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1 DGK activity was increased in lysates of insect cells in
2 DGK inhibition resulted in a dramatic reduction of cellu
3 DGK inhibitor R59949 injected into the vitreous dose dep
4 DGK zeta also coimmunoprecipitated and colocalized with
5 DGK zeta also coimmunoprecipitated with PKC alpha, sugge
6 DGK zeta, but not other DGKs, completely eliminated Ras
7 DGK-1, like DGK, has three cysteine-rich domains (CRDs),
8 DGK-1, the Caenorhabditis elegans ortholog of human neur
9 DGK-alpha inhibition and provision of IL-2 signals could
10 DGKs regulate Ras signaling by attenuating the function
11 , were upregulated in anergic T cells, and a DGK inhibitor restored interleukin 2 production in anerg
12 otein levels were significantly reduced by a DGK inhibitor, but tyrosinase and microphthalmia-associa
14 E (VtE) ameliorates DN in rat by activating DGK, and we recently reported that VtE specifically acti
15 These retinal hemodynamic parameters after DGK inhibition were comparable to those measured at base
16 ayed from five nondiabetic rat retinas after DGK inhibition and retinal PKC activities were assayed f
18 r, we show that diacylglycerol kinase alpha (DGK-alpha), which phosphorylates diacylglycerol to phosp
20 , which include loss of the GOA-1 G(o)alpha, DGK-1 diacylglycerol kinase, EAT-16 G protein gamma subu
26 ng clear that PA generated via the LPAAT and DGK pathways is also involved in the regulation of mTOR.
28 hat PA was generated sequentially by PLD and DGK in epidermal growth factor (EGF)-stimulated HCC1806
29 ospholipid biosynthesis, whereas the PLD and DGK pathways are activated in response to growth factors
31 re mediated by GOA-1 (a Galpha0 subunit) and DGK-1 (a diacylglycerol [DAG] kinase), both of which act
37 during symbiosis establishment, mediated by DGKs, are required for the mutualistic outcome of the Rh
38 study, we demonstrate that DAG metabolism by DGKs can serve a crucial function in viral clearance upo
39 DAG analogues that cannot be metabolized by DGKs, suggesting that DAG signaling can induce their int
40 tenuate local accumulation of signaling DAG, DGKs may regulate RasGRP activity and, consequently, act
43 1 metabotropic glutamate receptor-dependent DGK activity combined with a loss of Dgkkappa expression
44 se interested in the structure of eukaryotic DGKs, so that they know which expression strategies have
45 ur data support a causal function for excess DGK activity and defective Ras signaling in T cell anerg
46 porting this, we found that cells expressing DGK zeta S/D had higher DAG levels and grew more rapidly
48 domains that are thought to be important for DGK function including the cysteine-rich motifs and pote
50 iating this effect, we knocked down all four DGK isoforms expressed in the brain (beta, gamma, epsilo
51 nd the decrease of tyrosinase resulting from DGK inhibition could be blocked partially by protease in
54 otein that is significantly similar to human DGK-theta, DGKA, was identified in Dictyostelium discoid
55 amino acid residues are present in all human DGKs and likely define key residues required for the fun
58 ological inhibition of DGK-alpha activity in DGK-zeta-deficient T cells that received an anergizing s
62 MARCKS) phosphorylation site domain (PSD) in DGK zeta was phosphorylated in vitro by an active fragme
65 The ATP effect was abolished by inhibiting DGK and in the rdgA mutant, lacking functional DGK, impl
66 bservations that phosphatidylserine inhibits DGK-delta, and constitutively active RhoA inhibits DGK-t
67 lta, and constitutively active RhoA inhibits DGK-theta to identify the activity induced by alpha-thro
74 ey anergy target gene diacylglycerol kinase (DGK) alpha as a focal point, we identified early growth
75 ull-length Sus scrofa diacylglycerol kinase (DGK) alpha or the catalytic domain (alphacat) in Escheri
77 racellular signaling; diacylglycerol kinase (DGK) catalyzes the phosphorylation of DAG, which yields
79 activation of PKC and diacylglycerol kinase (DGK) coupled with upregulation of MAPK (mitogen-activate
82 gral membrane protein diacylglycerol kinase (DGK) from Escherichia coli has been reversibly unfolded
85 l blood flow studies, diacylglycerol kinase (DGK) inhibitor R59949, at various concentrations, was in
88 e identification of a diacylglycerol kinase (DGK) which also associates with both GTP- and GDP-bound
89 n to this problem for diacylglycerol kinase (DGK), an integral membrane protein from Escherichia coli
90 hospholipase D (PLD), diacylglycerol kinase (DGK), and lysophosphatidic acid acyltransferase (LPAAT).
92 acterized the role of diacylglycerol kinase (DGK), which phosphorylates DAG to generate phosphatidic
97 t genetic deletion of diacylglycerol kinase (DGK)zeta, a negative regulator of diacylglycerol-mediate
98 We demonstrated further that DAG kinases (DGKs) alpha and zeta, which terminate DAG-mediated signa
110 tightly regulated by diacylglycerol kinases (DGKs), is a lipid mediator linked to key biologic functi
111 ergy, we manipulated diacylglycerol kinases (DGKs), which are enzymes that terminate diacylglycerol-d
114 anergy-producing conditions, T cells lacking DGK-alpha or DGK-zeta proliferated and produced interleu
115 In the present study, we tested full-length DGK zeta and found that PKC alpha phosphorylated DGK zet
118 with wild-type DGK zeta or a control mutant (DGK zeta S/N) in which the same serines were changed to
119 rhabditis elegans ortholog of human neuronal DGK, inhibits neurotransmission to control behavior.
123 trate an agonist-induced activity of nuclear DGK-theta activity and a nuclear localization of DGK-del
126 little effect on the membrane association of DGK-theta, suggesting that a triad of enzyme, acidic lip
132 onstrate that generation of PA downstream of DGK-alpha is essential to connect expression of mutant p
133 eral T cells abolishes induced expression of DGK-alpha and other anergy genes and restores Ras/MAPK s
137 n in mast cells and reveal the importance of DGK activity during IgE sensitization for proper attenua
139 of the PA production, whereas inhibition of DGK decreased PA production only at the later stages of
140 sidase digestion revealed that inhibition of DGK reduced only the mature form of tyrosinase, and the
142 mice, we determined that the zeta isoform of DGK (DGKzeta) is necessary for the mechanically induced
147 ous application of phorbol esters or loss of DGK-1 (diacylglycerol kinase) rescues ric-8 mutant pheno
149 xpression of a constitutive-active mutant of DGK-alpha drove RCP-dependent invasion in the absence of
152 monstrate a synergistic and critical role of DGK isoforms in T cell development and tumor suppression
153 Ca(2+) regulation, we expressed a series of DGK alpha deletions spanning its regulatory domain in CO
155 SF1 to the CYP17 promoter, and silencing of DGK-theta expression inhibits cAMP-dependent CYP17 trans
156 alpha-thrombin induced the translocation of DGK-theta to the nucleus, implicating that this transloc
160 activity, inhibition of PLD2 but not PLD1 or DGK blocked the nuclear ERK activity in several cancer c
161 noblots) was broader than reported for other DGKs, indicating that DGKeta may play a more general rol
165 zeta and found that PKC alpha phosphorylated DGK zeta on serines within the MARCKS PSD in vitro and i
166 sults indicate that PKC alpha phosphorylates DGK zeta in cells, and this phosphorylation inhibits its
171 he phenyl-Sepharose binding of a recombinant DGK alpha fragment that included both the RVH domain and
172 Cultivation of TILs in low-dose IL-2 reduced DGK-alpha protein levels, increased steady-state phospho
178 ated DGK-alpha-deficient mice and found that DGK-alpha-deficient T cells had more diacylglycerol-depe
182 In contrast to previous studies showing that DGK isoforms decrease Ras activity, signaling downstream
184 ent and tumor suppression, and indicate that DGKs not only terminate DAG signaling but also initiate
186 the products of the PtdInsP 5-kinase and the DGK have been implicated in several Rac-regulated proces
190 We demonstrate that the zeta isoform of the DGK family (DGKzeta) is expressed in macrophages (Mphi)
193 onal novel isoform(s) account for all of the DGK-1 function necessary for one behavior, dopamine resp
196 ovel way to regulate Ras activation: through DGK zeta, which controls local accumulation of DAG that
198 two stop codon mutants predicted to truncate DGK-1 before its kinase domain that retained significant
201 ) had lower activity compared with wild-type DGK zeta or a control mutant (DGK zeta S/N) in which the
202 -acetate inhibited the activity of wild-type DGK zeta, but not DGK zeta S/D, in human embryonic kidne
204 ocytic choriomeningitis virus infection, yet DGK-deficient memory CD8(+) T cells exhibit impaired exp
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