dopaminergic Neuron Degeneration in Parkinson's Disease.

Biol Psychiatry 2019 05 19;85(9):769-781. Epub 2018 Dec 19.

Department of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Institute of Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, China; National Research Center for Geriatric Diseases, Xiangya Hospital, and Center for Medical Genetics, School of Life Science, Central South University, Changsha, Hunan, China. Electronic address:

Background: Death-associated protein kinase 1 (DAPK1) is a widely distributed serine/threonine kinase that is critical for cell death in multiple neurological disorders, including Alzheimer's disease and stroke. However, little is known about the role of DAPK1 in the pathogenesis of Parkinson's disease (PD), the second most common neurodegenerative disorder.

Methods: We used Western blot and immunohistochemistry to evaluate the alteration of DAPK1. Read More

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Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1.

Exp Neurol 2019 04 29;314:100-110. Epub 2019 Jan 29.

Department of Emergency Medicine, The First Affiliated Hospital of Kunming Medical University, No. 295 Xichang Road, Wu Hua District, Kunming 650032, Yunnan Province, China. Electronic address:

Emerging evidence has suggested a significant role of long non-coding RNAs (lncRNAs) in ischemic stroke by acting as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs) to regulate certain RNA transcripts. AK038897 is an lncRNA that was reported to be upregulated in rat brains in response to transient focal ischemia. We aimed to investigate the possible regulatory role of AK038897 in ischemic stroke. Read More

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miR-483-5p decreases the radiosensitivity of nasopharyngeal carcinoma cells by targeting DAPK1.

Lab Invest 2019 05 21;99(5):602-611. Epub 2019 Jan 21.

Department of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, Guangdong Province, People's Republic of China.

Recurrence or metastasis resulting from radioresistance are the main challenges for the treatment of nasopharyngeal carcinoma (NPC). A great deal of evidence supports the role of abnormal expression of miRNAs in radioresistance and malignancy. In some cancers, miR-483-5p is associated with inferior disease-specific survival. Read More

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Death-Associated Protein Kinase 1 as a Promising Drug Target in Cancer and Alzheimer's Disease.

Recent Pat Anticancer Drug Discov 2019 ;14(2):144-157

Fujian Key Laboratory for Translational Research in Cancer and Neurodegenerative Diseases, Institute for Translational Medicine, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350122, China.

Background: Death-Associated Protein Kinase 1 (DAPK1) plays an important role in apoptosis, tumor suppression and neurodegeneration including Alzheimer's Disease (AD).

Objective: This review will describe the diverse roles of DAPK1 in the development of cancer and AD, and the current status of drug development targeting DAPK1-based therapies.

Methods: Reports of DAPK1 regulation, function and substrates were analyzed using genetic DAPK1 manipulation and chemical DAPK1 modulators. Read More

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February 2020