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1 DAPK as a negative regulator of STAT3 emerges as therape
2 DAPK attenuated STAT3 activity directly by physical inte
3 DAPK is inactive in normal brain tissues, where it is fo
4 DAPK methylation was assessed by methylation-specific po
5 DAPK methylation, IL-10 lack of expression, COX-2 expres
6 DAPK phosphorylates at least one substrate in vitro and
7 DAPK promoter hypermethylation was found in IgM- B cells
8 DAPK suppresses translation in rabbit reticulocyte lysat
9 DAPK-1 and PTRN-1 physically interact in co-immunoprecip
10 DAPK-1 stimulatory peptides attenuate tryptic cleavage o
11 DAPK-1 was used as a model enzyme to develop selective p
12 in which death-associated protein kinase-1 (DAPK) activates zipper-interacting protein kinase (ZIPK)
13 reas no methylation was observed for APAF-1, DAPK, FANCF, FAS, P14, P21, P73, SOCS-3, and SURVIVIN.
14 ation dynamics of 4 TSGs (p15(INK4B), CDH-1, DAPK-1, and SOCS-1) were studied in sequential bone marr
16 NORE1A (15%), p14ARF (15%), p16INK4a (10%), DAPK (11%) and CRBP1 (9%), but promoter methylation was
17 and the cellular levels of phospho(Ser(308))-DAPK dramatically increase in response to GA treatment.
19 Mutation of Ser-289 to alanine results in a DAPK mutant with enhanced apoptotic activity, whereas th
21 has the most highly conserved elements of a DAPK consensus substrate, including a basic core followe
22 as DAPK siRNA knockdown and treatment with a DAPK inhibitor potentiated STAT3 activation, IL-6 mRNA e
24 -1, suggesting that ligand binding can alter DAPK-1 conformation and lock the enzyme onto its substra
27 d the levels of DAPK autophosphorylation and DAPK catalytic activity in response to tumor necrosis fa
31 revealed that methylation at the RASSF1A and DAPK loci, in addition to tumor stage and grade, were as
33 BRCA1, hMLH1, GSTP1, MGMT, CDH1, TIMP3, and DAPK), each rigorously characterized for association wit
35 owing selection in the presence of antisense DAPK cDNA, are more sensitive to tumor necrosis factor-i
36 enes (p16(INK4A), MGMT, GSTP1, RASSF1A, APC, DAPK, RARbeta, CDH1 and CDH13) in 175 primary pediatric
38 suppressing TNF-induced STAT3 activation as DAPK siRNA knockdown and treatment with a DAPK inhibitor
40 sphoinositide 3-kinase inhibitors attenuated DAPK dephosphorylation induced by mitochondrial toxins.
42 the phospho-acceptor site, creating a better DAPK-1 peptide consensus and demonstrated that the Km fo
43 apoptosis regulatory activities mediated by DAPK are controlled both by phosphorylation status and p
45 promoter methylation at CASP8, CDH1, CDH13, DAPK, MGMT, NORE1A, p14ARF and RARB2 in primary Wilms' t
46 e superfamily members, including CHK2, CHK1, DAPK-1, DAPK-3, DRAK-1, and AMPK, as Ser(20) kinases.
47 ponent of the 40S ribosomal subunit complex, DAPK selectively phosphorylates it at serine 235, one of
48 cell carcinoma tumors at BCL2, PTGS2 (COX2), DAPK, CDH1 (ECAD), EDNRB, RASSF1A, RUNX3, TERT, and TIMP
49 ilms' tumours and CASP8, CDH1, CDH13, CRBP1, DAPK, MGMT, MT1G, NORE1A, p16INK4a, SDHB and RARB2 in pr
50 ooth muscle cells demonstrate that decreased DAPK expression promotes a spontaneous, caspase-mediated
51 hese phosphatase holoenzymes dephosphorylate DAPK at Ser-308 in vitro and in vivo resulting in enhanc
52 oreover, concomitantly to dephosphorylation, DAPK is proteolytically processed by cathepsin after isc
55 n experiments are consistent with endogenous DAPK being associated with endogenous S6 in rat brain.
56 acting protein (CHIP) or DIP1/Mib1, enhanced DAPK degradation, and conversely, short interfering RNA
58 the N1347S mutation strikingly prevented ERK:DAPK-1-dependent apoptosis as defined by poly(ADP-ribose
61 P-3, 25% for p16INK4a, 21% for MGMT, 19% for DAPK, 18% for ECAD, 8% for p14ARF, and 7% for GSTP1, whe
65 wed methylation for p16 and 17% the same for DAPK, whereas only 6% of the samples displayed methylati
66 onic fibroblasts and neurons exhibit greater DAPK activity and increased sensitivity to cell death st
67 ted in cancer (p16(INK4A), APC, MGMT, GSTP1, DAPK, CDH1, CDH13, RARbeta and FHIT) in 24 primary TGCTs
68 ically, the signature of a miR-103/107 high, DAPK low, and KLF4 low expression profile correlated wit
70 identical to the previously described human DAPK, and it has a kinase domain and calmodulin-binding
71 on of DAPK-alpha, the mouse homolog of human DAPK has a negligible effect on tumor necrosis factor (T
72 existence of the alternatively spliced human DAPK-beta, and we examined the levels of DAPK autophosph
84 how that the death-associated protein kinase DAPK-1 acts as a negative regulator of wound closure.
86 silencing of death-activated protein kinase (DAPK) abrogated EFS-induced GLUT4 but not CD36 transloca
87 tivation of death associated protein kinase (DAPK) and consequently zipper-interacting protein kinase
88 of the p16, death-associated protein kinase (DAPK) and glutathione S-transferase P1 (GSTP1) genes usi
89 suppressors death-associated protein kinase (DAPK) and Kruppel-like factor 4 (KLF4) in CRC cells, res
91 tivation of death-associated protein kinase (DAPK) and the role of lysosome in neuroblastoma cells (S
92 mbers of the death-activated protein kinase (DAPK) family, an enzyme family of no known direct link t
96 f the mouse death-associated protein kinase (DAPK) have been identified and their roles in apoptosis
103 tivation of death-associated protein kinase (DAPK) occurs via dephosphorylation of Ser-308 and subseq
104 requency of death-associated protein kinase (DAPK) promoter hypermethylation has been noted in B-cell
105 ase (MGMT), death-associated protein kinase (DAPK), E-cadherin (ECAD), p14ARF, and glutathione S-tran
106 suppressor, death-associated protein kinase (DAPK), is a Ca(2+)/calmodulin-regulated Ser/Thr kinase w
107 C. elegans, death-associated protein kinase (DAPK-1) regulates epidermal morphogenesis, innate immuni
114 s of TNF-treated cell lines expressing mouse DAPK-beta suggests that the cytoprotective effect of DAP
117 These data highlight a naturally occurring DAPK-1 mutation that alters the oligomeric structure of
121 demonstrate that the cellular activities of DAPK are critical for antagonizing caspase-dependent apo
124 atory peptides attenuate tryptic cleavage of DAPK-1, suggesting that ligand binding can alter DAPK-1
125 nded to determine whether the degradation of DAPK in the absence of HSP90 activity is dependent on th
126 th geldanamycin (GA) leads to degradation of DAPK, and this degradation is attenuated by the proteaso
131 a suggests that the cytoprotective effect of DAPK is mediated through both intrinsic and extrinsic ap
133 Peg-IFN-alpha up-regulated the expression of DAPK and mTOR, which was associated with the suppression
135 llary RCC demonstrated a higher frequency of DAPK methylation (43%) than clear cell tumours (19%) (P=
139 lts uncover an unexpected interdependence of DAPK-1 and the microtubule cytoskeleton in maintenance o
142 man DAPK-beta, and we examined the levels of DAPK autophosphorylation and DAPK catalytic activity in
143 al HeLa cell lines with attenuated levels of DAPK expression, obtained following selection in the pre
147 04, Fisher's exact test), and methylation of DAPK was detected more frequently in older patients than
148 e results indicate that strict modulation of DAPK activities is critical for regulation of apoptosis
154 tion is also dependent on phosphorylation of DAPK at Ser(308), and the cellular levels of phospho(Ser
155 suggest that RSK-mediated phosphorylation of DAPK is a unique mechanism for suppressing the proapopto
158 into substrate preferences and regulation of DAPK, provide a foundation for proteomic investigations
159 cate that miR-103/107-mediated repression of DAPK and KLF4 promotes metastasis in CRC, and this regul
160 PK and mTOR, we further assessed the role of DAPK and mTOR in the peg-IFN-alpha-induced suppression o
162 the potential profound physiological role of DAPK in neuronal function and pathophysiology, the endog
166 Therefore, we determined the structure of DAPK catalytic domain, used a homology model of docked p
168 esidue extension of the carboxyl terminus of DAPK-beta distinguishes it from the human and mouse DAPK
171 , whereas silencing of mTOR had no effect on DAPK expression, suggesting mTOR may be a downstream eff
172 kinases in vivo has shown that only CHK1 or DAPK-1 can stimulate p53 transactivation and induce Ser(
173 he presence of hypoxia, thereby potentiating DAPK and KLF4 downregulation and hypoxia-induced motilit
176 c activity of PP2A also negatively regulates DAPK levels by enhancing proteasome-mediated degradation
177 noprecipitation showed that STAT3 restricted DAPK expression by promoter binding, thereby reinforcing
182 structure of the death domain, de-stabilizes DAPK-1 binding to ERK, and prevents ERK:DAPK-1-dependent
183 e ligands did, however, strikingly stimulate DAPK activity toward p53, a substrate that shows conserv
185 n vitro ubiquitination assays confirmed that DAPK is targeted for ubiquitination by both CHIP and DIP
189 +, and IgG- subpopulations demonstrated that DAPK hypermethylation was predominantly present in the I
190 using purified components demonstrated that DAPK phosphorylates CaMKK with a stoichiometry of nearly
191 eens and pharmacological tests, we find that DAPK-1 maintains epidermal tissue integrity through regu
197 In situ hybridization experiments show that DAPK mRNA expression is up-regulated in brain following
198 onsistent with previous studies showing that DAPK has a role in promoting caspase-independent cell de
201 e relationship between peg-IFN-alpha and the DAPK-mammalian target of rapamycin (mTOR) pathways.
202 ine L13a is phosphorylated at Ser(77) by the DAPK-ZIPK cascade, but EPRS is phosphorylated only at Se
203 al a previously undescribed function for the DAPK tumor suppressor family in regulation of epithelial
205 We examined whether a nuclear member of the DAPK family named DAPK3 or ZIP kinase had direct links t
207 ients, MSP amplification of a portion of the DAPK promoter followed by PCR product sequencing confirm
208 In conclusion, our data suggest that the DAPK-mTOR pathway is critical for anti-HCV effects of pe
211 ived peptide fragments were found to bind to DAPK; however, these had no stimulatory effect on its ac
215 conserved among protein kinases or unique to DAPK provided a link between structure and activity.
217 er proportion of B cells (1.074-6.026%) were DAPK hypermethylated than were T cells, monocytes, or ne
219 IP-1, thereby providing a mechanism by which DAPK activities can be regulated through proteasomal deg
220 of this kinase and the mechanisms via which DAPK elicits its biological action remain largely unknow
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