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Validated All-in-One™ qPCR Primer for DAPK1(NM_001288730.2) Search again
Product ID:
HQP152389
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DAPK, ROCO3
Gene Description:
death associated protein kinase 1
Target Gene Accession:
NM_001288730.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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].
Gene References into function
- To determine the extent of promoter hypermethylation in early lung tumorigenesis, we analyzed promoter methylation status of the p16, death-associated protein kinase (DAPK) and glutathione S-transferase P1 (GSTP1) genes
- upregulated significantly in acute myeloid leukemia patients whose white blood cell count was higher than 100 x 10(9)/L cells
- promoter methylation studied in 80 patients with head and neck squamous cell carcinoma (HNSCC)
- Results indicate that DAP-kinase exerts apoptotic effects by suppressing integrin functions and integrin-mediated survival signals, thereby activating a p53-dependent apoptotic pathway.
- Suppression of DAP kinase expression by DNA methylation might play a substantial role in the development of not only B-cell, but also T- and NK/T-cell lymphomas.
- DAP kinase binds to syntaxin 1A in a signal transduction pathway
- Frequent death-associated protein-kinase promoter hypermethylation is associated with brain metastases of solid tumors
- Hepatoma cells may escape from apoptosis through the loss or reduction of DAP-kinase expression, while the block of IFN-gamma signal transduction as well as the methylation of promoter region may reduce the expression of DAP-kinase protein.
- Loss of DAP-kinase function may be an early event in the transformation pathway to secondary leukemia via myelodysplasia.
- cellular activities of DAPK are critical for antagonizing caspase-dependent apoptosis to promote cell survival under normal cell growth conditions.
- DAPK promoter methylation and down-regulation is tightly associated with gastric atrophy, often contributes to the preneoplastic changes in gastric carcinogenesis.
- DAPK downregulation and methylation of the DAPK promoter may be involved in carcinogenesis of human uterine and ovarian tissues
- the expression of DAP kinase, p19ARF, p53, and p21WAF1 was significantly down-regulated in the chronically HIV-1SF2-infected HUT78 T cells
- Expression and phosphorylation of DAP kinase in hippocampus of patients with intractable temporal lobe epilepsy is significantly increased compared with autopsy controls.
- although DAP kinase alteration was relatively rare, DAP kinase alteration and/or p53 mutation may associate with tumor progression in soft-tissue LMSs
- DAP kinase is involved in TRAIL-mediated cell apoptosis and a demethylating agent may have a role in enhancing TRAIL-mediated apoptosis in some NSCLC cells by reactivation of DAP kinase
- DAP-kinase promoter methylation may be a potential prognostic marker for gastric cancer patients
- DAPK has a role as a sensor of mitochondrial membrane potential
- DAPK does not regulate radiation-induced cell death
- RSK-mediated phosphorylation of DAPK is a unique mechanism for suppressing the proapoptotic function of this death kinase in healthy cells as well as Ras/Raf-transformed cells.
- These data suggest that genetic variation in DAPK1 modulates susceptibility to LOAD.
- Aberrant methylation and hence silencing of TIMP3, SLC5A8, DAPK and RARbeta2, in association with BRAF mutation, may be an important step in PTC tumorigenesis and progression.
- The promoter hypermethylation of DAPK-1 is a marker of aggressive renal cell carcinoma and provides independent prognostic information on disease outcome.
- the apoptosis regulatory activities mediated by DAPK are controlled both by phosphorylation status and protein stability
- TIMP3, DAPK1 and AKR1B10 are important for squamous cell lung cancer tumorogenesis while AKR1B10 is potential oncogene whereas TIMP3 and DAPK1 are potential tumor suppressor genes.
- data highlight a naturally occurring DAPK-1 mutation that alters the oligomeric structure of the death domain, de-stabilizes DAPK-1 binding to ERK, and prevents ERK:DAPK-1-dependent apoptosis
- Aberrant hypermethylation on DAPK1 promoter is associated with the development of brain metastases from solid tumors
- suggest that DAPK-1 forms a multiprotein survival complex with cathepsin B countering the rate of TNFR-1-dependent apoptosis
- DAPK is found in two distinct immune complexes, one containing HSP90 and CHIP and a second complex containing only DIP1/Mib; strict modulation of DAPK activities by HSP90 heterocomplexes is critical for regulation of apoptosis and cellular homeostasis
- results showed RASSF1A & DAPK genes' promoter methylation occurred frequently in lung tumors, although prevalence of this alteration in these genes was not associated with smoking status of the patients or occurrence of mutations in K-ras, p53 & EGFR
- Promoter hypermethylation of DAPK was observed.
- 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.
- TIMP-3 promoter hypermethylation is elevated in HNSCC and is highly correlated with DAPK hypermethylation, implying a functional relationship between these genes.
- Sodium arsenite caused DAPK promoter hypermethylation and gene silencing which may be involved in arsenic-induced carcinogenesis.
- the DAPK gene epigenetically affected by methylation may be associated with the carcinogenesis of cholangiocarcinoma
- these findings establish a major role for DAPk and its specific interaction with PKD in regulating the JNK signaling network under oxidative stress.
- The promoter methylation of the DAPK gene is an important event during carcinogenesis and may have potential clinical application as a marker for the progression and prognosis of cancer.
- study reports that DAP kinase 1 promotes in vitro & in vivo phosphorylation of tropomyosin-1 on Ser283 & that this phosphorylation is essential for the H2O2-induced organization of the assembly of actin stress fibers in endothelial cells
- Exposure to arsenic may induce DAPK promoter hypermethylation and inactivate the function of DAPK in urothelial carcinoma. ...a key molecular event ...in the malignant phenotype of tumour arising in patients from arsenic-contaminated environments
- Methylation of the DAPK gene is associated with cell transformation in HPV and EBV infection in cervical cells
- a role for MAP1B in DAPK-1-dependent signaling in autophagy and membrane blebbing.
- Expression of dominant-negative and constitutively active death-associated protein kinase (DAPK) selectively inhibits T cell receptor-activated NF-kappaB and T cell activation.
- Methylation of DAPK1 was present in 80% of NSCLC tissues but only 14% of noncancerous tissues.
- These data highlight the existence of an alternative product of the DAPK-1 locus, and suggest that proteolytic removal of the C-terminal tail of s-DAPK-1 is required to stimulate maximally its membrane-blebbing function.
- Promoter methylation of death-associated protein kinase has a role in irradiation response in cervical cancer, although it might not directly be responsible for the cellular radiosensitivity
- Results show that the serine/threonine kinase death-associated protein kinase (DAPK) is involved in the signal transduction of neogenin.
- a novel interaction between DAPK and TSC2 proteins that has revealed a positive link between growth factor stimulation of DAPK and mTORC1 signaling that may ultimately affect autophagy, cell survival, or apoptosis.
- DAPK-ZIPK-L13a axis forms a unique regulatory module that first represses, then repermits inflammatory gene expression.
- results suggested that DAPK1 promoter methylation might play a significant role in the progression of chronic myeloid leukemia
- of promoter hypermethylation of TIMP3, CDH1, DAPK, RASSF1A, p16INK4A and MGMT, only the epigenetic silencing of TIMP3 and CDH1 predicted a better outcome in head and neck squamous cell carcinoma