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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Death-associated protein kinase 1

DAPK, death-associated protein kinase, DAP-kinase, DAPK1
Death-associated protein kinase 1 is a positive mediator of gamma-interferon induced programmed cell death. DAPK1 encodes a structurally unique 160-kD calmodulin dependent serine-threonine kinase that carries 8 ankyrin repeats and 2 putative P-loop consensus sites. It is a tumor suppressor candidate. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p16, amylin, Methylguanine-DNA Methyltransferase, POLYMERASE, E-cadherin
Papers on DAPK
DANGER is involved in high glucose-induced radioresistance through inhibiting DAPK-mediated anoikis in non-small cell lung cancer.
Youn et al., Pusan, South Korea. In Oncotarget, Feb 2016
In the current study, we showed that ionizing radiation-induced activation of the MEK-ERK-DAPK-p53 signaling axis is required for anoikis (anchorage-dependent apoptosis) of non-small cell lung cancer (NSCLC) cells in normal glucose media.
Quantitative proteomics reveals protein kinases and phosphatases in the individual phases of contextual fear conditioning in the C57BL/6J mouse.
Li et al., Vienna, Austria. In Behav Brain Res, Jan 2016
These include members of PKP signalling modules of mitogen-activated protein kinase (MAP3K10, RAF1, KSR2), Ca2+/calmodulin-dependent protein kinase (CaMKIIα, DAPK1), protein kinase C (PRKCD) and protein phosphatases 1, 2A, 2B(3) previously implicated in various learning paradigms.
Biophysical changes of ATP binding pocket may explain loss of kinase activity in mutant DAPK3 in cancer: A molecular dynamic simulation analysis.
Arsad et al., Kharagpur, India. In Gene, Jan 2016
UNASSIGNED: DAPK3 belongs to family of DAPK (death-associated protein kinases) and is involved in the regulation of progression of the cell cycle, cell proliferation, apoptosis and autophagy.
Regulation of autophagy by beclin 1 in the heart.
Sadoshima et al., Newark, United States. In J Mol Cell Cardiol, Dec 2015
Of these mechanisms, binding of Beclin 1 with Bcl-2 family proteins (Bcl-2/XL) that negatively regulate autophagy activity has been shown to be both positively and negatively regulated by various kinases, including DAPK, ROCK1, Mst1 and JNK1, in response to external stimuli.
[Chemical exposure, leukemia related DNA methylation changes and childhood acute leukemia].
Gao et al., Shanghai, China. In Zhonghua Yu Fang Yi Xue Za Zhi, Sep 2015
For the 8 genes analyzed, the methylation status of DAPK and PTEN and P73 in case group were significantly higher than that in control group (cases: 3.1% (4 cases), 16.0% (21 cases), 7.6% (10 cases); controls: 0.7% (1 case), 2.9% (4 cases), 0.7% (1 case); χ(2): 7.11, 16.90, 11.38; P value: 0.029, 0.000, 0.003).
Death-associated protein kinase 2: Regulator of apoptosis, autophagy and inflammation.
Geering, Basel, Switzerland. In Int J Biochem Cell Biol, Aug 2015
The three most conserved family members DAPK1/DAPK, DAPK2 and DAPK3/ZIPK share a high degree of homology in their catalytic domain, but differ significantly in their extra-catalytic structures and tissue-expression profiles.
The role of targeting kinase activity by natural products in cancer chemoprevention and chemotherapy (Review).
Cao et al., Changsha, China. In Oncol Rep, Aug 2015
Grifolin, a secondary metabolite isolated from the mushroom Albatrellus confluens, has been shown to inhibit cell growth and induce cell cycle arrest in multiple cancer cell lines by targeting extracellular signal-regulated kinase 1 or by upregulating death-associated protein kinase 1 (DAPK1) via p53.
5-Aza-CdR can reverse gefitinib resistance caused by DAPK gene promoter methylation in lung adenocarcinoma cells.
Li et al., Changchun, China. In Int J Clin Exp Pathol, 2014
To explore the relationship between death associated protein kinase (DAPK) gene promoter methylation and gefitinib resistance in Lung adenocarcinoma cell lines.
Cytogenetic analysis of epithelial ovarian cancer's stem cells: an overview on new diagnostic and therapeutic perspectives.
Triolo et al., In Eur J Gynaecol Oncol, 2014
The progression of EOC is characterized by a series of combined epigenetic aberrations, including the most important of those determined by the loss of methylation of certain regions of DNA encoding genes such as Ras-association domain-containing family 1 [(RASSF1A) tumor suppressor], death-associated protein kinase [(DAPK) protein kinase associated with the regulation of apoptosis], human sulfa- tase-I [(hSulf-1) sulfatase, which plays a key role in the regulation of apoptosis], breast cancer 1 gene [(BRCA1) tumor suppressor gene, involved in the processes of DNA repair], and HOXAI0 (gene required to promote many transcription factors).
DAPK1 Promoter Methylation and Cervical Cancer Risk: A Systematic Review and a Meta-Analysis.
Vinciguerra et al., Catania, Italy. In Plos One, 2014
OBJECTIVE: The Death-Associated Protein Kinase 1 (DAPK1) gene has been frequently investigated in cervical cancer (CC).
DAPk1 inhibits NF-κB activation through TNF-α and INF-γ-induced apoptosis.
Rho et al., Taejŏn, South Korea. In Cell Signal, 2012
our data findings suggest that DAPk1 can mediate the pro-apoptotic activity of TNF-alpha and INF-gamma via the NF-kappaB signaling pathways.
Impaired death-associated protein kinase-mediated survival signals in 5-fluorouracil-resistant human endometrial adenocarcinoma cells.
Tanaka et al., Ibaraki, Japan. In Oncol Rep, 2012
acquisition of fluorouracil-resistance may be accompanied by impairment of common apoptotic signals regulating both DAPK-dependent and DAPK-independent pathways.
Promoter hypermethylation of death-associated protein kinase and p16 genes in vulvar lichen sclerosus.
Carvalho et al., Rio de Janeiro, Brazil. In J Low Genit Tract Dis, 2012
There was no statistically significant difference in the percentage of methylation of the DAPK genes (Fisher test, p = .190) and p16 gene (Fisher test, p = .316) between the vulvar lichen sclerosus group (study) and the control group.
Azacytidine inhibits the proliferation of human promyelocytic leukemia cells (HL60) by demethylation of MGMT, DAPK and p16 genes.
Luo et al., Chongqing, China. In Hematology, 2012
The CpG islands of p16, DAPK and MGMT genes are hypermethylated in HL60 cells. Azacytidine inhibits proliferation of leukemic cells by hypomethylation of p16, DAPK and MGMT genes.
Increased DAPK1 but decreased CCL2 plasma levels of nucleic acids in patients with stable angina.
Marc et al., Ljubljana, Slovenia. In Biochem Med (zagreb), 2010
Stable angina patients had 5.1-times higher plasma level of DAPK1 nucleic acids (mRNA and DNA) than controls.
DAPK1 interaction with NMDA receptor NR2B subunits mediates brain damage in stroke.
Lu et al., New Orleans, United States. In Cell, 2010
Here, we report that cerebral ischemia recruits death-associated protein kinase 1 (DAPK1) into the NMDA receptor NR2B protein complex in the cortex of adult mice.
Blocking the deadly effects of the NMDA receptor in stroke.
Wang et al., Vancouver, Canada. In Cell, 2010
In this issue, Tu et al. (2010) demonstrate that ischemic injury promotes the association of death-associated protein kinase 1 with the NMDA receptor, thereby potentiating its activity, and show that disrupting this association reduces damage to the brain.
Downregulation of death-associated protein kinase 1 (DAPK1) in chronic lymphocytic leukemia.
Plass et al., Columbus, United States. In Cell, 2007
Study shows that loss or reduced expression of DAPK1 underlies cases of heritable predisposition to chronic lymphocytic leukemia (CLL) and epigenetic silencing of DAPK1 by promoter methylation occurs in almost all sporadic CLL cases.
Chronic lymphocytic leukemia: keeping cell death at bay.
Debatin, Ulm, Germany. In Cell, 2007
Raval et al. (2007) now implicate dowregulation of the expression of the kinase DAPK1 both genetically and epigenetically in familial and sporadic CLL.
Lack of CpG island methylator phenotype defines a clinical subtype of T-cell acute lymphoblastic leukemia associated with good prognosis.
Torres et al., Córdoba, Spain. In J Clin Oncol, 2005
PATIENTS AND METHODS: Methylation-specific polymerase chain reaction was used to analyze methylation of the ADAMTS-1, ADAMTS-5, APAF-1, ASPP-1, CDH1, CDH13, DAPK, DIABLO, DKK-3, LATS-1, LATS-2, NES-1, p14, p15, p16, p57, p73, PARK-2, PTEN, sFRP1/2/4/5, SHP-1, SYK, TMS-1, and WIF-1 genes in samples from 50 consecutive T-ALL patients (19 children and 31 adults).
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