ライフサイエンスコーパス: LOX

1 LOX contains a prominent tyrosine in the substrate bindi

2 LOX expression was analyzed by using RNA-sequencing, PCR

3 LOX in colorectal cancer synergizes with hypoxia-inducib

4 LOX inhibition attenuated hepatic stellate cell activati

5 LOX is a target for cancer therapy, and thus the search

6 LOX of animals, plants, and prokaryotes contain iron as

7 LOX overexpression in colorectal cancer cells also induc

8 LOX overexpression is associated with poor cancer outcom

9 LOX-1 promotes endothelial activation and dysfunction by

10 LOX-like 3 (Loxl3) associates with Stat3 in the nucleus

11 LOXs share a conserved C-terminal catalytic domain but d

12 p65- nuclear factor kappa B, lipoxygenase-1 (LOX-1) and toll-like receptor 4 (p < 0.05).

13 The lectin-like oxidized LDL receptor 1 (LOX-1) is a key player in the development of atheroscler

14 eceptor Lectin-like Oxidized LDL Receptor-1 (LOX-1) is associated with vascular dysfunction, and LOX-

15 through lectin-like oxidized LDL receptor-1 (LOX-1) signaling, and glycosylation removal from L5 atte

16 ceptor, lectin-like oxidized LDL receptor-1 (LOX-1), and alphabeta amyloid peptide, which together co

17 oxidized low-density lipoprotein receptor-1 (LOX-1), one of the scavenger receptors for oxidized low-

18 oxidized low-density lipoprotein receptor-1 (LOX-1).

19 PLY triggered neutrophil recruitment in a 12-LOX-dependent manner in vitro.

20 Although 12-LOX is a proposed therapeutic target to protect pancreat

21 ted signaling pathways mediated by direct 12-LOX oxidation of 2-AA-LPC and 2-AA-LPE.

22 2-AA-LPC, 2-AA-LPE, and their downstream 12-LOX oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LP

23 h residual inflammation induced by PLY in 12-LOX-deficient mice indicates that 12-LOX-independent pat

24 data suggested that dietary sugar induces 12-LOX signaling to increase risks of breast cancer develop

25 that human platelet-type 12-lipoxygenase (12-LOX) can directly catalyze the regioselective and stereo

26 12-Lipoxygenase (12-LOX) is a key enzyme in arachidonic acid metabolism, and

27 e previously showed that 12-lipoxygenase (12-LOX), which is required to generate the PMN chemoattract

28 es the production of the 12-lipoxygenase (12-LOX)-dependent lipid inflammatory mediator hepoxilin A3,

29 nd that either depletion or inhibition of 12-LOX impairs both exocrine pancreas growth and unexpected

30 gic inhibition-to interrogate the role of 12-LOX in pancreatic development.

31 ovide new insight into the requirement of 12-LOX in pancreatic organogenesis and islet formation, and

32 both the depletion and the inhibition of 12-LOX.

33 ocked by morpholino-directed depletion of 12-LOX.

34 ves into the lungs of mice induced robust 12-LOX-dependent neutrophil migration into the airways, alt

35 Importantly, a potent and selective 12-LOX inhibitor, ML355, significantly inhibited the produc

36 g zebrafish development demonstrated that 12-LOX-generated metabolites of arachidonic acid increase s

37 Y in 12-LOX-deficient mice indicates that 12-LOX-independent pathways also contribute to PLY-triggere

38 catalyzed by the consecutive actions of 12R-LOX and epidermal LOX3.

39 Because 13-LOX pathway products comprise compounds involved in inse

40 The 13-LOX enzyme identified here accumulated in the plastid en

41 Four 13-lipoxygenases (13-LOXs) produce JA precursors in Arabidopsis (Arabidopsis

42 identified LOX3 and LOX4 as the principal 13-LOXs responsible for vegetative growth restriction after

43 is (Arabidopsis thaliana) leaves, but the 13-LOXs responsible for growth restriction have not yet bee

44 In this respect, 15-lipoxygenase-1 (15-LOX-1) is a key enzyme that catalyzes the formation of l

45 f cysteinyl leukotrienes (cysLTs) and 12-/15-LOX metabolites were produced in the airways during AAI

46 at mice deficient in the gene encoding 12/15-LOX (Alox15) are profoundly susceptible to invasive aspe

47 ce after disease onset, with 5-LOX and 12/15-LOX being downregulated and upregulated, respectively.

48 date that small molecules that target 12/15-LOX can prevent progression of beta-cell dysfunction and

49 Consistent with a role for 12/15-LOX in promoting oxidative stress, its chemical inhibiti

50 Together, these data indicate that 12/15-LOX is a critical player in induction of the earliest as

51 cosanoid network, we hypothesized that 12/15-LOX is also active during invasive aspergillosis.

52 Inhibition of 12/15-LOX provides a potential therapeutic approach to prevent

53 have been shown to selectively target 12/15-LOX with high potency.

54 ed with WT macrophages, monocytes from 12/15-LOX(-/-) mice displayed diminished trafficking, which wa

55 We also observed that macrophages from 12/15-LOX(-/-) mice exhibit diminished migratory response to m

56 igated the role of 12/15-lipoxygenase (12/15-LOX) in TF expression.

57 12/15-Lipoxygenase (12/15-LOX) is induced in beta-cells and macrophages during T1D

58 he lung were blunted in the absence of 12/15-LOX, although neutrophil antifungal activity was intact.

59 survival allowed the identification of 12/15-LOX-dependent induction of IL-17A and IL-22.

60 ssociated with very early (6 and 12 h) 12/15-LOX-dependent inflammatory cytokine (IL-1alpha, IL-1beta

61 The influence of activating 15-LOX on the AA metabolite network was then investigated e

62 However, 15-LOX appears to be the most critical factor for the defic

63 uggested that activating 15-lipoxygenase (15-LOX) is a promising strategy to intervene the arachidoni

64 Thus, we provide a novel 15-LOX-1 inhibitor that inhibits cellular NO production and

65 Inhibition of 15-LOX-1 holds promise to interfere with regulated cell dea

66 -target actions, we found that: 1) COX or 15-LOX-1 inhibitors elevate inflammatory leukotriene levels

67 In this study, a novel potent 15-LOX-1 inhibitor, 9c (i472), was developed and structure-

68 ion increases SPM levels, and 4) that the 15-LOX-1 inhibitor 3887 suppresses SPM formation in M2 macr

69 (15(S)-HETE), the major product of human 15-LOXs 1 and 2, induced TF expression and activity in a ti

70 causes further suppression of the HIF-1alpha/LOX/ITGA5/FN1 axis.

71 Manoalide, a PLA2 inhibitor or Zileuton, a 5-LOX inhibitor with VPC reversed the protective effects o

72 esized that propofol would directly affect 5-LOX function.

73 y mutation of F177 and/or Y181 to alanine (5-LOX-F177A, 5-LOX-Y181A, 5-LOX-F177/Y181A) resulted in de

74 Specific inhibitors of COX-2 and 5-LOX decreased formation of HKD2 and HKE2 Platelets did n

75 flammatory leukotriene levels, 2) FLAP and 5-LOX inhibitors reduce leukotrienes in M1 but less so in

76 lowered cPLA2 activity along with COX2 and 5-LOX mRNA levels.

77 as the principal metabolites of COX-2 and 5-LOX, respectively.

78 ion in animal models, and because COX- and 5-LOX-derived eicosanoids are thought to contribute to Abe

79 For 5-LOX-F177A and 5-LOX-F177/Y181A, formation of 5-LOX products was dramatic

80 riments on fMLP-stimulated neutrophils and 5-LOX-transfected human embryonic kidney cells, propofol a

81 their ability to inhibit COX-1, COX-2 and 5-LOX.

82 ed their interaction with NF-kB, COX-2 and 5-LOX.

83 from obese individuals exhibited decreased 5-LOX levels and reduced 5-LOX Ser271 phosphorylation and

84 /Y181A) resulted in delayed and diminished 5-LOX membrane association in A23187-stimulated cells.

85 rmacophores led to the discovery of a dual 5-LOX/sEH inhibitor, which was subsequently optimized in t

86 tigating the therapeutic potential of dual 5-LOX/sEH inhibitors in other inflammation- and fibrosis-r

87 ic acid from the nuclear membrane-embedded 5-LOX-activating protein (FLAP).

88 atory event and require cells that express 5-LOX and COX-2 for their biosynthesis.

89 F177 and/or Y181 to alanine (5-LOX-F177A, 5-LOX-Y181A, 5-LOX-F177/Y181A) resulted in delayed and dim

90 se pockets were functionally important for 5-LOX activity.

91 For 5-LOX-F177A and 5-LOX-F177/Y181A, formation of 5-LOX produ

92 phosphorylation and distinct intracellular 5-LOX redistribution.

93 In Fig.3c, the arrow labeled '5-LOX' should be aimed at the plot measuring LXB(4), and t

94 synthetic crossover of the 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) pathways.

95 Merging of 5-lipoxygenase (5-LOX) and soluble epoxide hydrolase (sEH) pharmacophores

96 Potential pro-inflammatory 5-lipoxygenase (5-LOX) inhibition potential (IC50 0.76-0.92mg/mL) of the p

97 clooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) pathways, participate in the induction of protectiv

98 e cyclooxygenase (COX) and 5-lipoxygenase (5-LOX) pathways.

99 step reaction catalyzed by 5-lipoxygenase (5-LOX) requiring the formation of 5-HPETE [5(S)-hydroperox

100 tenuated the production of 5-lipoxygenase (5-LOX)-related arachidonic acid (AA) derivatives in the pe

101 and its subsequent transformation to LTA4 5-LOX is thought to receive arachidonic acid from the nucl

102 two pockets can be used to explore a novel 5-LOX inhibitor in the future.

103 vivo and defined the biosynthetic roles of 5-LOX and COX-2, using inhibitors and incubations with exo

104 as accompanied by a rapid translocation of 5-LOX from nucleus to cytoplasm in both ECs and VSMCs, pot

105 agenesis was performed for the residues of 5-LOX in the vicinity of propofol, and we evaluated the fu

106 X-F177A and 5-LOX-F177/Y181A, formation of 5-LOX products was dramatically reduced relative to 5-LOX-

107 ve the X-ray crystallographic structure of 5-LOX, and examined the binding site(s) of propofol on 5-L

108 henyl-2-picrylhydrazyl), and inhibition of 5-LOX, COX-1-2, and inducible nitric oxide synthase (iNOS)

109 lls, propofol attenuated the production of 5-LOX-related AA derivatives.

110 ts were identified near the active site of 5-LOX.

111 e examined the influence of the FY cork on 5-LOX activity and membrane binding in HEK293 cells in the

112 xamined the binding site(s) of propofol on 5-LOX.

113 uced neuroinflammation via activating PLA2/5-LOX/LTB4 cascade using a partial frontal lobe resection

114 oves outcomes after SBI by activating PLA2/5-LOX/LTB4 cascade.

115 ase A2/5-lipoxygenase/leukotriene-B4 (PLA2/5-LOX/LTB4) axis is an important inflammatory signaling pa

116 hibited decreased 5-LOX levels and reduced 5-LOX Ser271 phosphorylation and distinct intracellular 5-

117 i-propofol (AziPm), we photolabeled stable 5-LOX protein, which had been used to solve the X-ray crys

118 alveolar-like MDM (aMDM) to HDM suppressed 5-LOX expression and product formation, while triggering p

119 Uncapping the 5-LOX active site by mutation of F177 and/or Y181 to alani

120 nases (COXs), 5-lipoxygenase (LOX), or the 5-LOX-activating protein (FLAP).

121 ducts was dramatically reduced relative to 5-LOX-wild type (wt).

122 iLtJ female mice after disease onset, with 5-LOX and 12/15-LOX being downregulated and upregulated, r

123 Y181 to alanine (5-LOX-F177A, 5-LOX-Y181A, 5-LOX-F177/Y181A) resulted in delayed and diminished 5-LOX

124 phere is similar to iron ligands of coral 8R-LOX and soybean LOX-1 but is not overlapping.

125 he adjusted mean concentration of 12-HETE, a LOX pathway product, was 56.2% higher (95% credible inte

126 imal inhibitory concentrations (IC(50)) in a LOX enzyme activity assay.

127 Oxidized LDL (a LOX-1 ligand) increased angiotensin II-induced vasoconst

128 y, SPPL2a/b-deficient mice, which accumulate LOX-1 NTFs, develop larger and more advanced atheroscler

129 outcome, irrespective of HIF-1 In addition, LOX was expressed by tumor cells in the bone marrow from

130 us the search for therapeutic agents against LOX has been widely sought.

131 All LOX belong to the same gene family, and they are widely

132 whether high glucose (HG) or diabetes alters LOX-PP expression and thereby influences AKT pathway and

133 gy and pathway analyses linked TNF-alpha and LOX expression in patients with EoE, which was validated

134 y, increased expression levels of COL1A1 and LOX were associated with decreased survival in thyroid c

135 lar that correlate with type VI collagen and LOX, both of which are associated with increased type I

136 the PKIE measured in macrophages for COX and LOX oxygenation of AA is similar to KIEs determined in p

137 possible implications for the use of COX and LOX pathway inhibitors for lung cancer therapy.

138 Eicosanoids derived from AA via the CYP and LOX biosynthetic pathways were positively associated wit

139 is associated with vascular dysfunction, and LOX-1 has been shown to interact with angiotensin II rec

140 tion, and regional blood flow in the FME and LOX tumor xenografts.

141 Lysyl oxidase (LOX) and LOX-like (LOXL) proteins are copper-dependent metalloenz

142 droxylase 2 (LH2) or lysyl oxidase (LOX) and LOX-like 2 (LOXL2) were significantly upregulated in lat

143 tyric acid immunostaining of the medulla and LOX were compared between the praying mantis and two rel

144 vated protein kinase p38 phosphorylation and LOX-1 translocation to the surface.

145 ine arteries from late pregnant wildtype and LOX-1 overexpressing mice were incubated overnight with

146 lable LOX inhibitor CCT365623 with good anti-LOX potency, selectivity, pharmacokinetic properties, as

147 either anti-CD40.Env gp140/poly-ICLC or anti-LOX-1.Env gp140/poly-ICLC induced balanced antibody and

148 ia coordinated copper transport in the ATP7A-LOX axis.

149 ATP7A silencing was also found to attenuate LOX activity and metastasis of Lewis lung carcinoma cell

150 The resulting microneedle-based LOX biosensor displays an interference-free lactate dete

151 Faba bean LOX preferred free fatty acids (FFAs) over triacylglycer

152 optimization yielded the orally bioavailable LOX inhibitor CCT365623 with good anti-LOX potency, sele

153 phenes (AMTs) as potent, orally bioavailable LOX/LOXL2 inhibitors, we report herein the discovery of

154 y ATP7A as a therapeutic target for blocking LOX- and LOXL-dependent malignancies.

155 In turn, both LOX and IL6 were acting in concert to promote RANKL-depe

156 observed with eicosanoids derived from AA by LOX enzymes.

157 Little is known about metal selection by LOX and the adjustment of the redox potentials of their

158 SPPL2a/b control cellular LOX-1 NTF levels which, following self-association via t

159 with particular focus on the lobula complex (LOX).

160 Few data are available concerning LOX in ccRCC.

161 for LOX or are located at a highly conserved LOX catalytic domain, which is relatively invariant in t

162 COL1A1, COL1A2, COL3A1, COL5A1, POSTN, CTGF, LOX, TGFbeta1, PDGFRA, TNC, BGN, and TSP2 were significa

163 ne genes such as SOD (superoxide dismutase), LOX (lipoxygenase), PAL (phenylalanine ammonia lyase), a

164 ort herein the discovery of a series of dual LOX/LOXL2 inhibitors, as well as a subseries of LOXL2-se

165 oxidase propeptide (LOX-PP), released during LOX processing, has been implicated in promoting apoptos

166 in conditions characterized by dysfunctional LOX activity, such as obesity.

167 ime in ccRCC, a detailed study of endogenous LOX and also investigated their transcriptomic profile.

168 We found that endogenous LOX is overexpressed in ccRCC, is involved in a positive

169 D1 as well as extracellular matrix Cu enzyme LOX activity in wound tissues.

170 Esophageal epithelial LOX might have a role in the development of fibrosis wit

171 el positive feedback mechanism in epithelial LOX induction through fibroblast-derived TNF-alpha secre

172 TNF-alpha-mediated epithelial LOX upregulation was recapitulated in 3-dimensional orga

173 We investigated regulation of epithelial LOX expression as a novel biomarker and functional effec

174 last-derived TNF-alpha stimulates epithelial LOX expression through activation of nuclear factor kapp

175 s the catalytic metal, whereas fungi express LOX with iron or with manganese.

176 athogenic variants in 6 genes (COL3A1, FBN1, LOX, PRKG1, SMAD3, and TGFBR2) were identified in 26 ind

177 X-PP (rLOX-PP) or HG medium and examined for LOX-PP expression, AKT and caspase-3 activation.

178 red amino acids cause haploinsufficiency for LOX or are located at a highly conserved LOX catalytic d

179 Mounting evidence suggests a role for LOX-1 in various steps of the atherosclerotic process, f

180 emic delivery of the conditioned medium from LOX-overexpressing colorectal cancer cells promoted tumo

181 a-repressed miR-142-3p, which targets HIF1A, LOX and ITGA5, causes further suppression of the HIF-1al

182 We show that a high LOX expression in primary tumors from patients with colo

183 Notably, higher LOX, ITGA5, or FN1, or lower miR-142-3p levels are assoc

184 EK293 cells, along with immunoprecipitation, LOX enzymatic activity, solid-phase binding assays, and

185 ger receptor cysteine-rich (SRCR) domains in LOX-like (LOXL) 2.

186 DG, and is sustained by further increases in LOX and allene oxide cyclase mRNA and protein levels.

187 s accumulating, there is growing interest in LOX-1 as a potential therapeutic target.

188 ese data suggest that a missense mutation in LOX is associated with aortic disease in humans, likely

189 uencing was used to investigate mutations in LOX in an additional 410 probands from unrelated familie

190 the conclusion that rare genetic variants in LOX predispose to thoracic aortic disease.

191 regnancy, but not in conditions of increased LOX-1 expression, suggesting that STBEVs (via LOX-1) pla

192 In retinas of diabetic rats, increased LOX-PP level, decreased AKT phosphorylation, and increas

193 his study suggest that hyperglycemia-induced LOX-PP overexpression may contribute to retinal vascular

194 Silencing of ATP7A inhibited LOX activity in the 4T1 mammary carcinoma cell line, res

195 Inhibiting LOX reduces collagen cross-linking and fibronectin assem

196 this impairment to reduced 15-lipoxygenase (LOX) activity rather than altered DHA cellular uptake.

197 hrough the activation of 12/15-lipoxygenase (LOX)/12-HETE signaling, altering neuronal morphology and

198 key SPM biosynthetic enzyme 5-lipoxygenase (LOX) in vascular cells.

199 ting cyclooxygenases (COXs), 5-lipoxygenase (LOX), or the 5-LOX-activating protein (FLAP).

200 bean exhibited high lipase and lipoxygenase (LOX) activities, with pH optima being 8.0 and 6.0, respe

201 uding cyclooxygenase (COX) and lipoxygenase (LOX) has revealed far lower values.

202 ncluding cyclooxygenase (COX), lipoxygenase (LOX), or cytochrome P450 (CYP).

203 ivo, and further evidence that lipoxygenase (LOX) pathway contributes to volatile production in intac

204 pression of genes encoding 13-lipoxygenases (LOXs) and phospholipase A-Igamma3 (At1g51440), a plastid

205 Overall, the mantis LOX is more similar to the LOX of the locust than the mo

206 In PTEN-null GBM models, LOX inhibition markedly suppresses macrophage infiltrati

207 Moreover, LOX-mediated 5-hydroxyeicosatetraenoic acids (HETE) and

208 O(2) delivery to hypoxic (FME) and normoxic (LOX) human melanoma xenografts in a murine window chambe

209 L5-injected wild-type but not LOX-1(-/-) mice showed longer QTc compared to L1-injecte

210 orter ATP7A is necessary for the activity of LOX and LOXL enzymes.

211 to a mechanism that controls the binding of LOX to collagen and is based on differential BMP1- and A

212 vious studies showing that the deficiency of LOX in mice or inhibition of lysyl oxidases in turkeys a

213 Here, we show that the function of LOX-1 is controlled proteolytically.

214 view discusses the discovery and genetics of LOX-1; describes existing evidence supporting the role o

215 ly, silencing or pharmacologic inhibition of LOX activity blocked dissemination of colorectal cancer

216 Pharmacologic inhibition of LOX reduced tumor burden and collagen remodeling in muri

217 Inhibition of LOX-dependent subendothelial matrix stiffening alone sup

218 We describe a pharmacological inhibitor of LOX, CCT365623, which disrupts EGFR cell surface retenti

219 carcinoma cell line, resulting in a loss of LOX-dependent mechanisms of metastasis, including the ph

220 However, little is known about modulators of LOX-1-mediated responses.

221 pH 6.4, which is close to the pH optimum of LOX.

222 s the first to validate direct regulation of LOX and LOXL2 by the miR-200/ZEB1 axis, defines a novel

223 tective mechanism via negative regulation of LOX-1 signaling.

224 bes existing evidence supporting the role of LOX-1 in atherogenesis and its major complication, myoca

225 As evidence supporting the vital role of LOX-1 in atherogenesis keeps accumulating, there is grow

226 medicinal chemistry discovery of a series of LOX inhibitors bearing an aminomethylenethiophene (AMT)

227 Studies of the genetic structure of LOX-1 have also uncovered various genetic polymorphisms

228 We noted a significant suppression of LOX-1 expression that in turn suppressed apoptosis as we

229 ing body of work supporting the targeting of LOX and calls for greater efforts in developing therapeu

230 rt the concept of pharmacologic targeting of LOX pathway to inhibit liver fibrosis and promote its re

231 These vaccines bind to either CD40 or LOX-1, two dendritic cell surface receptors with differe

232 velope protein (Env gp140) to either CD40 or LOX-1, two endocytic receptors on dendritic cells (DCs),

233 n overexpressed, the SRCR repeats from other LOX family members can catalyze protein deacetylation/de

234 erols as substrates, and together with other LOX pathway enzymes, it formed specific volatile product

235 r that is >300-fold selective for LOXL2 over LOX.

236 bitor of LOXL2 that is highly selective over LOX and other amine oxidases.

237 Notably, while overall LOX/LOXL2-catalyzed collagen cross-links were enriched i

238 XCAT, a fusion of bacterial lactate oxidase (LOX) and catalase (CAT), which irreversibly converts lac

239 mmobilization of the enzyme lactate oxidase (LOX) by drop-casting procedure.

240 Lysyl oxidase (LOX) and LOX-like (LOXL) proteins are copper-dependent m

241 lysyl hydroxylase 2 (LH2) or lysyl oxidase (LOX) and LOX-like 2 (LOXL2) were significantly upregulat

242 poxia-induced ECM re-modeler, lysyl oxidase (LOX) as a key inducer of chemoresistance by developing c

243 lular matrix modifying enzyme lysyl oxidase (LOX) correlates with metastatic dissemination to the bon

244 1, which directly upregulates lysyl oxidase (LOX) expression.

245 tylimination as a function of lysyl oxidase (LOX) family members.

246 collagen crosslinking by the lysyl oxidase (LOX) family of enzymes.

247 The lysyl oxidase (LOX) family of extracellular proteins plays a vital role

248 aling increased expression of lysyl oxidase (LOX) in mesothelial and ovarian cancer cells to promote

249 Lysyl oxidase (LOX) is a secreted copper-dependent amine oxidase that c

250 Lysyl oxidase (LOX) is a secreted copper-dependent amine oxidase whose

251 lso cleaves and activates the lysyl oxidase (LOX) precursor, the enzyme catalyzing the initial step i

252 Lysyl oxidase (LOX) remodels the tumour microenvironment by cross-linki

253 Lysyl oxidase (LOX), a collagen cross-linking enzyme, has not been inve

254 t HG-induced up-regulation of lysyl oxidase (LOX), a collagen-cross-linking enzyme, in retinal capill

255 the secretory enzymes such as lysyl oxidase (LOX), while Atox1 in the nucleus functions as a Cu-depen

256 , ATP7A, and the proenzyme of lysyl oxidase (LOX; copper-loaded via ATP7A) are all in close proximity

257 Lysyl oxidases (LOXs) play a central role in extracellular matrix remode

258 Lysyl oxidase propeptide (LOX-PP), released during LOX processing, has been implic

259 on to the lectin-like oxidized LDL receptor (LOX-1).

260 um, normal medium and exposed to recombinant LOX-PP (rLOX-PP) or HG medium and examined for LOX-PP ex

261 Results indicate that HG up-regulates LOX-PP expression and reduces AKT activation.

262 rLOX-PP were examined for changes in retinal LOX-PP levels, AKT phosphorylation, and the number of ac

263 Mechanistically, secreted LOX functions as a potent macrophage chemoattractant via

264 In vitro, tumor-secreted LOX supported the attachment and survival of colorectal

265 Since LOX is an established player in cancer cell migration, o

266 to iron ligands of coral 8R-LOX and soybean LOX-1 but is not overlapping.

267 s, Galectin-1, Fibronectin, Heparan Sulfate, LOX, FAK1), cell cycle genes (USP16, S1P complexes), and

268 ication, myocardial ischemia; and summarizes LOX-1 modulation by some naturally occurring compounds a

269 odels of breast cancer metastasis, targeting LOX, or its downstream effects, significantly inhibited

270 linical rationale for developing and testing LOX inhibitors to overcome chemoresistance in TNBC patie

271 ants in 7 genes (PKD1, COL3A1, SMAD3, TGFB2, LOX, MYLK, and YY1AP1) in 14/384 cases in the study coho

272 a ATP7A) are all in close proximity and that LOX activity is reduced upon Atox1 silencing in the cell

273 aken together, our findings demonstrate that LOX enhances platelet activation and thrombosis.

274 Here, we find that LOX regulates the epidermal growth factor receptor (EGFR

275 In vivo experimental studies show that LOX overexpression in colorectal cancer cells or systemi

276 We show that LOX regulates EGFR by suppressing TGFbeta1 signalling th

277 Thus, we show that LOX regulates EGFR cell surface retention to drive tumou

278 Collectively, our findings show that LOX supports colorectal cancer cell dissemination in the

279 ating characteristic analyses suggested that LOX upregulation indicates disease complications and fib

280 Unlike in most insects the LOX of the praying mantis consists of five nested neurop

281 Expression of the LOX and LOXL2 isoforms is directly regulated by miR-200

282 Expression of the LOX variants p.Ser280Arg and p.Ser348Arg resulted in sig

283 ity against melanoma cells, specifically the LOX IMVI and SK-MEL-28 cell lines.

284 and proteomics analyses, we report that the LOX precursor is proteolytically processed by the procol

285 We noted that the LOX sequence between the BMP1- and ADAMTS-processing sit

286 from both mouse strains, suggesting that the LOX-1 pathway may be involved in complicated pregnancies

287 erall, the mantis LOX is more similar to the LOX of the locust than the more closely related cockroac

288 g with AA cyclization and shunting AA to the LOX pathway under physiological conditions.

289 Functionally, LOXL2, as opposed to LOX, is the principal isoform that crosslinks and stabil

290 TBEVs contribute to vascular dysfunction via LOX-1 and AT1 receptors during pregnancy.

291 L5 can modulate cardiac repolarization via LOX-1-mediated alteration sarcolemmal ionic currents.

292 OX-1 expression, suggesting that STBEVs (via LOX-1) play a role in normal adaptations to pregnancy.

293 ding pocket (Tyr(215) in Aerococcus viridans LOX) that is partially responsible for securing a flexib

294 Here we investigated whether LOX/HIF1 endows colorectal cancer cells with full compet

295 they reveal a novel mechanism through which LOX-driven IL6 production by colorectal cancer cells imp

296 While LOX-generated collagen cross-linking metabolites have be

297 Individuals with LOX variants had fusiform enlargement of the root and as

298 resentation and greater durability than with LOX-1.IMPORTANCE An effective vaccine to prevent HIV-1 i

299 Correspondingly, YAP1-LOX and beta1 integrin-SPP1 signaling correlates positiv

300 pression of five key genes (RARG, ID1, ZIC1, LOX and DHRS3), a pattern validated in 63 human adherent