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1                                              p38delta binds to ACO1, and p38delta expression in p38ga
2                                              p38delta can be activated by MKK3 and MKK6, known activa
3                                              p38delta counteracts the activity of its downstream targ
4                                              p38delta is highly expressed in salivary gland, pituitar
5                                              p38delta phosphorylates ATF-2 and PHAS-I, but not MAPK-a
6 t on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal kinase, another stress-
7 n kinase C isoforms, Ras, MEKK1, MEK3, and a p38delta-extracellular signal regulated kinase 1/2 compl
8 rding this inverse regulation, we describe a p38delta-ERK1/2 complex that may coordinate these change
9                               Thus, aberrant p38delta-PKD1 signaling in neutrophils may underlie deve
10 se 3 (MLK3) and IB2 synergistically activate p38delta but not the MAPKs JNK-1 and p38alpha.
11 accompanied by increased levels of activated p38delta, and synergistic activation of p38delta by MLK3
12                        caMEK6 also activates p38delta, but p38delta inhibits the caMEK6-dependent act
13 sent studies suggest that PKCdelta activates p38delta leading to increased p21(Cip1) promoter activit
14  keratinocyte differentiation that activates p38delta phosphorylation leading to increased differenti
15                  p38delta binds to ACO1, and p38delta expression in p38gamma/delta(-/-) cells fully r
16 ovel regulatory pathway involving CITED2 and p38delta, which may be critical for the maintenance of a
17 38gamma were involved in induction, ERK2 and p38delta played no role in TNF-alpha-dependent promoter
18 8alpha, which increases gene expression, and p38delta, which decreases gene expression.
19 MAPK (MAPK14) proteins p38gamma (MAPK12) and p38delta (MAPK13) were recently shown to modulate the im
20                                 p38alpha and p38delta are the most abundant isoforms expressed by all
21 activated the p38 MAPK isoforms p38alpha and p38delta in wild-type (Mkk3+/+) mesangial cells, but not
22             Thus, activation of p38alpha and p38delta is dependent on the activation of upstream MKK3
23 -state culture conditions, both p38alpha and p38delta isoforms are increasingly phosphorylated activa
24 tion is required for subsequent p38alpha and p38delta MAPK activation and collagen stimulation by TGF
25 st a critical role for the MKK3-p38alpha and p38delta MAPK pathway in mediating VEGF164 isoform-speci
26    However, opposing actions of p38alpha and p38delta negate any effect on TonEBP/OREBP activity.
27 of dominant negative mutants of p38alpha and p38delta resulted in marked inhibition of TGF-beta1-indu
28                 In macrophages, p38alpha and p38delta were abundant, but p38beta was undetected.
29                                 p38alpha and p38delta were also expressed by neutrophils, CD4+ T cell
30 p38 MAPk isoforms studied, only p38alpha and p38delta were detected in neutrophils.
31  because of opposing effects of p38alpha and p38delta, and effects of inhibitors of p38 depend on whi
32 ctivation of p38 MAPK isoforms, p38alpha and p38delta, and stimulation of pro-alpha1(I) collagen by T
33 xplained by opposing effects of p38alpha and p38delta, both of which are activated by high NaCl and i
34 er MAP kinases including ERK2, p38alpha, and p38delta and showed little inhibitory activity against a
35                   In addition, p38alpha- and p38delta-MAPK were identified as suppressors of AR expre
36 e positive and negative roles of p38beta and p38delta in AP-1 regulation, MKK6 stimulates AP-1-depend
37            Evidence implicating p38gamma and p38delta (p38gamma/p38delta) in inflammation are mainly
38                                 p38gamma and p38delta (p38gamma/p38delta) regulate inflammation, in p
39 her, our results establish that p38gamma and p38delta are central to colitis-associated colon cancer
40 Together, our results establish p38gamma and p38delta as key components in innate immune responses.
41 esponse to injury, and validate p38gamma and p38delta as potential targets for cancer therapy.
42  Here, we show that deletion of p38gamma and p38delta impaired the innate immune response to lipopoly
43         We analyzed the role of p38gamma and p38delta in colon cancer associated to colitis using the
44  p38alpha with selectivity over p38gamma and p38delta isoforms.
45 owever, the role of the related p38gamma and p38delta kinases has remained unclear.
46                                 p38gamma and p38delta were necessary to maintain steady-state levels
47 in mammals (p38alpha, p38beta2, p38gamma and p38delta).
48             p38alpha, p38beta, p38gamma, and p38delta are four isoforms of p38 mitogen-activated prot
49  the first time that p38alpha, p38gamma, and p38delta down-regulate fibulin 3 expression.
50 ly members (p38alpha, p38beta, p38gamma, and p38delta) that are activated by MKK3 and MKK6.
51 ily, including ERK5, p38alpha, p38gamma, and p38delta, and that the activation of certain kinases act
52 specific for the combination of PKCdelta and p38delta and is not produced by replacing PKCdelta with
53 e apoptosis, promotes identical PKCdelta and p38delta-ERK1/2 activity changes, leading to similar mor
54        Protein kinase C delta (PKCdelta) and p38delta are key proteins in a cascade that stimulates k
55 53 is an intermediary in this regulation, as p38delta expression increases p53 mRNA, protein, and pro
56 embers, with p38beta higher in 3T3 cells but p38delta only detected in the EMT-6 line.
57          caMEK6 also activates p38delta, but p38delta inhibits the caMEK6-dependent activation.
58 e regulation of the focal adhesion kinase by p38delta in the human breast cell lines.
59  cell growth is synergistically regulated by p38delta isoform, whereas nuclear factor kappa B (NFsmal
60                      In addition, concurrent p38delta activation and extracellular signal-regulated k
61   We further show that exogenously expressed p38delta increases p21(Cip1) mRNA and protein and that p
62 s define a previously unappreciated role for p38delta in breast cancer development and evolution by r
63 indings strongly suggest an in vivo role for p38delta in promoting cell proliferation and tumor devel
64 ylated, and FHF can serve as a substrate for p38delta in vitro.
65                        This study implicates p38delta mitogen-activated protein kinase (MAPK) as a do
66                                 Importantly, p38delta and PKD1 conversely regulate PTEN activity in n
67 ced susceptibility to skin carcinogenesis in p38delta-null mice involves a defect in proliferative re
68 th lung metastasis; however, mice deleted in p38delta (PyMT/p38delta(-/-)) exhibited delayed primary
69  to IB2(Delta1-436) and can thereby increase p38delta interaction with IB2(Delta1-436).
70 PRMT5 knockdown is associated with increased p38delta phosphorylation, suggesting that PRMT5 impacts
71 tivated protein kinase (MAPK) delta isoform (p38delta) is a poorly studied member of the MAPK family.
72            Here, we show that p38 MAP kinase p38delta is required for recruitment of neutrophils into
73                            The novel kinase, p38delta, has a nucleotide sequence encoding a protein o
74 ressing kinase-inactive p38gamma and lacking p38delta.
75                   In addition, cells lacking p38delta also displayed an increased cell-matrix adhesio
76                  We report that mice lacking p38delta gene exhibited a marked resistance to developme
77                     This study proposes MAPK p38delta protein as a key factor in breast cancer.
78 g to IB2 facilitates recruitment of the MAPK p38delta (SAPK4), while failing to stimulate binding of
79 , involucrin (hINV), via a Ras, MEKK1, MEK3, p38delta signaling cascade.
80 propose that PKCdelta activates a MEKK1/MEK3/p38delta MAPK cascade to increase p53 levels and p53 dri
81 ing module in which IB2 scaffolds a MLK3/MKK/p38delta kinase cascade.
82               Silencing of p38alpha, but not p38delta, using siRNA suppressed MDA-MB-468 cell prolife
83 ated p38delta, and synergistic activation of p38delta by MLK3 and IB2 is further enhanced by FHF2.
84 ation of p38alpha and a lesser activation of p38delta in LPS-stimulated macrophages.
85 ctive form of MEK6, an upstream activator of p38delta, can also produce cell death when coupled with
86 e other p38 isoforms, the kinase activity of p38delta is not blocked by the pyridinyl imidazole, 4-(4
87 2 minimally inhibited the kinase activity of p38delta.
88                         Dot-blot analysis of p38delta mRNA in 50 human tissues revealed a distributio
89                                   Binding of p38delta to IB2 is mediated by the carboxyl-terminal hal
90 will be needed to define the contribution of p38delta to macrophage, neutrophil, and T cell functions
91    Global and myeloid-restricted deletion of p38delta in mice results in decreased alveolar neutrophi
92 resent study, we have assessed the effect of p38delta deficiency on skin tumor development in vivo by
93 nant form of p38 in monocytes; expression of p38delta was low and p38beta was undetected.
94       We demonstrate a direct interaction of p38delta with PKCdelta and MEK3 and show that exogenous
95            Also, siRNA-mediated knockdown of p38delta enhances the activation of TonEBP/OREBP.
96                                      Lack of p38delta resulted in reduced primary tumor size and bloc
97 TonEBP/OREBP activity, but overexpression of p38delta reduces it.
98 alpha, but primarily mono-phosphorylation of p38delta.
99 n tissues revealed a distribution profile of p38delta that differs from p38alpha.
100                   FHF-induced recruitment of p38delta to IB2 is accompanied by increased levels of ac
101 ular level, we demonstrate that targeting of p38delta in breast cancer cells, MCF-7 and MDA-MB-231 re
102 VHL, resulting in degradation of p38alpha or p38delta.
103  reverted by knocking out either p38gamma or p38delta or by inhibiting the mTOR pathway with rapamyci
104 duced by replacing PKCdelta with PKCalpha or p38delta with p38alpha.
105                   In this model, PKCdelta or p38delta knockdown results in reduced p53 and p21(Cip1)
106                               Like p38alpha, p38delta is activated by cellular stress and proinflamma
107 ng increases MKK4, which activates p38gamma, p38delta, and JNK2 to phosphorylate p53 on Ser-33 and ca
108 nine, the corresponding residue in p38gamma, p38delta, and the JNKs, rendered all five inhibitors ine
109 2, JNK3); p38s (p38alpha, p38beta, p38gamma, p38delta) and ERK5.
110                          Silencing p38gamma, p38delta, or JNK2 partially rescued G(1) arrest from SEP
111 n cancer model in wild-type (WT), p38gamma-, p38delta-, and p38gamma/delta-deficient (p38gamma/delta(
112                                     p38gamma/p38delta interacts with the TPL2/A20 Binding Inhibitor o
113                       Additionally, p38gamma/p38delta regulates TPL2 mRNA translation by modulating t
114  levels are dramatically reduced in p38gamma/p38delta-deficient (p38gamma/delta(-/-)) cells and tissu
115                  This could obscure p38gamma/p38delta roles, since TPL2 is essential for regulating i
116  implicating p38gamma and p38delta (p38gamma/p38delta) in inflammation are mainly based on experiment
117              p38gamma and p38delta (p38gamma/p38delta) regulate inflammation, in part by controlling
118 xcellent tool to elucidate specific p38gamma/p38delta functions.
119          These results suggest that p38gamma/p38delta govern innate immune responses by regulating ME
120                        We show that p38gamma/p38delta posttranscriptionally regulates the TPL2 amount
121 deltaKIKO macrophages revealed that p38gamma/p38delta-regulated numerous genes implicated in innate i
122 D) was phosphorylated at Ser444 via p38gamma/p38delta.
123 es by MKK6 and/or arsenite, whereas p38gamma/p38delta inhibits or has no effect on the stimulation.
124                                     PKCdelta/p38delta signaling, a key controller of keratinocyte pro
125 understand the relationship between PKCdelta/p38delta and PRMT5/MEP50 signaling.
126 describe an opposing action between PKCdelta/p38delta MAPK signaling and PRMT5/MEP50 epigenetic silen
127  is an example of crosstalk between PKCdelta/p38delta signaling and PRMT5/MEP50 epigenetic silencing.
128                We further show that PKCdelta/p38delta signaling suppresses MEP50 expression, leading
129            We further show that the PKCdelta/p38delta keratinocyte differentiation cascade reduces PR
130 sis; however, mice deleted in p38delta (PyMT/p38delta(-/-)) exhibited delayed primary tumor formation
131                                Reciprocally, p38delta overexpression induced IL-6 biosynthesis.
132                                        SAPK4/p38delta phosphorylated eEF2K at Ser359 in vitro, causin
133 cts that was phosphorylated rapidly by SAPK4/p38delta, but poorly by SAPK2/p38, SAPK3/p38gamma, SAPK1
134 expression of a catalytically inactive SAPK4/p38delta mutant, suggesting that SAPK4/p38delta may medi
135 st that activates all SAPKs, including SAPK4/p38delta.
136 SAPK4/p38delta mutant, suggesting that SAPK4/p38delta may mediate the inhibition of eEF2K by this str
137 skin tumor development in vivo by subjecting p38delta knockout mice to a two-stage 7,12-dimethylbenz(
138 itogen-activated protein kinases here termed p38delta.
139 ted to play an important role in terminating p38delta activation responsible for IL-6 biosynthesis.
140 ncreases p21(Cip1) mRNA and protein and that p38delta knockdown or expression of dominant-negative p3
141 a new member of the p38 MAPK family and that p38delta likely has functions distinct from that of p38a
142                            This finding that p38delta isoform promotes the phosphorylation of ERK1/2
143     Taken together, these data indicate that p38delta is a new member of the p38 MAPK family and that
144                        We also observed that p38delta was strongly activated by MKK3 and MKK6, while
145           Sequence comparisons revealed that p38delta is approximately 60% identical to the other thr
146 e Cancer Genome Atlas database revealed that p38delta is highly expressed in all types of human breas
147          The data presented herein show that p38delta has many properties that are similar to those o
148               Recent studies have shown that p38delta, a p38 family member, functions as an important
149            Our previous studies suggest that p38delta exists in association with protein partners.
150 se assays and inhibitor studies suggest that p38delta is the p38 isoform responsible for the regulati
151                       Lastly, we explore the p38delta:PROTAC:VHL complex to explain the different sel
152                             Furthermore, the p38delta isoform was identified as a novel and predomina
153 orylation, suggesting that PRMT5 impacts the p38delta signaling complex.
154 sion, and PRMT5 dimethylates proteins in the p38delta complex.
155 e methyltransferase 5 (PRMT5) as part of the p38delta signaling complex.
156 , CITED2 up-regulation in vitro requires the p38delta isoform, which is specifically phosphorylated b
157                    We further show that this p38delta-ERK1/2 complex relocates into the nucleus in re
158                              The p38alpha to p38delta mitogen-activated protein kinases (MAPKs) are c
159  late differentiating erythroblasts, whereas p38delta mRNA is only expressed and active during the te
160 an also produce cell death when coupled with p38delta.
161   We show that coexpression of PKCdelta with p38delta produces profound apoptosis-like morphological

 
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