ライフサイエンスコーパス: LAP

1 LAP blockade is a general property of melanin pigments,

2 LAP depends upon reactive oxygen species (ROS) generated

3 LAP initiated 20 years ago, has been described for all h

4 LAP is not developing, has not been adopted for intermed

5 LAP is required for efficient degradation of the engulfe

6 LAP is triggered by engagement of the TIM4 receptor by e

7 LAP neutrophils also displayed slower kinetics ( approxi

8 LAP was required for TLR9 trafficking into a specialized

9 LAP+ and LAP- fractions were analyzed by immunofluoresce

10 LAPs have a role in insect defense and act as a regulato

11 and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated con

12 There were 7881 (17.8%) LAP and 36,359 (82.2%) OPEN performed in an average of 4

13 Nasal anti-CD3 induced a LAP(+) regulatory T cell that secreted high levels of IL

14 ll plants, whereas the stress-induced acidic LAPs (LAP-A) are expressed only in a subset of the Solan

15 synthesis of two transcriptional activators (LAP-1 and -2) and a transcriptional repressor (LIP).

16 P levels are significantly reduced, allowing LAP-mediated activation of the late promoter.

17 entional methods for leucine aminopeptidase (LAP) and pyrrolidonyl arylamidase (PYR) testing can be c

18 s, and the reference leucine aminopeptidase (LAP).

19 l-Leucine aminopeptidases (LAPs) are implicated in the progress of many pathologica

20 Leucine aminopeptidases (LAPs) are present in animals, plants, and microbes.

21 Three distinct clusters emerged among LAP participants: a high responder group (high level of

22 tes or sera of mice engineered to contain an LAP C33S mutation.

23 mage, it was shown that the tomato LAP-A and LAP-N and the Arabidopsis thaliana LAP1 and LAP2 are mol

24 es, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE.

25 teria infection on host Hsp60 expression and LAP-mediated bacterial adhesion, invasion, and transepit

26 tration results in expansion of Foxp3(+) and LAP(+) regulatory T cells (Tregs), suggesting oral deliv

27 duced a significant increase in Foxp3(+) and LAP(+) T cells in in vitro cultures.

28 different promoter activities of the HAP and LAP varieties.

29 gulatory elements differ between the HAP and LAP varieties.

30 ool to dissect the functions of the LAP* and LAP isoforms.

31 LAP+ and LAP- fractions were analyzed by immunofluorescence and m

32 Discordances between NucAmino and LAP occurred in 512 (16.9%) of the 3,029 sequences conta

33 ulosis to evade killing by NADPH oxidase and LAP.

34 the active form of C/EBP-beta (also known as LAP), acting as a critical molecular unit that controls

35 AP), latent TGF-beta and/or active TGF-beta (LAP/TGF-beta) is localized on the cell surface of Foxp3(

36 strated that only the full-length C/EBP beta/LAP* served as a true activator for Mn-SOD, whereas LAP,

37 d and activate the latent form of TGF-beta1 (LAP-TGF-beta1).

38 ungal particles that are normally cleared by LAP.

39 ignment that was preferable to that found by LAP in that it was more likely to codon align insertions

40 0001), only 15% of patients were operated by LAP and intermediate (or major) resections were performe

41 The proportion of resections performed by LAP was inversely related to annual caseload.

42 Phagocytosis by LAP macrophages was reduced approximately 40% compared t

43 y WTR (aHR 1.9 [1.4-2.6]) and black women by LAP (aHR 2.2 [1.4-3.5]).

44 a transposable 13-amino acid peptide called LAP (LplA Acceptor Peptide).

45 l autoimmune encephalomyelitis, CD4(+)CD25(+)LAP(+) cells exhibit more potent suppressive activity th

46 CD4(+)CD25(+)LAP(+) cells express elevated levels of Foxp3 and Treg-a

47 ro, the suppressive function of CD4(+)CD25(+)LAP(+) cells is both cell contact and soluble factor dep

48 We further show that CD4(+)CD25(+)LAP(+) cells suppress myelin oligodendrocyte glycoprotei

49 de (LAP) on their cell surface (CD4(+)CD25(+)LAP(+) cells).

50 otent suppressive activity than CD4(+)CD25(+)LAP(-) cells, and the suppression is TGFbeta dependent.

51 dependent; this contrasts with CD4(+)CD25(+)LAP(-) cells, which are mainly cell contact dependent.

52 sing CD4(+) regulatory T cells (CD4(+)CD25(-)LAP(+) cells with upregulated IL-10 and transforming gro

53 following adoptive transfer of CD4(+)CD25(-)LAP(+) regulatory T cells from nasal anti-CD3-treated an

54 ate that nasal anti-CD3 induces CD4(+)CD25(-)LAP(+) regulatory T cells that suppress lupus in mice an

55 CD4(+)LAP(+) T cells are hypoproliferative compared with CD4(+

56 In vitro generated CD4(+)LAP(+)Foxp3(-) T cells were suppressive in vitro, inhibi

57 Adoptive transfer of orally induced CD4(+)LAP(+) Tregs ameliorated metabolic and cytokine abnormal

58 -6 abrogated the in vitro induction of CD4(+)LAP(+) T cells by STAT3-dependent inhibition of Lrrc32 (

59 The in vitro activation of CD4(+)LAP(-) T cells results in the generation of LAP(+) Tregs

60 These CD4(+)LAP(+) T cells lack Foxp3 but express TGF-betaR type II

61 ls are hypoproliferative compared with CD4(+)LAP(-) T cells, secrete IL-8, IL-9, IL-10, IFN-gamma, an

62 T reg cell LAP-TGF-beta plays an important role in the suppression

63 sible for the abnormal neutrophil chemotaxis LAP.

64 specific derivatization of azide-conjugated LAP in cells.

65 re we describe the consequences of defective LAP in vivo.

66 with a reasonable selectivity versus dizinc LAP.

67 cell surface receptor for the latent domain (LAP) of the multifunctional cytokine TGF-beta.

68 Here we report that C/EBPbeta (LAP) DNA binding is inhibited by N-terminal sequences an

69 Ectopic expression of p34 C/EBPbeta (LAP) inhibited Ras(V12)-mediated transformation of NIH 3

70 y of another isoform of C/EBPbeta, C/EBPbeta-LAP, and might control liver biology through the regulat

71 ntify all patients who underwent an elective LAP or OPEN between 2007 and 2012.

72 ls in Caco-2 cells and consequently enhanced LAP-mediated L. monocytogenes adhesion but not invasion

73 The entire LAP completes in less than 20 min while using only a ten

74 that the CD4(+)CD25(+) subset that expresses LAP functions in a TGFbeta-dependent manner and has grea

75 than commercial colorimetric and fluorescent LAP substrates, respectively.

76 Three-year LRFS for R0 resection was 86% for LAP cancer and 84% for RRC (P = 0.817).

77 g required for autophagy, is dispensable for LAP induced by uptake of microbes or dead cells.

78 dditional surface localization mechanism for LAP/TGF-beta, which may play an important role in contro

79 APs as well as suggesting new mechanisms for LAP action in the defense of solanaceous plants against

80 PAMPs and melanin removal, are necessary for LAP activation and fungal killing.

81 why its inhibitory activity is selective for LAP*.

82 in 10 min and that it is highly specific for LAP fusion proteins over all endogenous mammalian protei

83 Of 100 exenterative operations, 55 were for LAP cancer and 45 for RRC.

84 l and highly sensitive fluorescent assay for LAPs based on substituted aminopyridines as fluorescent

85 ith increase in the frequencies of Foxp3(+), LAP(+), and GARP(+) T cells.

86 was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosy

87 By 10 months, colonies derived from LAP+ cells increased so that up to 35% of the liver was

88 Macrophages from LAP patients had a lower level of expression of 12-lipox

89 ed with long-acting cabotegravir (GSK1265744 LAP) pharmacokinetic variability, the current study was

90 oth IM and SC locations following GSK1265744 LAP administration.

91 understand the biodistribution of GSK1265744 LAP and its associated pharmacokinetics.

92 to a maximum volume at 2days post-GSK1265744 LAP administration, while the Vehicle depot did not sugg

93 employed to examine the temporal GSK1265744 LAP biodistribution in rat following either IM or SC adm

94 of macrophages trafficking to the GSK1265744 LAP and Vehicle depot sites.

95 The GSK1265744 LAP depot volume increased rapidly by day 2 in the IM in

96 resent in the depot region of the GSK1265744 LAP injected gastrocnemius while the Vehicle injected ga

97 ated a population of gastrointestinal-homing LAP(+)Foxp3(-) Treg cells.

98 However, the molecular mechanism(s) of how LAP/TGF-beta is anchored on the cell membrane is unknown

99 However, it remains unclear how LAP shapes both the activation and outcome of the immune

100 ve characterized a novel population of human LAP(+) Tregs that is different from classic CD4(+)Foxp3(

101 are due to defective engulfment and impaired LAP-mediated clearance of apoptotic germ cells as miR-47

102 and Capnocytophaga sp were most abundant in LAP.

103 cis together indicates sites of future BL in LAP.

104 e critical for early detection of changes in LAP activity and for screening potent LAP inhibitors.

105 ynergistic interaction of this consortium in LAP causation is possible and is the subject of ongoing

106 Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like

107 old-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants

108 For R0 resections only, DFS in LAP cancer was 76% and 57% in RRC (P = 0.212).

109 from diseased (DD) and healthy sites (DH) in LAP and from healthy sites in HS and HC and analyzed by

110 Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFal

111 to B6D2F1 Ags, and 3) allografts enriched in LAP(+), Foxp3(+), and CD4(+) T cells, with few CD8(+) T

112 r systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflamma

113 R0 rates were significantly higher in LAP cancer than in RRC (91% vs 62%, P = 0.001).

114 Hepatocyte-specific expression of hLAL in LAP-Tg/KO triple mice reduced the liver size to the norm

115 ponents of the autophagy pathway involved in LAP.

116 which the LTBP-binding cysteine residues in LAP TGF-beta1 were mutated to serine precluding covalent

117 , LPS-induced hyper-inflammatory response in LAP can be partially modulated by periodontal therapy.

118 However, the clinical effect of this SNP in LAP is ethnicity dependent, destructive (increases LAP i

119 was strongly associated and site-specific in LAP.

120 ethnicity dependent, destructive (increases LAP incidence), and complex with mechanisms still to be

121 lomyelitis, diabetes, and lupus) by inducing LAP(+) regulatory T cells.

122 Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated

123 When dying cells are injected into LAP-deficient mice, they are engulfed but not efficientl

124 Of interest, both the large isoform (LAP-2) and the small isoform (LIP) of C/EBP-beta can exe

125 C/EBP beta is expressed as three isoforms, LAP* (liver-activating protein), LAP, and LIP (liver-inh

126 -hLAL transgene with lal(-/-) knockout (KO) (LAP-Tg/KO) triple mice.

127 anoic acid, and the most efficiently labeled LAP clones were isolated by fluorescence activated cell

128 nts, whereas the stress-induced acidic LAPs (LAP-A) are expressed only in a subset of the Solanaceae.

129 The neutral LAPs (LAP-N and its orthologs) are constitutively expressed an

130 We conclude that regulation of LIP/LAP ratios during ER stress is a novel mechanism for mod

131 It is shown here that the LIP/LAP ratio decreased by 5-fold during the early phase of

132 The LIP/LAP ratio is a critical factor in C/EBPbeta-mediated gen

133 tion rates during ER stress controls the LIP/LAP ratio.

134 enase ( approximately 30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 +/- 50 pg/10(6) c

135 dence limits of agreement with measured mean LAP exceeded +/-18 mm Hg both for the overall group and

136 was largely restored in macrophages missing LAP components (Nox2, Rubicon, Beclin, Atg5, Atg7, or At

137 this assay was a useful tool for monitoring LAP activities in extracts from cancer cell lines, as we

138 The neutral LAPs (LAP-N and its orthologs) are constitutively expres

139 nes required for canonical autophagy but not LAP do not display defective dying cell clearance, infla

140 n of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-

141 For both sexes, quartile 4 of LAP carried increased risks for tobacco-exposed persons

142 The ability of LAP to attenuate autoimmunity likely occurs through the

143 f the engulfed corpse, and in the absence of LAP, engulfment of dead cells results in increased produ

144 hibits NADPH oxidase-dependent activation of LAP by excluding the p22phox subunit from the phagosome.

145 LCMS proteomic analysis of LAP-TAP-purified proteins from HeLa cells containing a t

146 th subsequent metalloproteolytic cleavage of LAP represents a major mechanism of TGF-beta activation

147 Consequences of LAP deficiency include a decreased capacity to clear dyi

148 Here, we describe the engagement of LAP upon uptake of apoptotic, necrotic, and RIPK3-depend

149 , and recombinant IL-2 induced expression of LAP on naive CD4(+) T cells, independent of Foxp3 or exo

150 L-10 or TGF-beta prevented the generation of LAP(+) Tregs and Foxp3(+) Tregs in vivo, and the LAP(+)

151 )LAP(-) T cells results in the generation of LAP(+) Tregs, which is further amplified by IL-8.

152 g mechanisms predicting the heterogeneity of LAP activity, severity, and response to treatment.

153 The impact of LAP to immune regulation is best characterized in profes

154 acterial titers), and restored impairment of LAP phagocytes.

155 o acids further solidified the importance of LAP* in the induction of Mn-SOD and emphasized the cruci

156 of the OPEN, P<0.0001) and the incidence of LAP biopsies increased after 2009.

157 Th2 responses, resulted in the induction of LAP(+) regulatory T cells and suppression of ongoing art

158 s was associated with a lack of induction of LAP(+) regulatory T cells.

159 lerance, strongly decreased the induction of LAP(+) Tregs.

160 A approximately 10(7) library of LAP variants was displayed on the surface of yeast cells

161 Although the mechanism of LAP-A action is unknown, it has been presumed that LAP p

162 ped an in vitro model to study modulation of LAP(+) on CD4(+) T cells.

163 nerates a newly differentiated population of LAP(high)CD103(high) CD8(TGF-beta) Treg cells, which rep

164 Herein, we provide a detailed review of LAP and its known roles in the immune response and provi

165 These data provide insight into the role of LAP as a virulence factor during intestinal epithelial i

166 ovide a rationale for revisiting the role of LAP* in the regulation of other genes and in pathways su

167 molecular event, requires the active site of LAP, and results in the removal of 12 N-terminal amino a

168 More than a third of LAP+ fetal hepatocytes expressed ductal markers.

169 RNA against ANLN increased survival times of LAP-MYC mice, compared to mice given a control siRNA.

170 cheme was used to tag and image a variety of LAP fusion proteins in multiple mammalian cell lines wit

171 In plants, there are two classes of LAPs.

172 as TGF-beta1 contained in complex with only LAP could not be activated by stirring when studied as e

173 In our LAP participants, distinct patterns of LPS response were

174 s an exoprotease, leucine aminopeptidase (PA-LAP), which is coexpressed with several known virulence

175 data support a model whereby full-length PA-LAP is activated in a two-step process; proteolytic clea

176 by expressing the full-length proform of PA-LAP recombinantly in Escherichia coli (here termed, rLAP

177 read-out of a 5-parameter liver assay panel (LAP) on a portable, easy-to-use, fast and cost-efficient

178 Long-Acting Parenterals (LAPs) have been used in the clinic to provide sustained

179 ic surface protein, leucine amino peptidase (LAP).

180 have identified latency-associated peptide (LAP) and IL-1 receptor type I and II (CD121a/CD121b) as

181 eta complexed to latency-associated peptide (LAP) is expressed on the cell surface of activated but n

182 l that expresses latency-associated peptide (LAP) on its surface.

183 egs that express latency-associated peptide (LAP) on their cell surface (CD4(+)CD25(+)LAP(+) cells).

184 des that express latency-associated peptide (LAP) on their cell surface but do not express Foxp3.

185 d a CD4(+)CD25(-)latency-associated peptide (LAP)(+) regulatory T cell that secreted high levels of I

186 that express the latency-associated peptide (LAP), a membrane-bound TGF-beta1.

187 of TGF-beta, the latency-associated peptide (LAP), and having regulatory properties in human peripher

188 ession levels of latency-associated peptide (LAP), CD103, PD-1, PD-L1, and CTLA-4, as compared with p

189 at pro-TGF-beta, latency-associated peptide (LAP), latent TGF-beta and/or active TGF-beta (LAP/TGF-be

190 in complex with latency-associated peptide (LAP), which is disulfide bonded via Cys33 to latent TGF-

191 dependent CD4(+) latency-associated peptide (LAP)-positive Tregs by oral administration of anti-CD3 a

192 associated with latency-associated peptide (LAP).

193 -bound TGF-beta (latency-associated peptide [LAP]) and have been shown to play an important role in t

194 e substrate, called "LplA Acceptor Peptide" (LAP).

195 -induced localized aggressive periodontitis (LAP) in African-American adolescents has been documented

196 Localized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis lin

197 sed with localized aggressive periodontitis (LAP) present an in vivo phenotype with depressed chemota

198 cts with localized aggressive periodontitis (LAP) who had proximal bone loss but minimal proximal car

199 gent for localized aggressive periodontitis (LAP), an aggressive form of periodontal disease that occ

200 ponse in localized aggressive periodontitis (LAP).

201 ren with Localized Aggressive Periodontitis (LAP).

202 toxin in localized aggressive periodontitis (LAP).

203 ren with localized aggressive periodontitis (LAP).

204 etallo-aminopeptidases (MAPs), PfA-M1 and Pf-LAP.

205 In contrast, inhibition of Pf-LAP was lethal to parasites early in the life cycle, pri

206 e onset of Hb degradation suggesting that Pf-LAP has an essential role outside of Hb digestion.

207 li cells employ LC3-associated phagocytosis (LAP) by recruiting autophagy member proteins to clear ap

208 LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC

209 ophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles,

210 pathway termed LC3-associated phagocytosis (LAP), which promotes fungal killing.

211 ermed MAPLC3A (LC3)-associated phagocytosis (LAP), which results in optimal degradation of the phagoc

212 light chain 3 (LC3)-associated phagocytosis (LAP).

213 germ cells via LC3-associated phagocytosis (LAP).

214 ight-chain 3 (LC3)-associated phagocytosis" (LAP), lacked such defects.

215 athway called "LC3-associated phagocytosis" (LAP).

216 Here we show that plant LAPs are bifunctional.

217 chaperones and a new function for the plant LAPs as well as suggesting new mechanisms for LAP action

218 xpression of latency-associated polypeptide (LAP)/TGF-beta and after adoptive transfer also their pro

219 ges in LAP activity and for screening potent LAP inhibitors.

220 direct measurements of left atrial pressure (LAP) via catheterization in 100 patients with HCM.

221 d in patients with locally advanced primary (LAP) cancer and recurrent rectal cancer (RRC).

222 arteannuin B; the low artemisinin producers (LAPs), which include the 'Meise', 'Iran#8', 'Iran#14', '

223 ity index (VAI), lipid accumulation product (LAP), body adiposity index (BAI) and the waist-to-height

224 e considered the lipid accumulation product (LAP; [WC enlargement*triglycerides]).

225 d alignment program Local Alignment Program (LAP) using 115,118 human immunodeficiency virus type 1 (

226 cross-breeding of liver-activated promoter (LAP)-driven tTA transgene and (tetO)7-CMV-hLAL transgene

227 arboring deletions of the core LAT promoter (LAP) region.

228 teractors includes lamina-associated protein LAP-1, myocyte nuclear envelope protein Syne1, BetaM its

229 t not the liver-enriched activating protein (LAP) version, represses ATF4 transcription.

230 -enriched transcriptional activator protein (LAP) isoform of CCAAT/enhancer binding protein beta (C/E

231 is a receptor for Listeria adhesion protein (LAP) during Listeria monocytogenes infection.

232 demonstrated that Listeria adhesion protein (LAP) promotes adhesion to intestinal epithelial cells an

233 beta propeptide [latency associated protein (LAP)], and a latent TGF-beta binding protein (LTBP).

234 e isoforms, LAP* (liver-activating protein), LAP, and LIP (liver-inhibitory protein).

235 -length (liver-enriched activating protein* (LAP*)) isoform but not the slightly shorter (LAP) isofor

236 sing localization and affinity purification (LAP)-tagged dynein/dynactin subunits from bacterial arti

237 The AAPC of the incidence of real LAP increased more than that of real OPEN (7.0% vs 1.3%)

238 REDUCE LAP-HF I (Reduce Elevated Left Atrial Pressure in Patien

239 eft Atrial Pressure in Heart Failure (REDUCE LAP-HF I), the first randomized controlled trial of a de

240 ssure in Patients with Heart Failure (REDUCE LAP-HF) study was an open-label, single-arm, phase 1 stu

241 d practice of laparoscopic liver resections (LAP), compared to open resections (OPEN).

242 sed to a 13-amino acid recognition sequence (LAP), catalyzed by a mutant of the Escherichia coli enzy

243 LAP*)) isoform but not the slightly shorter (LAP) isoform.

244 her, we concluded that inducible Ag-specific LAP(+) Tregs can suppress asthmatic lung inflammation an

245 eration, and transfer of sorted OVA-specific LAP(+) Tregs in vivo inhibited allergic eosinophilia and

246 Caco-2 cells more susceptible to subsequent LAP-mediated adhesion and translocation.

247 +)CD25(-) T cells, makes these cells surface LAP/TGF-beta-positive.

248 Furthermore, surface LAP/TGF-beta forms a complex with the molecular chaperon

249 er, is not involved in GARP-mediated surface LAP/TGF-beta.

250 P78 reduced the expression levels of surface LAP/TGF-beta.

251 The surface LAP/TGF-beta contains high-glycosylated, furin-processed

252 The optimal catalyst system (LAP 8-5-47) provided alpha-amino amides from an aldehyde

253 TCRgammadelta+LAP+ cells express antigen presentation molecules and fu

254 + regulatory T cells, although TCRgammadelta+LAP+ cells do not themselves express Foxp3.

255 Identification of TCRgammadelta+LAP+ regulatory cells provides an avenue for understandi

256 P-A catalytic site mutants demonstrated that LAP-A chaperone activity was independent of its peptidas

257 We found that LAP activation also requires the genetic, biochemical or

258 alizing Abs against cytokines, we found that LAP induction was decreased in the presence of IL-6 and

259 Treg-mediated suppression and indicates that LAP is an authentic marker able to identify a TGFbeta-ex

260 action is unknown, it has been presumed that LAP peptidase activity is essential for regulating wound

261 Collectively, these data suggested that LAP-A has a role in modulating essential defenses agains

262 onolayers than a lap mutant, suggesting that LAP is involved in transepithelial translocation, potent

263 The LAP [leucine-rich and postsynaptic density-95/Discs larg

264 The LAP receptor is a stress response protein, Hsp60, but th

265 The LAP(+) Tregs strongly suppressed naive CD4(+) T cell pro

266 me rural adults of Xinjiang was high and the LAP was an effective indicator for the screening of MetS

267 and WHtR were all greater than 0.7, and the LAP was the index that most accurately identified MetS s

268 +) Tregs and Foxp3(+) Tregs in vivo, and the LAP(+) Tregs could also be generated concomitantly with

269 of the DBR2 gene from varieties of both the LAP and the HAP groups.

270 Its selectivity for the LAP* isoform also makes helenalin acetate an interesting

271 protein, Hsp60, but the precise role for the LAP-Hsp60 interaction during Listeria infection is unkno

272 just upstream of the ATG start codon in the LAP varities, which might be the reason for the differen

273 f these, biopsies accounted for 29.9% of the LAP (7.3% of the OPEN, P<0.0001) and the incidence of LA

274 ice lacking any of several components of the LAP pathway show increased serum levels of inflammatory

275 resting tool to dissect the functions of the LAP* and LAP isoforms.

276 Furthermore, disruption of the LAP-A hexameric structure increased chaperone activity.

277 lin acetate binds to the LAP* but not to the LAP isoform, explaining why its inhibitory activity is s

278 nt with this, helenalin acetate binds to the LAP* but not to the LAP isoform, explaining why its inhi

279 he clinical response to treatment within the LAP cohort.

280 ls of this response were observed within the LAP group.

281 Thus, LAPs not only could become new diagnostic or prognostic

282 pecific ligation of 10-azidodecanoic acid to LAP in cells, in nearly quantitative yield after 30 min.

283 siRNAs were delivered to LAP-MYC mice, which develop hepatoblastoma, using lipid

284 induced damage, it was shown that the tomato LAP-A and LAP-N and the Arabidopsis thaliana LAP1 and LA

285 Upon transplantation, LAP+ late gestation fetal hepatocytes formed hepatic, en

286 in pathway have clinical utility in treating LAP and other oral diseases associated with infection, i

287 PRRs, for reasons that are poorly understood LAP does not substantially contribute to Mtuberculosis c

288 estine lamina propria, where they upregulate LAP, downregulate IFN-gamma via ATF-3 expression and acq

289 Assays using LAP-A catalytic site mutants demonstrated that LAP-A cha

290 apoptotic germ cells by Sertoli cells using LAP.Although phagocytic clearance of apoptotic germ cell

291 The AUC of VAI, LAP and WHtR were all greater than 0.7, and the LAP was

292 phagocytes, in particular macrophages, where LAP has instrumental roles in the clearance of extracell

293 rved as a true activator for Mn-SOD, whereas LAP, LIP, and C/EBP delta functioned as potential repres

294 culation on the putative mechanisms by which LAP may regulate immune function, perhaps through the me

295 systemic levels of endotoxin associated with LAP.

296 ssion of TGF-beta on DCs in association with LAP is one of the mechanisms by which immature DCs limit

297 Through its association with LAP, TGF-beta is maintained in a latent form that must b

298 ree of systemic diseases, and diagnosed with LAP.

299 Fifty-nine individuals with LAP were treated by mechanical debridement and systemic

300 In primary neutrophils from persons with LAP, PDK1 expression and activation levels were signific