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Inhibition of DAPK1 by deleting a catalytic domain or a death domain of DAPK1 rescues the Excitatory pyramidal neurons in the entorhinal cortical layer II region synaptic loss
in Alzheimer's disease (AD) brains, elevated DAPK1 levels showed co-relation with the increase of APP (show APP ELISA Kits) phosphorylation. Combined together, these results suggest that DAPK1 promotes the phosphorylation and amyloidogenic processing of APP (show APP ELISA Kits), and that may serve a potential therapeutic target for AD.
This study demonstrate that phosphorylation of Tau at Serine 262 by the kinase domain of DAPK1 mediates spine damage and the subsequent neuronal death in ischemic stroke.
DAPK1-p53 (show TP53 ELISA Kits) interaction is a preferred target for therapeutic intervention of stroke.
Suggest that DAPK1 is a novel regulator of tau protein abundance, and that DAPK1 upregulation might contribute to tau-related pathologies in Alzheimer disease.
the DAPK1-p53 (show TP53 ELISA Kits) interaction is a signaling point of convergence of necrotic and apoptotic pathways
a new function of DAPK in suppressing TNF (show TNF ELISA Kits)-induced STAT3 (show STAT3 ELISA Kits) activation, was identified.
TSC2 (show TSC2 ELISA Kits) binds to the death domain of DAPK. This interaction is required for TSC2 (show TSC2 ELISA Kits) to reduce DAPK protein levels and half-life. DAPK is regulated by the lysosome pathway. Lysosome inhibition blocks TSC2 (show TSC2 ELISA Kits)-mediated degradation of DAPK.
Results identify DAPK as a molecule required for full production of IL-1beta (show IL1B ELISA Kits) and functional assembly of the NLRP3 (show NLRP3 ELISA Kits) inflammasome.
Study reports that cerebral ischemia recruits death-associated protein kinase 1 (DAPK1) into the NMDA receptor NR2B (show GRIN2B ELISA Kits) protein complex in the cortex of adult mice.
DAPK1 methylation is associated with the risk of gastrointestinal cancer.
downregulation of HOXC9 (show HOXC9 ELISA Kits) releases its transcriptional inhibition of DAPK1, resulting in the activation of the DAPK1-Beclin1 (show BECN1 ELISA Kits) pathway, which induces autophagy in glioblastoma cells
findings evidence a positive correlation between SIRT1 (show SIRT1 ELISA Kits) and BCL6 (show BCL6 ELISA Kits) expression increase in follicular lymphomas (FL) . SIRT1 (show SIRT1 ELISA Kits) methylation decreases in FL and diffuse large-B cell lymphomas (DLBCL)and this parallels the increase of KLF4 (show KLF4 ELISA Kits), DAPK1 and SPG20 (show SPG20 ELISA Kits) methylation
results suggest that DAPK1 is an important prognostic marker and therapeutic target for bladder cancer and have identified possible therapeutic agents for future testing in bladder cancer models with low DAPK1 expression
Study provides evidence that DAPK1 is a negative-feedback regulator of the RIG-I (show DDX58 ELISA Kits) pathway. RIG-I (show DDX58 ELISA Kits)-mediated antiviral signaling activates DAPK1 kinase activity and DAPK1 inactivates RIG-I (show DDX58 ELISA Kits) RNA sensing by direct phosphorylation of RIG-I (show DDX58 ELISA Kits).
Meta-analysis suggested that aberrant methylation of DAPK promoter was associated with head and neck squamous cell carcinoma.
our study characterized DAPK1 as a novel transcriptional target of BRMS1 (show BRMS1 ELISA Kits). Transcriptional activation of DAPK1 might be another important mechanism accounting for the metastasis suppressive activity of BRMS1 (show BRMS1 ELISA Kits).
The result suggests that DAPK promoter methylation is significantly increased in bladder cancer patients compared to normal controls. DAPK promoter methylation could serve as a biomarker for bladder cancer detection and management.
Down-regulation of mRNA expression was found in cases in which CASP8 (show CASP8 ELISA Kits), TMS1 (show SERINC3 ELISA Kits) and DAPK were hypermethylated.
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.
death-associated protein kinase 1
, death-associated protein kinase 1-like
, DAP kinase 1