ライフサイエンスコーパス: arginase

1 , including PGE2, inducible NO synthase, and arginase.

2 4Ralpha mediates IL-13-induced production of arginase.

3 nfiltration of M2-type macrophages producing arginase.

4 d kidney activity of the Mn-dependent enzyme arginase.

5 Arginase 1 (40-fold) and IL-10 (265-fold) were higher in

6 A majority of OSM(+) neutrophils expressed arginase 1 (72.5% +/- 12%), suggesting an N2 phenotype.

7 these enzymes, a pegylated human recombinant arginase 1 (AEB1102), reduces plasma arginine in murine

8 n, such as stripes of macrophages expressing arginase 1 (ARG1) and mannose receptor, C type 1 (MRC1).

9 Arginase 1 (Arg1) and nitric oxide synthases compete for

10 Of the RAGs examined, only arginase 1 (Arg1) expression correlated with the increas

11 ginase deficiency is caused by deficiency of arginase 1 (ARG1), a urea cycle enzyme that converts arg

12 In contrast with PD-L1, arginase 1 (Arg1), which exerts T cell suppression at an

13 n markers, were specifically responsible for arginase 1 activity.

14 reduced inducible nitric oxide synthase and arginase 1 and displayed a reduced T-cell suppressive ac

15 ell proliferation and express high levels of Arginase 1 and iNOS.

16 This process is under tight control by arginase 1 and is of functional importance during ischem

17 er cells stimulated with palmitate, enhanced arginase 1 and lower leukotriene B4 (LTB4) levels were d

18 m of l-Arginine (l-Arg), through the enzymes arginase 1 and NO synthase 2 (NOS2), is well documented

19 hat rodent and human RBCs contain functional arginase 1 and that pharmacological inhibition of argina

20 and decreased M2 macrophages that expressed Arginase 1 and were found in inflammatory zone protein (

21 More specifically, G-MDSCs producing arginase 1 are associated with a higher incidence of nos

22 MDSCs expressing arginase 1 are induced by PI.

23 r cells expressing inducible NO synthase and arginase 1 are induced.

24 show that the lactate-induced expression of arginase 1 by macrophages has an important role in tumou

25 erse physiological and anatomical markers of arginase 1 deficiency and therefore may be of therapeuti

26 Arginase 1 deficiency is a urea cycle disorder associate

27 Moreover, Nr4a2 transcriptionally activates arginase 1 expression by directly binding to its promote

28 We find that the loss of arginase 1 expression results in decreased dendritic com

29 eptors led to strikingly increased levels of arginase 1 gene expression and protein activity in infec

30 rophages induced NO synthase 2 and inhibited arginase 1 gene expression.

31 Hepatic arginase 1 gene therapy using adeno-associated virus res

32 alpha levels and the expression of M2 marker Arginase 1 in inflammatory-elicited macrophages.

33 e (iNOS), reactive oxygen species (ROS), and arginase 1 inhibitors.

34 9) had significantly higher mononuclear cell arginase 1 mRNA, protein, and enzyme activity; lower NOS

35 cells via a CD18-mediated contact-dependent arginase 1 release.

36 by adoptively transferring MDSC or injecting arginase 1 to noninjured mice.

37 MDSCs expressing arginase 1 were measured by flow cytometry.

38 ls of MDSC mediators S100A8/A9, S100A12, and arginase 1 were significantly increased.

39 ulating factor 1 receptor (CSF-1R)-dependent arginase 1(+) myeloid cells enhanced NO-dependent tumor

40 es express significantly increased levels of arginase 1, a biomarker of the alternatively activated M

41 n the peritoneum, which expressed functional arginase 1, and potently suppressed T cell proliferation

42 High initial levels of G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were associated

43 Decompartmentalized hemoglobin, arginase 1, asymmetric dimethylarginine, and adenine nuc

44 on as in wild-type mice, though TSLP-induced arginase 1, CCL2, and matrix metalloproteinase 12 messen

45 ced expression of protumor type 2 molecules (arginase 1, Fizz 1, Mgl, and IDO), number of M2-type mac

46 pression of the pro-Th1 mediators Fizz-1 and arginase 1, indicating that it could promote proinflamma

47 d 1 and 2, but not CD40, TGF-beta signaling, arginase 1, or iNOS, inhibited nTreg proliferation in co

48 markers for alternative activation, such as Arginase 1, with concomitant downregulation of inducible

49 nciding with an induction of MDSC expressing arginase 1.

50 phenotype as determined by the expression of arginase 1.

51 r and expression of an M2 macrophage marker, arginase-1 (Arg 1) was lower in tumors from ogr1(-/-) mi

52 increased gene expression for the M2 markers Arginase-1 (Arg-1) and Fizz-1, which are classically ind

53 Arginase-1 (Arg-1) was found promote suppression because

54 nd involved complement, activating FcRs, and Arginase-1 (Arg1) activity.

55 Arginase-1 (Arg1) also metabolizes l-arginine but does n

56 alternative macrophage activation including arginase-1 (ARG1) and mannose receptor (CD206).

57 we demonstrate that expression of the enzyme arginase-1 (Arg1) during acute or chronic lung inflammat

58 expression of the anti-inflammatory mediator arginase-1 (P = 0.005), and a sustained reduction in ski

59 educing anti-inflammatory cytokine IL-10 and arginase-1 activities, suggesting a dominant classically

60 mouse population infected with Mtb, enhanced arginase-1 activity was associated with increased lung i

61 and expressed macrophage mannose receptors, arginase-1 activity, and IL-10.

62 Intravascular venous levels of arginase-1 and cell-free plasma hemoglobin increase imme

63 that aged stored blood has higher levels of arginase-1 and cell-free plasma hemoglobin.

64 red a Wnt6-dependent induction of macrophage Arginase-1 and downregulation of TNF-alpha.

65 shown that the mRNA expression levels of the arginase-1 and inducible NO synthase genes, which charac

66 RHI correlated negatively with arginase-1 and positively with l-arginine (P = .001).

67 haracterized by the up-regulation of YM1 and arginase-1 and the down-regulation of inducible nitric o

68 t inhibition of the anti-inflammatory factor arginase-1 by c-Jun.

69 Arginase-1 expression was reduced in the brain during la

70 Both iNOS and arginase-1 expression were reduced in peritoneal macroph

71 sion as evidenced by increased expression of arginase-1 in CD11b(+)Gr1(+) cells, diminished M1 functi

72 l co-culture system, we show that macrophage arginase-1 is the only factor required by M2 macrophages

73 ic tumors of Bcl11b(F/F)/CD4-Cre mice, their arginase-1 levels were severely reduced.

74 and correlates with hypoargininemia and high arginase-1 levels.

75 fferentially regulating cyclooxygenase-2 and arginase-1 levels.

76 vitamin D in skin homeostasis, and implicate arginase-1 upregulation as a previously unreported mecha

77 Here, we identify extrahepatic arginase-1(+) Id2(+) fetal ILC precursors that express a

78 macrophages and a concomitant enhancement in arginase-1(+) M2 macrophages.

79 Plg/Pla also increased M2 markers (CD206 and arginase-1) and secretory products (transforming growth

80 Pulmonary endothelial deletion of arginase-1, a downstream target of HIF-2alpha, likewise

81 t with the expression of IFN-gamma, but also Arginase-1, a functional antagonist of the iNOS pathway,

82 In addition, the expression of arginase-1, a marker for anti-inflammatory macrophages,

83 602S/S individuals resist induction of host arginase-1, an enzyme that depletes cellular arginine st

84 (EndoPAT), and plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine were measure

85 teins: vascular endothelial growth factor-A, Arginase-1, and CCL2, similarly shown in tumor-associate

86 including LIGHT, sphingosine kinase 1, CCL1, arginase-1, and costimulatory molecules, CD16/32, ICAM-1

87 vated iNKT cells, and inducible NO synthase, arginase-1, and IL-10 produced by MDSCs, contributed to

88 ve Mvarphi activation markers, such as YM-1, arginase-1, and interleukin-10 by activation of mer rece

89 atory phenotype with reduced iNOS, increased Arginase-1, and lower wound tumor necrosis factor alpha

90 DSCs not only produced high levels of NO and arginase-1, but also greatly increased levels of chemoki

91 egulation of genes relevant to MDSCs such as arginase-1, IDO1, PDL1, and IL-10 at the injection site.

92 ny genes were similarly perturbed, including Arginase-1, IL-10, TREM1, and IFN signaling, revealing t

93 type counterparts due to lower expression of arginase-1, IL6, and phospho-Stat3.

94 Both subsets produced Arginase-1, inducible nitric oxide synthase (iNOS), and

95 d from S. aureus biofilms revealed increased arginase-1, inducible NO synthase, and IL-10 expression,

96 y elevated expression of mannose receptor-1, Arginase-1, interleukin-10 and transforming growth facto

97 s previously associated with AA-MPhis (e.g., arginase-1, mannose receptor, CCL2, CCL17, and CCL22).

98 companied by reduced expression of CD206 and arginase-1, markers for AAMs.

99 rleukin-10, transforming growth factor-beta, arginase-1, matrix metalloproteinase and vascular endoth

100 oduction of the immune-suppressive cytokines arginase-1, TGF-beta, and IL-10 by MDSC, concomitant wit

101 correlated with increased serum activity of arginase-1, which was elevated in TB patients coinfected

102 ker iNOs and diminish that of the M2 markers Arginase-1, Ym-1, and FIZZ-1.

103 i infection resulted in accumulation of high arginase-1-expressing macrophages in the lung, which for

104 a indicate that helminth coinfection induces arginase-1-expressing type 2 granulomas, thereby increas

105 reventing a subsequent increase in CD163 and arginase-1.

106 inflammatory macrophage mannose receptor and arginase-1.

107 Controlling for arginase 2 mRNA/protein did not impact any functional ou

108 our-necrosis factor-alpha production through arginase-2 activity.

109 Neonatal CD71(+) cells express the enzyme arginase-2, and arginase activity is essential for the i

110 atory mediators tumor necrosis factor-alpha, arginase-2, interleukin-1beta, interleukin-6, and interf

111 Helicobacter pylori arginase, a bimetallic enzyme, is crucial for pathogenes

112 production in the glioma microenvironment of arginase, a marker of myeloid suppressor cells, which is

113 el molecular mechanism drives OxLDL-mediated arginase activation, endothelial NOS uncoupling, endothe

114 ylcarboxamidoadenosine (NECA) increased both arginase activity (EC(50)=261.8 nM) and TIMP-1 productio

115 tory cytokines, whereas late MDSCs expressed arginase activity and anti-inflammatory interleukin 10 (

116 iR-210 modulated MDSC function by increasing arginase activity and nitric oxide production, without a

117 Induction of arginase activity and parasite growth involved C-type le

118 Mechanistically, IND reduced arginase activity as well as NO and reactive oxygen spec

119 lation with IFN-gamma, we observed that MPhi arginase activity did not inhibit production of NO deriv

120 ively with lung function and positively with arginase activity in CF airway fluid.

121 The rapid increase in arginase activity in human aortic endothelial cells expo

122 ceptors, because mannose injection decreased arginase activity induction and parasite load in vitro a

123 Arginase activity induction in macrophages is an escape

124 (+) cells express the enzyme arginase-2, and arginase activity is essential for the immunosuppressive

125 Finally, we demonstrate that the arginase activity of neuroblastoma impairs NY-ESO-1-spec

126 Neuroblastoma arginase activity results in inhibition of myeloid cell

127 However, arginase activity was high in CF airway fluid and minima

128 CD11b(+)GR-1(+) myeloid cells with enhanced arginase activity, identified as myeloid-derived suppres

129 with tetrahydrobiopterin oxidation and high arginase activity, leading to endothelial nitric oxide s

130 )-dependent mechanism that is independent of arginase activity, PD-1-PD-L1 expression, and interleuki

131 ever, L-arginine supply can be restricted by arginase activity, resulting in inefficient NO output an

132 press T-cell proliferation through increased arginase activity.

133 hages, determined by cytokine production and arginase activity.

134 ine aortic intima with a concomitant rise in arginase activity.

135 children cannot be fully explained by plasma arginase activity.

136 ed (13)C probe, [6-(13)C]-arginine, to image arginase activity.

137 hesis pathway, it relies mainly upon its own arginase-AdoMetDC/ODC pathway to acquire the polyamines

138 ach of targeting secreted arginine through l-arginase, along with targeting microenvironment-secreted

139 nd the substrate arginine (via inhibition of arginase), among other targets.

140 Under the same conditions, the enzymes arginase and agmatinase accelerate substrate hydrolysis

141 t (in contrast to the mechanisms employed by arginase and agmatinase) is believed to involve attack b

142 f a diverse set of enzymatic proteins (e.g., arginase and glutamine synthase).

143 dulated through small-molecule inhibitors of arginase and inducible nitric oxide synthase, suggesting

144 Blocking arginase and inducible NO synthase did not restore B lym

145 bited Th2 ACT, consistent with a key role of arginase and M2 macrophages in myeloma elimination by Th

146 the suggested competitive metabolism by the arginase and NO synthase pathways.

147 ough arginine depletion in the media using l-arginase and NOS inhibition in cancer cells using N(G)-n

148 inine utilization pathway by an inhibitor of arginase and ornithine decarboxylase protected the mice

149 he AM symbiosis, the enzymatic activities of arginase and urease, and fungal gene expression in the e

150 m-induced CD11b(+)Gr1(+) cells express Arg1 (arginase) and Nos2 (inducible NO synthase) and suppress

151 whereas vascular endothelial growth factor, arginase, and TNF-alpha production were significantly le

152 abolism, principally mediated by the enzymes arginase (Arg) and inducible nitric oxide synthase (iNOS

153 g inducible nitric oxide synthase (iNOS) and arginase (ARG), are typical in asthmatic airway epitheli

154 However, the importance of arginase (ARG), the first enzyme of the polyamine pathwa

155 lism (IDO1, IDO2, Trp 2,3-dioxygenase [TDO], arginase [ARG] 1, ARG2, inducible NO synthetase) were ev

156 endothelial NO synthase (iNOS and eNOS) and arginase (Arg1 and Arg2) expression and enzyme activity

157 e cellular processes, is a substrate for two arginases-Arg1 and Arg2-having different expression patt

158 the expression of the mitochondrial form of arginase ARG2 in PDA and that ARG2 silencing or loss res

159 We find that the mitochondrial form of arginase (ARG2), which hydrolyzes arginine into ornithin

160 Arginase, arginine deiminase and arginine decarboxylase

161 s by upregulating the production of iNOS and arginase, as well as MMP-9 and VEGF.

162 f inducible nitric oxide synthase (iNOS) and arginase, as well as other suppressive mechanisms, allow

163 -derived NO is functionally active following arginase blockade.

164 microglia was required for the induction of arginase by IL-4.

165 Plasma levels of arginine, arginase, cell-free hemoglobin, ADMA, symmetric-dimethyl

166 associated with an increase in intracellular arginase concentration detected using a spectrophotometr

167 -(13)C]-arginine is linearly correlated with arginase concentration in vitro.

168 of T cells, suggesting that parasite-derived arginase contributes to the overall quality of the host

169 Clinical features of arginase deficiency include elevated plasma arginine lev

170 Arginase deficiency is caused by deficiency of arginase

171 % of plasma arginine levels in subjects with arginase deficiency were above the normal range despite

172 In neonatal and adult mice with arginase deficiency, AEB1102 reduced the plasma arginine

173 an arginine-reducing agent in patients with arginase deficiency.

174 reduces plasma arginine in murine models of arginase deficiency.

175 t the functional abnormalities that occur in arginase deficiency.

176 urea cycle disorders and the only to examine arginase deficiency.

177 We found that C57BL/6 mice infected with arginase-deficient (arg(-)) L. major failed to completel

178 to determine how single-copy and double-copy arginase deletion affects cortical circuits in mice.

179 e extended these results by demonstrating an arginase-dependent ability of AML blasts to polarize sur

180 the hypothesis that neuroblastoma creates an arginase-dependent immunosuppressive microenvironment in

181 Cs potently inhibited T cells in a partially arginase-dependent manner.

182 Knock out of Plasmodium arginase did not alter arginine depletion in infected mi

183 ds were analyzed for their inhibition of the arginase enzyme from Leishmania (Leishmania) amazonensis

184 This indicates that the HKDM-encoded arginase enzyme produces the urea used by the E. ictalur

185 In persistent infection, arginase-expressing gMDSCs (and circulating arginase) in

186 se data demonstrate the capacity of expanded arginase-expressing gMDSCs to regulate liver immunopatho

187 Furthermore, we found that arginase-expressing MPhis preferred L-citrulline over L-

188 To gain insight on how loss of arginase expression affects the excitability and synapti

189 hypoxia, dietary nitrate suppressed cardiac arginase expression and activity and markedly elevated c

190 We report that arginase expression and activity were induced in macroph

191 HIF-2alpha stability, which causes increased arginase expression and dysregulates normal vascular NO

192 MAPK family members are involved in iNOS and arginase expression following LPS stimulation.

193 lenocytes secreted more IL-10, had increased arginase expression in macrophages and dendritic cells,

194 e derived based on an Interleukin-12beta and arginase expression ratio.

195 lic tracer analysis demonstrated that plasma arginase flux was unchanged by P. berghei infection.

196 crobial activity and the capacity to inhibit arginase from Leishmania were evaluated in spray-dried p

197 high inhibitory capacity against the enzyme arginase from Leishmania.

198 Plasmodium berghei ANKA with or without the arginase gene.

199 ombinant cellular assay overexpressing human arginase I (CHO cells).

200 of a pegylated form of the catabolic enzyme arginase I (peg-Arg I) has shown some promise as a thera

201 elevation of cAMP results in upregulation of arginase I and increased polyamine synthesis.

202 the expression of immunosuppressive factors arginase I and iNOS.

203 suppressed T cell responses by expression of arginase I and production of reactive oxygen species and

204 , as associated with increased expression of arginase I and the cytokines IL10 and IL4.

205 analyses reinforced the association between arginase I expression and enzymes involved in prostaglan

206 The basis for high arginase I expression in macrophages in vivo is incomple

207 Our findings also suggest that induction of arginase I expression is stochastic; that is, difference

208 /EBPbeta to the IL-4 response element of the arginase I gene.

209 Arginase I induction by IL-4 requires binding of the tra

210 elucidate mechanisms involved in modulating arginase I induction by IL-4, the prototypical activator

211 Arginase I is a marker of murine M2 macrophages and is h

212 omo sapiens mediator complex subunit 23 gene/arginase I locus.

213 ther they rapidly and synergistically induce arginase I mRNA, protein, and promoter activity in murin

214 eneic T cells and in the use of either IL-17/arginase I or IFN-gamma/inducible nitric oxide synthase

215 Inhibition of arginase I or ODC abrogates L. amazonensis replication i

216 titution of the Mn(2+) metal center in human Arginase I with Co(2+) (Co-hArgI) results in an enzyme t

217 ly, treatment of crystalline Mn(2+)(2)-human arginase I with Zn(2+) reveals for the first time the st

218 increased protein and mRNA levels for iNOS, arginase I, and arginase II; although the induction of a

219 IL-4 and 8-bromo-cAMP individually induce arginase I, but together they rapidly and synergisticall

220 Immunohistochemistry confirmed that arginase I, ODC, and cyclooxygenase2 expression was high

221 Our data implicate arginase I, ODC, PGE2, and TGF-beta in the failure to mo

222 The plasma levels of arginase I, ornithine decarboxylase (ODC), transforming

223 of arginase II was more robust than that for arginase I.

224 ) is required for optimal catalysis by human arginase I.

225 ociated anti-inflammatory interleukin 10 and arginase I.

226 yl)hexanoic acid, compound 9, inhibits human arginases I and II with IC50s of 223 and 509 nM, respect

227 selected lead compounds cocrystallized with arginases I and II.

228 Finally, rescue of arginase-I activity after STAT3 blockade restored MDSC's

229 f STAT3 signaling also resulted in decreased arginase-I activity.

230 phorylated STAT3 levels that correlated with arginase-I expression levels and activity.

231 ration and IFN-gamma production and had high arginase-I expression.

232 demonstrate that the suppressive function of arginase-I in both infiltrating and circulating MDSC is

233 Analysis of the human arginase-I promoter region showed multiple STAT3-binding

234 rylated STAT3 binds to multiple sites in the arginase-I promoter.

235 lls were phenotyped as CD11b+, CD33+, CD34+, arginase-I+, and ROS+.

236 urea level correlating with increased renal Arginase II activity, hyperargininemia, and increased ki

237 atopoiesis through aberrantly high levels of arginase II activity.1 AML is a clinically, genetically,

238 reased following siRNA-mediated knockdown of arginase II and decreased when arginase II was overexpre

239 High arginase II expression correlates with poor survival for

240 inhibitor (ERK pathway) completely abolished arginase II expression while actually enhancing iNOS ind

241 while both the ERK and p38 pathways regulate arginase II induction in LPS-stimulated macrophages, iNO

242 ted iNOS expression while it only attenuated arginase II induction.

243 Arginase II is expressed and released from AML blasts an

244 Arginase II is the predominant isoform expressed and cre

245 Arginase II promoter activity was increased by approxima

246 Arginase II promoter activity was unaffected by a p38 in

247 vely active RAS mutant increased LPS-induced arginase II promoter activity, while transfection with a

248 t or a vector expressing MKP-3 inhibited the arginase II promoter activity.

249 , and arginase II; although the induction of arginase II was more robust than that for arginase I.

250 knockdown of arginase II and decreased when arginase II was overexpressed.

251 l and human cord blood CD71(+) cells express arginase II, and this enzymatic activity inhibits phagoc

252 in and mRNA levels for iNOS, arginase I, and arginase II; although the induction of arginase II was m

253 Arginase-II (Arg-II), the type-II L-arginine-ureahydrola

254 unique and previously unreported phenotype (arginase(+)/IL-1beta(+)) that augmented neurite growth a

255 en reduced IL-4Ralpha expression and reduced arginase, IL-1beta, and CCL2 expression was confirmed us

256 death by a mechanism involving activation of arginase in high inducible nitric oxide synthase-express

257 We investigated the role of parasite-derived arginase in secondary (memory) anti-Leishmania immunity

258 arginase-expressing gMDSCs (and circulating arginase) increased most in disease phases characterized

259 ase 1 and that pharmacological inhibition of arginase increases export of eNOS-derived nitrogen oxide

260 T. musculi excreted/secreted factor-mediated arginase induction.

261 By contrast, arginase inhibition did not improve postischemic recover

262 The protective effect of arginase inhibition was lost in the presence of a NOS in

263 A higher potency of arginase inhibition was observed with fisetin, which was

264 chol group on apigenin drastically decreased arginase inhibition.

265 Finally, combined treatment with arginase inhibitor and arginine rescued the suppression

266 ce were given blood from eNOS(-/-) mice, the arginase inhibitor failed to protect against ischemia-re

267 Additionally, when the specific arginase inhibitor l-norvaline was used to treat E. icta

268 NOS) inhibitor aminoguanidine hydrochloride, arginase inhibitor N-hydroxy-nor-l-arginine (nor-NOHA),

269 ion and increased infection were reversed by arginase inhibitor Nor-NOHA but were reproduced by adopt

270 from eNOS(-/-) mice were protected when the arginase inhibitor was given with blood from wild-type d

271 oxy-Nor-L-arginine (Nor-NOHA) was used as an arginase inhibitor.

272 t alpha,alpha-disubstituted amino acid-based arginase inhibitors.

273 gh adoptive transfer of MDSC or injection of arginase into noninjured mice.

274 xists based on the functional copy number of arginase: intrinsic excitability is altered, there is de

275 f arginine to ornithine by parasites or host arginase is a proposed mechanism of arginine depletion.

276 BCT-100, a pegylated human recombinant arginase, leads to a rapid depletion in extracellular an

277 response in aged mice resulted in attenuated arginase (M2a associated), IL-1beta, and chemokine ligan

278 ulline was less effective as a substrate for arginase-mediated L-ornithine production compared with L

279 ponding recruitment of CCR2(+)/IL-4Ralpha(+)/arginase(+) myeloid cells in vivo.

280 ng antibody or a specific inhibitor of the l-arginase-nitric oxide pathway (N(G)-monomethyl l-arginin

281 Studies using arginase-null mutants show that Leishmania-derived argin

282 e findings highlight for the first time that arginase of all Helicobacter gastric pathogens utilizes

283 resence of these two residues exclusively in arginase of other Helicobacter gastric pathogens, which

284 Using H. pylori arginase, our studies reveal that the interactions of Hi

285 is taken up is primarily metabolized by the arginase pathway to produce the polyamines required for

286 se-null mutants show that Leishmania-derived arginase plays an important role in disease pathogenesis

287 f this study was to test the hypothesis that arginase reciprocally controls NO formation in RBCs by c

288 while the role of MAPKs in the regulation of arginase remains unclear.

289 ressive CD11c(+) microglia and extracellular arginase, resulting in arginine catabolism and reduced l

290 Inhibitors of arginase significantly improved postischemic functional

291 In vivo blockade of arginase strongly inhibited Th2 ACT, consistent with a k

292 of L-arginine to ornithine and urea by host arginase supports Leishmania proliferation in macrophage

293 conservation of the signature motifs in all arginases, the H. pylori homolog has a non-conserved mot

294 tration of adeno-associated virus expressing arginase, there is near-total recovery of the abnormalit

295 proliferation in vivo, whereas addition of L-arginase to cultured keratinocytes stimulated proliferat

296 kin (IL)10, transforming growth factor-beta, arginase type II, chemokine (C-C motif) ligand 22 (CCL22

297 Plasma arginase was not elevated in those with malaria, and pla

298 Arginases were expressed by stimulated Ms, but competiti

299 plete arginine, MDSCs express high levels of arginase, which catalyzes the breakdown of arginine into

300 significantly to the inhibitory activity of arginase, while the hydroxyl group at position 5 did not