戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
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
13 yltrimethylammonium chloride, also activated DGK alpha.
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
17 ey residues required for the function of all DGKs.
18 r, we show that diacylglycerol kinase alpha (DGK-alpha), which phosphorylates diacylglycerol to phosp
19                 Diacylglycerol kinase-alpha (DGK-alpha) was more highly expressed in CD8-TILs compare
20 , which include loss of the GOA-1 G(o)alpha, DGK-1 diacylglycerol kinase, EAT-16 G protein gamma subu
21                          Heterogeneity among DGK family members indicates that individual DGKs may ha
22                              Both anergy and DGK-alpha overexpression were associated with defective
23 OGPOGPO-NH2, substituting KGE, KGD, EGK, and DGK for the YGX sequence.
24             In contrast, GOA-1 (Goalpha) and DGK-1 (diacylglycerol kinase) appear to negatively regul
25      The Rac-associated PtdInsP 5-kinase and DGK copurify by liquid chromatography, suggesting that t
26 ng clear that PA generated via the LPAAT and DGK pathways is also involved in the regulation of mTOR.
27             While inhibition of both PLD and DGK had no effect on the overall ERK activity, inhibitio
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
30 inated Ras activation induced by RasGRP, and DGK activity was required for this mechanism.
31 re mediated by GOA-1 (a Galpha0 subunit) and DGK-1 (a diacylglycerol [DAG] kinase), both of which act
32 cent IIC9 cells indicates that DGK-theta and DGK-delta are both present.
33               In addition, a monoclonal anti-DGK-theta antibody inhibited the alpha-thrombin-stimulat
34 ty requires recruitment of the beta-arrestin-DGK complex to activated 7TMRs.
35 ylating the MARCKS PSD, PKC alpha attenuates DGK zeta activity.
36 tant for the termination of DAG signaling by DGK-1 in vivo.
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
41       Finally, overexpression of kinase-dead DGK zeta in Jurkat cells prolonged Ras activation after
42                       Furthermore, decreased DGK activity also promotes thymic lymphomagenesis accomp
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
47  more rapidly compared with cells expressing DGK zeta S/N that could not be phosphorylated.
48 domains that are thought to be important for DGK function including the cysteine-rich motifs and pote
49 lerance to amino acid substitutions seen for DGK and other membrane proteins.
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
52 K and in the rdgA mutant, lacking functional DGK, implicating DGK.
53                                 We generated DGK-alpha-deficient mice and found that DGK-alpha-defici
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
56                                  To identify DGK domains and amino acid residues critical for termina
57  mutant, lacking functional DGK, implicating DGK.
58 ological inhibition of DGK-alpha activity in DGK-zeta-deficient T cells that received an anergizing s
59 o, we analyzed 20 dgk-1 mutants defective in DGK-1-controlled behaviors.
60     In vivo anergy induction was impaired in DGK-alpha-deficient mice.
61                              LXXLL motifs in DGK-theta mediate a direct interaction of SF1 with the k
62 MARCKS) phosphorylation site domain (PSD) in DGK zeta was phosphorylated in vitro by an active fragme
63 DGK family members indicates that individual DGKs may have unique functions.
64 t as a functional unit during Ca(2+)-induced DGK alpha activation.
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
68                                Thus, type IV DGKs regulate RasGRPs, but the downstream effects differ
69     Diacylglycerol kinase alpha is an 82-kDa DGK isoform that is activated in vitro by Ca(2+).
70                                  DAG kinase (DGK) terminates DAG signaling by converting it to phosph
71  and silenced by ATP, suggesting DAG-kinase (DGK) involvement.
72 dly increases nuclear diacylglycerol kinase (DGK) activity and PA production.
73                       Diacylglycerol kinase (DGK) activity was important for these lipid metabolic ch
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
76                       Diacylglycerol kinase (DGK) catalyzes the conversion of diacylglycerol to phosp
77 racellular signaling; diacylglycerol kinase (DGK) catalyzes the phosphorylation of DAG, which yields
78                       Diacylglycerol kinase (DGK) converts DG into phosphatidic acid.
79 activation of PKC and diacylglycerol kinase (DGK) coupled with upregulation of MAPK (mitogen-activate
80                   The diacylglycerol kinase (DGK) family of enzymes plays critical roles in lipid sig
81                       Diacylglycerol kinase (DGK) from Escherichia coli contains three transmembrane
82 gral membrane protein diacylglycerol kinase (DGK) from Escherichia coli has been reversibly unfolded
83 eric membrane protein diacylglycerol kinase (DGK) from Escherichia coli.
84         We found that diacylglycerol kinase (DGK) inhibitor II (R59949) decreased caspase-3/7 activit
85 l blood flow studies, diacylglycerol kinase (DGK) inhibitor R59949, at various concentrations, was in
86                       Diacylglycerol kinase (DGK) plays a key role in cellular processes by regulatin
87                       Diacylglycerol kinase (DGK) terminates diacylglycerol (DAG) signaling by phosph
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).
91  D (PLD1 and PLD2) or diacylglycerol kinase (DGK), two enzyme classes involved in PA production.
92 acterized the role of diacylglycerol kinase (DGK), which phosphorylates DAG to generate phosphatidic
93 pholipase D (PLD) and diacylglycerol kinase (DGK).
94 ic acid, catalyzed by diacylglycerol kinase (DGK).
95 which is catalyzed by diacylglycerol kinase (DGK).
96                       Diacylglycerol kinase (DGK)zeta is a negative regulator of diacylglycerol-depen
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
99                                 DAG kinases (DGKs) convert DAG into phosphatidic acid, resulting in t
100 cerol (DAG) and the activity of DAG kinases (DGKs) in membranous structures.
101                                 DAG kinases (DGKs) metabolize DAG by converting it to phosphatidic ac
102                Diacylglycerol (DAG) kinases (DGKs) are a family of enzymes that convert DAG to phosph
103                Diacylglycerol (DAG) kinases (DGKs) regulate the intracellular levels of two important
104                      Diacylglycerol kinases (DGKs) catalyze the ATP-dependent phosphorylation of diac
105                      Diacylglycerol kinases (DGKs) inhibit diacylglycerol (DAG) signaling by phosphor
106                      Diacylglycerol kinases (DGKs) phosphorylate diacylglycerol (DAG) to terminate it
107                      Diacylglycerol kinases (DGKs) phosphorylate diacylglycerol produced during stimu
108                      Diacylglycerol kinases (DGKs) terminate signalling from diacylglycerol by conver
109 ically interact with diacylglycerol kinases (DGKs), enzymes that degrade DAG.
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
112                      Diacylglycerol kinases (DGKs), which negatively regulate Ras activity, were upre
113 ible cDNA with substantial homology to known DGKs.
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
116                                  DGK-1, like DGK, has three cysteine-rich domains (CRDs), a pleckstri
117                      We found that a mutant (DGK zeta S/D) in which serines within the MARCKS PSD wer
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.
120  the activity of wild-type DGK zeta, but not DGK zeta S/D, in human embryonic kidney 293 cells.
121                          We isolated a novel DGK, which we designated DGKiota, from human retina and
122 ibroblasts results in an increase in nuclear DGK activity.
123 trate an agonist-induced activity of nuclear DGK-theta activity and a nuclear localization of DGK-del
124 efore, it is expected that the activation of DGK would ameliorate DN.
125 facial association and catalytic activity of DGK-theta are independently regulated.
126 little effect on the membrane association of DGK-theta, suggesting that a triad of enzyme, acidic lip
127 s form a previously uncharacterized clade of DGK domain proteins.
128                     Coimmunoprecipitation of DGK zeta and RasGRP was enhanced in the presence of phor
129                     Thus, precise control of DGK activity is essential for proper signal transduction
130 ing distinct temporal and spatial control of DGK activity to each isozyme.
131 es may serve as the messengers downstream of DGK and PLA2, respectively.
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
134 glycerol levels by conditional expression of DGK-zeta attenuates cell growth.
135              Here we show that a fraction of DGK-zeta is found in the nucleus, where it regulates the
136 s that impair the physiological functions of DGK-1.
137 n in mast cells and reveal the importance of DGK activity during IgE sensitization for proper attenua
138                                Inhibition of DGK activity attenuates the binding of SF1 to the CYP17
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
141                Pharmacological inhibition of DGK-alpha activity in DGK-zeta-deficient T cells that re
142 mice, we determined that the zeta isoform of DGK (DGKzeta) is necessary for the mechanically induced
143                              Ten isoforms of DGK have been identified, and we show that DGKzeta is th
144 theta activity and a nuclear localization of DGK-delta.
145 but not others, regulate the localization of DGK-zeta.
146 by alternating the intracellular location of DGK-zeta.
147 ous application of phorbol esters or loss of DGK-1 (diacylglycerol kinase) rescues ric-8 mutant pheno
148  into TM1 and flanking sites, in a mutant of DGK lacking the two native Cys residues.
149 xpression of a constitutive-active mutant of DGK-alpha drove RCP-dependent invasion in the absence of
150         Twelve enhanced stability mutants of DGK were obtained using a simple screen.
151                            Overexpression of DGK-alpha resulted in a defect in T cell receptor signal
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
154           The nuclear-localization signal of DGK-zeta is located in a region that is homologous to th
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
157                  A complete understanding of DGK catalytic and regulatory mechanisms, as well as phys
158                                  A family of DGKs has been identified in multicellular organisms over
159 ing conditions, T cells lacking DGK-alpha or DGK-zeta proliferated and produced interleukin 2.
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
162                      DGK zeta, but not other DGKs, completely eliminated Ras activation induced by Ra
163  in regulating cellular DG levels than other DGKs.
164                            Homology to other DGKs was apparent in domains that are thought to be impo
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
167                 It has been shown to possess DGK activity when assayed using a medium-chain diacylgly
168 F stimulation, suggesting that PLD2 precedes DGK activation.
169  exons containing the stop codons to produce DGK-1 isoforms that contain the kinase domain.
170                               Using purified DGK-theta, we show that this isoform is subject to dual
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
173 phobic core of the lipid bilayer surrounding DGK in reconstituted membranes.
174                                          Ten DGK family isozymes have been identified to date, which
175  DGKzeta inhibits PKCalpha activity and that DGK activity is required for this inhibition.
176 tively regulates the EGL-30 pathway and that DGK-1 antagonizes the EGL-30 pathway.
177               These results demonstrate that DGK-theta is the isoform responsive to alpha-thrombin st
178 ated DGK-alpha-deficient mice and found that DGK-alpha-deficient T cells had more diacylglycerol-depe
179                          We report here that DGK alpha and zeta synergistically promote T cell matura
180 ted from quiescent IIC9 cells indicates that DGK-theta and DGK-delta are both present.
181                        Finally, we show that DGK-theta directly interacts with, and is activated by,
182 In contrast to previous studies showing that DGK isoforms decrease Ras activity, signaling downstream
183                   These results suggest that DGK regulates melanogenesis via modulation of the posttr
184 ent and tumor suppression, and indicate that DGKs not only terminate DAG signaling but also initiate
185                                          The DGK alpha regulatory region includes tandem C1 protein k
186 the products of the PtdInsP 5-kinase and the DGK have been implicated in several Rac-regulated proces
187 GK peptide has lower thermostability and the DGK peptide is the least thermostable.
188                              We identify the DGK-3 diacylglycerol kinase as a thermal memory molecule
189  KGE and KGD sequences, and the least in the DGK sequence.
190  We demonstrate that the zeta isoform of the DGK family (DGKzeta) is expressed in macrophages (Mphi)
191 s sequence appears to be a new member of the DGK family that we refer to as DGKeta.
192                               Members of the DGK family undergo alternative splicing, generating the
193 onal novel isoform(s) account for all of the DGK-1 function necessary for one behavior, dopamine resp
194 e downstream effects differ depending on the DGK.
195          Lastly, our study revealed that the DGKs involved in the symbiosis form a previously unchara
196 ovel way to regulate Ras activation: through DGK zeta, which controls local accumulation of DAG that
197                                        Thus, DGK activity plays opposing roles in the expansion of CD
198 two stop codon mutants predicted to truncate DGK-1 before its kinase domain that retained significant
199                                          Two DGK family members, delta and eta, contain a sterile alp
200           In n-octylglucoside, the wild-type DGK had a thermal inactivation half-life of 6 min at 55
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
203 ernalization and CCP dynamics, compared with DGK inhibition.
204 ocytic choriomeningitis virus infection, yet DGK-deficient memory CD8(+) T cells exhibit impaired exp

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top