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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.
Death-associated protein kinase (DAPK) is regulated by DANGER which binds directly to DAPK and inhibits catalytic activity.
cellular activities of DAPK are critical for antagonizing caspase (show CASP3 ELISA Kits)-dependent apoptosis to promote cell survival under normal cell growth conditions.
Our meta-analysis results reveal that DAPK promoter methylation might be associated with tumor metastasis and poor prognosis in NSCLC patients, although no correlation with histological types and TNM (show ODZ1 ELISA Kits) stage in NSCLC patients were found.
Results identified MGMT (show MGMT ELISA Kits) and DAPK1 as predictors of nodal metastasis in oral and oropharyngeal squamous cell carcinoma with a high predictive value and specificity and sensitivity.
Viral infection induced DAPK1-IRF7 (show IRF7 ELISA Kits) and DAPK1-IRF3 (show IRF3 ELISA Kits) interactions and overexpression of DAPK1 enhanced virus-induced activation of the interferon (show IFNA ELISA Kits)-stimulated response element (ISRE) and IFN-beta (show IFNB1 ELISA Kits) promoters and the expression of the IFNB1 (show IFNB1 ELISA Kits) gene.
DAPK1 is highly expressed in the peritumoral region of glioblastoma multiforme brain neoplasms.
A significant strong association between DAPK1 promoter methylation and CC was shown and confirmed independently by histological tumor type, method used to evaluate methylation and source of control samples.
miR (show MLXIP ELISA Kits)-191-DAPK1 axis may play an important role modulating the response of ovarian endometriosis and endometrioid carcinoma cells to TNF-alpha (show TNF ELISA Kits).
The authors discuss evidence suggesting potential contributions of DAPK in the regulation of gut (show GUSB ELISA Kits) inflammation and intestinal homeostasis. [review]
Besides mediating the anticancer effect, pDAPK(S308) may serve as a predictive biomarker for Raf (show RAF1 ELISA Kits) inhibitors combination therapy, suggesting an ideal preclinical model that is worthy of clinical translation.
These data define a novel link between DAPK and HSF1 (show HSF1 ELISA Kits) and highlight a positive-feedback loop in DAPK regulation under mild inflammatory stress conditions in colorectal tumors.
high DAPK1 expression causes increased cancer cell growth and enhanced signaling via the mTOR (show FRAP1 ELISA Kits)/S6K (show RPS6KB1 ELISA Kits) pathway; evaluation of breast cancer patient data sets revealed that high DAPK1 expression associates with worse outcomes in women with p53 (show TP53 ELISA Kits)-mutant cancers
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