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1 MKP-1 also provided neuroprotection in vivo in a lentivi
2 MKP-1 coordinates both myoblast proliferation and differ
3 MKP-1 deficiency in monocytes and macrophages promotes a
4 MKP-1 is a potential target for modulating regional effe
5 MKP-1 overexpression is also observed with unpredictable
6 MKP-1 serves as a master-regulator of macrophage phenoty
7 MKP-1 was regulated by innate recognition signals and it
8 MKP-1(-/-) mice experienced amplified injury.
9 MKP-1(-/-) or wild-type mice were ventilated with very h
10 MKP-5 controlled JNK to coordinate muscle stem cell prol
11 d to induction of MAP-kinase phosphatase -1 (MKP-1) and dephosphorylation of ERK1/2 in the mammospher
12 ological contribution of MAPK phosphatase 1 (MKP-1) as a nuclear antagonist of both p38 MAPK and JNK
13 ogen-activated protein kinase phosphatase 1 (MKP-1) in blood monocytes, and hematopoietic MKP-1-defic
14 ERK1/2, stabilization of MAPK phosphatase 1 (MKP-1), and induction of TNF-alpha with concomitant down
16 e considered the role of MAPK phosphatase 1 (MKP-1/DUSP1), which catalyzes dephosphorylation and inac
18 ogen-activated protein kinase phosphatase-1 (MKP-1) and enhanced GC inhibition of LPS-induced IL-6.
19 eased phosphorylation of MAPK phosphatase-1 (MKP-1) concomitant with inhibited phosphorylation of p38
20 tivated protein kinase (MAPK) phosphatase-1 (MKP-1) have increased fatty acid oxidation and are prote
22 tivated protein kinase (MAPK) phosphatase-1 (MKP-1) is a critical negative regulator of the MAPKs.
23 ogen-activated protein kinase phosphatase-1 (MKP-1) is a key deactivator of MAP kinases, known effect
24 ogen-activated protein kinase phosphatase-1 (MKP-1) mRNA expression, which inhibits p-p38, was analyz
26 tment, the expression of MAPK phosphatase-1 (MKP-1) was significantly upregulated in human monocytes
27 hanced the expression of MAPK phosphatase-1 (MKP-1), a critical negative regulator of MAPKs that driv
28 ogen-activated protein kinase phosphatase-1 (MKP-1), a negative regulator of ERK1/2, through a protea
29 ogen-activated protein kinase phosphatase-1 (MKP-1), also known as dual specificity phosphatase-1 (DU
30 ogen-activated protein kinase phosphatase-1 (MKP-1), an inducible nuclear phosphatase, by regulating
34 the epitope sequence recognized by the M-18 MKP-1 antibody revealed extensive phosphorylation of two
36 Recent studies show that MAPK phosphatase-3 (MKP-3) promotes gluconeogenic gene transcription in hepa
43 e found that upon LPS stimulation, MKP-1 and MKP-2 accumulated with different kinetics: MKP-1 level p
47 ingly, enhanced stabilities of the MKP-1 and MKP-2 mutants were not associated with decreased ubiquit
48 S stimulation had little effect on MKP-1 and MKP-2 protein levels, but hindered their detection by an
50 two C-terminal serine residues in MKP-1 and MKP-2 to alanine decreased their half-lives, while mutat
52 Remarkably, the stability of both MKP-1 and MKP-2 was markedly decreased in macrophages in the prese
54 We found that Prdx1 bound to both MKP-1 and MKP-5, but dissociated from MKP-1 when the Prdx1 peroxid
55 lipid profiles; however, both MKP-1(+/-) and MKP-1(-/-) mice had significantly less aortic root ather
56 had cytotoxic effects, induced autophagy and MKP-1 expression, and enhanced Dox-induced apoptosis in
57 orer cytoplasmic export of nuclear IRAK3 and MKP-1 stabilization, resulting in increased p38MAPK acti
58 arian tumor-derived cell lines MKP-Liver and MKP-Lung cells reproduce in vivo EMT and represent the f
59 for the p53(DBD).(DP)JNK (274 +/- 14 nm) and MKP-5.(DP)JNK (55 +/- 8 nm) complexes were established;
60 f 3A-KO VSMCs with p53 siRNA reduced p21 and MKP-1 levels and completely restored growth without affe
62 he expression of negative regulators such as MKP-1 may have significant therapeutic potential for tre
65 ight and serum lipid profiles; however, both MKP-1(+/-) and MKP-1(-/-) mice had significantly less ao
71 cates that suppression of JNK1/2 activity by MKP-1 maintains PARP-1 levels and suggests that MKP-1-me
73 ve effects of p38 and JNK MAPK inhibition by MKP-1 without consequence to ERK activation in this stri
74 by preventing its rapid dephosphorylation by MKPs and that the simultaneous activation of p53 and JNK
75 USP9/MKP-4 is unique among these cytoplasmic MKPs in containing a conserved PKA consensus phosphoryla
76 +/+), heterozygous MKP-1(+/-), and deficient MKP-1(-/-) mice were exposed to sea level (SL), Denver a
80 and genetic tools to demonstrate that DUSP1/MKP-1 is an essential non-redundant regulator of UV-indu
81 dual-specificity protein phosphatase DUSP10/MKP-5 negatively regulates muscle stem cell function in
89 ivation of both ERK1/2 and p38alpha by DUSP9/MKP-4 is mediated by a conserved arginine-rich kinase in
90 antibody demonstrates that endogenous DUSP9/MKP-4 is phosphorylated on Ser-58 in response to the PKA
92 PKA signaling and that attenuation of DUSP9/MKP-4 function can mediate cross-talk between the PKA pa
94 ution inhibits both the interaction of DUSP9/MKP-4 with ERK2 and p38alpha in vivo and its ability to
95 ct the intrinsic catalytic activity of DUSP9/MKP-4, phospho-mimetic (Ser-58 to Glu) substitution inhi
96 dy, we identified the MAPK phosphatase Dusp9/MKP-4 by transcriptome analysis as selectively expressed
98 bone marrow megakaryocytes (MKs), embryonic MKPs were CD45(-) and represent an abundant population i
99 ransgenic mice where the Dusp4 gene encoding MKP-2 has been knocked out (MKP-2(-/-) mice), we show th
107 ed IL-6 and TNF-alpha production by BMM from MKP-1(-/-) mice was significantly reduced as compared wi
108 o both MKP-1 and MKP-5, but dissociated from MKP-1 when the Prdx1 peroxidatic cysteine Cys52 was over
110 d primary hippocampal cultures prepared from MKP-2(-/-) mice with no effect on EPSC amplitude observe
112 h these alterations in hippocampal function, MKP-2(-/-) mice show deficits in spatial reference and w
113 ndings strongly suggest that CD49f(H)CD41(H) MKPs are fundamental to promote FL development, as propo
114 Moreover, after removing CD49f(H)CD41(H) MKPs from purified E11.5 FL hepatoepithelial-enriched ce
115 medium conditioned by E11.5 CD49f(H)CD41(H) MKPs produced a partial effect on CD49f(D) cells, induci
118 MKP-1) in blood monocytes, and hematopoietic MKP-1-deficiency in atherosclerosis-prone mice accelerat
124 These results also demonstrate that hepatic MKP-1 overexpression in obesity is causally linked to th
127 tor and MED14, 4.7 kbp upstream of the human MKP-1 gene transcription start site, enhanced binding of
131 esult of MKK3/6 activation and a decrease in MKP-1 expression, thereby leading to an increase in the
132 w that long-term potentiation is impaired in MKP-2(-/-) mice compared with MKP-2(+/+) controls wherea
136 Although hypoxia up-regulated VEGF levels in MKP-1(+/+) MEFs eightfold, only a 70% increase in VEGF e
137 l p-p38 was expressed mostly in microglia in MKP-3 KO mice, and their selective pharmacological inhib
142 ion of the two C-terminal serine residues in MKP-1 and MKP-2 to alanine decreased their half-lives, w
143 to sulfonic acid, which in turn resulted in MKP-1 oxidation-induced oligomerization and inactivity t
146 induced ERK1/2 phosphorylation by increasing MKP-1 expression via a cAMP-PKA-dependent signaling path
151 wn to mediate VitD enhancement of GC-induced MKP-1 production in monocytes via increased production o
153 MKP-1 or NAC treatment blocked 4-HNE-induced MKP-1 degradation, thereby protecting cell from apoptosi
155 pressant treatment normalizes stress-induced MKP-1 expression and behavior, and mice lacking MKP-1 ar
158 increased accumulation of p53, which induces MKP-1, p21, and WIP1, leading to inhibition of G(1) to S
160 l mechanism that implicates PKCepsilon-IRAK3-MKP-1 signaling in the regulation of MAPK activity and i
162 d MKP-2 accumulated with different kinetics: MKP-1 level peaked at approximately 1 h, while MKP-2 lev
163 ptin receptor-deficient (db/db) mice lacking MKP-1 are also resistant to the development of hepatic s
165 y analyses of livers from db/db mice lacking MKP-1 showed suppression of peroxisome proliferator-acti
167 sistent mechanical allodynia in mice lacking MKP-3 (postoperative day 21), concurrently with persiste
169 ndings identify a regulatory circuit linking MKP-1 signaling in DCs, production of polarizing cytokin
172 with immune-suppressive properties modulate MKP-1 expression as part of their mechanism of action.
173 n of the critical anti-inflammatory molecule MKP-1 in response to beta2 -agonists, as well as impaire
175 ents revealed that CD4(+) T cells from naive MKP-2(-/-) mice had decreased cell proliferation and IL-
177 lational modification in the accumulation of MKP-1 and MKP-2 in macrophages following LPS stimulation
178 al cells revealed the specific activation of MKP-5, resulting in decreased p38MAPKalpha activity.
180 ments showed that bone marrow derived DCs of MKP-2(-/-) mice had impaired capability in antigen prese
181 dings demonstrate that chronic deficiency of MKP-1 leads to decreased atherosclerosis via mechanisms
185 dings strongly suggest that dysregulation of MKP-3 prevents spontaneous resolution of acute postopera
188 sion, it markedly enhanced the expression of MKP-1 in cells stimulated by LPS, in a similar manner an
191 c stress promoted the S-glutathionylation of MKP-1, targeting MKP-1 for proteasomal degradation.
192 -induced oligomerization and inactivation of MKP-5 so that activation toward p38MAPK was maintained.
193 P-1 expression and enhanced DEX induction of MKP-1 in both patients with SS asthma and patients with
195 horylated ERK1/2, whereas siRNA knockdown of MKP-1 blocked progestin-mediated ERK1/2 dephosphorylatio
199 crophage content was increased in lesions of MKP-1LeuKO mice compared to mice that received wildtype
200 varian cancer cells expressed high levels of MKP-1 and PARP-1 proteins, and that silencing MKP-1 or P
201 on and migration and showed that the loss of MKP-1 activity is a critical step in monocyte priming an
203 diabetic conditions resulted in the loss of MKP-1 protein levels, the hyperactivation of ERK and p38
207 induced cell death whereas overexpression of MKP-1 protects macrophages against metabolic stress-indu
209 ovide new insights into a functional role of MKP-1 in oxidative stress-induced cell death by regulati
210 2 deactivation, further supporting a role of MKP-1 in the anti-inflammatory mechanism of mapracorat.
213 kout, an antagonist, or a local silencing of MKP-1 attenuates depressive-like behaviors, pointing to
215 horylation of p38 MAP kinase, a substrate of MKP-1, as well as alpha smooth muscle actin (alphaSMA) e
217 n, this study identified the upregulation of MKP-1 by vitamin D as a novel pathway by which vitamin D
219 t studies have identified novel functions of MKPs in development, the immune system, and cancer.
221 rior to LPS stimulation had little effect on MKP-1 and MKP-2 protein levels, but hindered their detec
224 p4 gene encoding MKP-2 has been knocked out (MKP-2(-/-) mice), we show that long-term potentiation is
225 to inhibiting hepatic fatty acid oxidation, MKP-1 promotes hepatic lipogenic gene expression through
226 97 and its cofactor, UBXD8, destabilize p21, MKP-1, and SIRT1, three established mRNA targets of the
227 at dendritic cell (DC)-expressed phosphatase MKP-1, a negative regulator of the MAP kinases, programm
228 we have identified nuclear MAPK phosphatase MKP-1 as a novel molecular target of ROS in TGF-beta sig
229 ear dual-specificity MAP kinase phosphatase (MKP) DUSP2, a known regulator of the ERK and p38 MAPKs,
231 vented its inactivation by MAPK phosphatase (MKP)-5; however, JNK was still able to phosphorylate c-J
237 togen-activated protein kinase phosphatases (MKPs) play key roles in inflammation and immune mediated
238 togen-activated protein kinase phosphatases (MKPs), directly inactivate MAPKs through dephosphorylati
242 which are inactivated by MAPK phosphatases (MKPs), represent a central signaling node in the regulat
245 the post-translational regulation of a plant MKP in vivo, adding an additional regulatory layer to MA
247 on of Prdx1-Cys52 was enhancing in the Prdx1:MKP-5 complex with increasing amounts of H(2)O(2) concen
249 The embryonic megakaryocyte progenitors (MKPs) in the E11.5 FL were identified as CD49f(H) CD41(H
250 s by overexpressing glutaredoxin 1 protected MKP-1 from degradation and normalized monocyte adhesion
251 MKP-1-deficient bone marrow into LDL-R(-/-) (MKP-1LeuKO) mice accelerated high-fat diet (HFD)-induced
253 iting the expression of a negative regulator MKP-1, which in turn leads to enhanced MAPK ERK activati
255 Introduction of a degradation-resistant MKP-1 mutant effectively attenuated luteolin-induced JNK
257 KP-1 and PARP-1 proteins, and that silencing MKP-1 or PARP-1 increased cisplatin sensitivity in resis
258 While mapracorat alone did not stimulate MKP-1 expression, it markedly enhanced the expression of
261 il a novel pathway consisting of superoxide, MKP-1, and JNK for luteolin's cytotoxicity in lung cance
262 esting that inhibition of the JNK suppressor MKP-1 plays a major role in luteolin-induced lung cancer
265 appaBalpha with MKP-1, and demonstrated that MKP-1 was a pivotal feedback control for both MAP kinase
266 -1 expression was supported by findings that MKP-1 and PR mRNA levels were significantly correlated i
273 Collectively, these findings suggest that MKP-1 is a critical mediator of anti-proliferative and a
274 Therefore, our data strongly suggest that MKP-1 might be the key regulator of vascular densities t
275 ogenic actions of the MAPKs and suggest that MKP-5 may serve as a target to promote muscle stem cell
276 -1 maintains PARP-1 levels and suggests that MKP-1-mediated cisplatin resistance can be bypassed by P
277 crophage activation, our study suggests that MKP-2 is essential to the pathogenic response of EAE, an
280 the ERK and p38 MAPKs, is unique amongst the MKP family in being able to bind to both ERK3 and ERK4.
282 Surprisingly, enhanced stabilities of the MKP-1 and MKP-2 mutants were not associated with decreas
283 oid response element 4.6 kbp upstream of the MKP-1 gene were significantly lower in monocytes from pa
284 n the glucocorticoid response element of the MKP-1 promoter in monocytes were analyzed by means of ch
285 6-kbp glucocorticoid response element of the MKP-1 promoter in the presence of GM-CSF in U937 cells.
286 esterone response elements downstream of the MKP-1 transcription start site to up-regulate MKP-1 prom
292 priming effects of metabolic stress, whereas MKP-1 overexpression blunted both MAPK activation and mo
293 the underlying molecular mechanism by which MKP-1 expression is negatively regulated during S. pneum
294 Here we investigated the mechanisms by which MKP-2 modulates central nervous system (CNS) inflammatio
295 as to determine the mechanisms through which MKP-1 deficiency in monocytes and macrophages promotes a
298 is impaired in MKP-2(-/-) mice compared with MKP-2(+/+) controls whereas neuronal excitability, evoke
300 nteractions of p38, ERK or IkappaBalpha with MKP-1, and demonstrated that MKP-1 was a pivotal feedbac
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