ライフサイエンスコーパス: CLP

1 CLP caused an increase in renal capillary permeability a

2 CLP caused bone marrow (BM) and thymus atrophy, decrease

3 CLP caused substantial increases in mRNAs for IL-1beta a

4 CLP decreased pancreatic SP-D levels and caused severe p

5 CLP did not promote OC formation from bone marrow cells

6 CLP increased levels of cytokines (IL-1beta, IL-6, and T

7 CLP is not absolutely crucial, however; some 5LO activit

8 CLP promoted OC formation and bone resorption and expres

9 CLP TRPV1KO mice exhibited significant hypothermia, hypo

10 CLP-1, the mouse homolog of human hexamethylene bis-acet

11 CLP-activation of TLR4-mediated nuclear factor-kappaB an

12 CLP-assisted US thrombolysis resulted in restoration of

13 CLP-induced bone loss was prevented by Zoledronic acid.

14 CLP-induced markers of mitochondrial biogenesis and mito

15 CLPs come from a wide range of taxonomic groups-from sin

16 precipitation experiments indicated that 5LO-CLP complex formation in MM6 cells was increased by stim

17 at on cell stimulation, formation of the 5LO-CLP complex augments the translocation from cytosol to n

18 After CLP, NLRP3(-/-) mice showed reduced plasma levels of IL-

19 se in plasma and the peritoneal cavity after CLP, peak at 8 hours after infection, and are higher in

20 y monocytes into the peritoneal cavity after CLP, which is dependent on VLA-4, is impaired in above m

21 +) hematopoietic stem-progenitor cells after CLP improves long-term survival by 65%.

22 longer and suffered less organ damage after CLP.

23 n greater apoptosis and Fas expression after CLP and a decrease in glycoprotein 130 expression on LSE

24 ricular frozen sections before and 8 h after CLP revealed the presence of NLRP3 and IL-1beta proteins

25 injury with higher serum amylase 24 h after CLP.

26 was not affected significantly 18-24 h after CLP.

27 ts in echo/Doppler parameters in heart after CLP.

28 IKK inhibitor (IKK 16; 1 mg/kg) 1 hour after CLP or LPS administration attenuated these effects.

29 In addition, receipt of AB103 12 hours after CLP attenuated inflammatory cytokine responses and neutr

30 Receipt of AB103 24 hours after CLP still protected 63% of mice (5 of 8).

31 among mice treated with AB103 12 hours after CLP was 100% (8 of 8), compared with 17% among untreated

32 Two hours after CLP, an i.p. injection of 200 mug/kg of anti-rat NPCT an

33 At 10 mg/kg administered 6 hours after CLP, MnTMPyP did not alter blood pressure, but blocked s

34 Samples were harvested 20 hours after CLP.

35 by echocardiography before and 6 hours after CLP.

36 on was significantly decreased 6 hours after CLP.

37 f T cells was also evident at 16 hours after CLP.

38 t 58 hrs and 100% mortality at 154 hrs after CLP.

39 d by echocardiography before and 6 hrs after CLP.

40 1(+) CD11b(+) MDSCs gradually increase after CLP, reaching approximately 88% of the bone marrow myelo

41 ils, and increased acute kidney injury after CLP, and also had significantly higher mortality after t

42 MDSCs from septic mice into naive mice after CLP increased proinflammatory cytokine production, decre

43 e survival rate of CD36-deficient mice after CLP was 58% compared with 17% in control mice.

44 ves survival of MAIR-II-deficient mice after CLP.

45 Using an acute sepsis model after CLP, we found that iNOS-/- mice had a comparable level o

46 Mortality after CLP was reduced even when type I IFN responses were bloc

47 Similar effects were observed after CLP and FLAP knockdown in human primary macrophages as w

48 sponse, was elevated in several organs after CLP, and its expression was inhibited by H2S treatment.

49 he variability in physiologic response after CLP in mice and determined peaks in the temporal distrib

50 ells progressively decreased in spleen after CLP with a concomitant increase within the peritoneal ca

51 usion that mMCP-4 can enhance survival after CLP at least in part by limiting detrimental effects of

52 h post-CLP did not confer protection against CLP-triggered cardiac dysfunction, apoptosis and inflamm

53 ce (FACETS) or current local practice alone (CLP), using concealed computer-generated randomisation.

54 Control-ODN or iCpG-ODN did not alter CLP-induced cardiac dysfunction.

55 l, effects were similar for isolated CLO and CLP, except for ABCA4-ARHGAP29.

56 o significant differences between FACETS and CLP.

57 ve-transfer approaches, we show that HSC and CLP sensitivity to chronic LPS depends on hematopoietic-

58 thousands crystalline particles of CLP I and CLP II before and after compression.

59 the same compression conditions of CLP I and CLP II were observed and characterized quantitatively.

60 zed for quantitative comparison to CLP I and CLP II.

61 ic overexpression of S1P1 suppressed LSK and CLP cell proliferation in vivo.

62 in patients taking antidepressants, such as CLP.

63 ced cardiac-myocyte apoptosis and attenuated CLP-induced Fas and Fas ligand expression in the myocard

64 bsence of the TGFBIp gene in mice attenuated CLP-induced sepsis.

65 ice with anti-CXCR3 significantly attenuated CLP-induced hypothermia, decreased systemic cytokine pro

66 CpG-ODN significantly attenuated CLP-induced myocardial apoptosis and increased myocardia

67 Because CLP-induced inflammation involves response to fecal cont

68 nd fetal SNPs near TPM1 and NOG1 and between CLP and fetal SNPs at ABCA4-ARHGAP29, THADA, FOXE1, and

69 tify complex patterns of coevolution between CLPs and their various hosts.

70 ymorphs (I and II) of clopidogrel bisulfate (CLP) was determined to illustrate pressure distribution

71 fy the polymorphs of clopidogrel bisulphate (CLP).

72 perinuclear was clearly compromised in both CLP- and FLAP-deficient cells.

73 esponsiveness of MNCs was only attenuated by CLP, and a larger proportion of these neurons displayed

74 the genetics of infection mechanisms used by CLPs, particularly into the role of gene duplication and

75 severe deficiencies in all B lineage cells, CLP, LMPP, and total Flt3(+) MPP in bone marrow than the

76 ctional effects of four APs: chlorpromazine (CLP), haloperidol (HAL), risperidone (RIS) and clozapine

77 pine (QTP; 8.51 mug/capita/day), citalopram (CLP; 5.45 mug/capita/day), and venlafaxine (VLF; 3.59 mu

78 ing antidepressants, including Clomipramine (CLP), have an increased risk of osteoporotic fracture.

79 o-B cells and impairment in B cell-committed CLPs.

80 ymal progenitors reduced B-lineage committed CLPs, while conditional Cxcl12 or Scf deletion from IL-7

81 In contrast, CLP increased the proportion of SON neurons displaying s

82 In the positive control CLP group, median survival was 36 h (range 24-48 h).

83 TLR3 deficiency significantly decreased CLP-induced cardiac-myocyte apoptosis and attenuated CLP

84 tures derived from EBF1- and FOXO1-deficient CLPs.

85 uency of Ki-67(+) HSCs and severely depletes CLPs and B precursors.

86 Antibiotic administration during CLP revealed an important role for hepatocyte LPS cleara

87 o control bacterial burden in tissues during CLP-induced polymicrobial sepsis.

88 ing collagen-like peptide (CLP) to yield ELP-CLP conjugates that show a remarkable reduction in the i

89 s a member of chitinase-like protein family (CLPs) able to induce the proliferation of imaginal disc

90 e identify ecological conditions that favour CLPs over their simple lifecycle counterparts and highli

91 Although LMPP and Flt3(+) CLP contain precursors for NK and dendritic cell lineage

92 Second, although Flt3(-) CLPs are less common in the BM, they are abundant in the

93 enes are expressed by MPP3 cells and Flt3(-) CLPs, the latter only give rise to B cells in the spleen

94 Following CLP, compared with immunocompetent WT mice, NOD/SCID/IL2

95 6a, miR-122, miR-210) in the blood following CLP.

96 Intriguingly, following CLP, Nlrp3(-/-) peritoneal cells (primarily neutrophils)

97 inase (ERK) phosphorylation levels following CLP.

98 on factor identified as a candidate gene for CLP in human populations, with targeted deletion in mice

99 d dithiocarbamates-methyl isothiocyanate for CLP.

100 spina bifida; and trifluralin and maneb for CLP.

101 CXCR4 was required for CLP positioning near Interleukin-7(+) (IL-7) cells and f

102 Bone marrow cells from CLP-treated mice had normal OC precursor frequency, but

103 e apoptosis, and rescued humanized mice from CLP-induced mortality.

104 nce of cytokines and histones in plasma from CLP mice.

105 I significantly impeded pDC development from CLPs.

106 /IFN-I/Flt3 axis in pDC differentiation from CLPs.

107 onal DCs (cDCs) and pDCs were generated from CLPs in response to FL, whereas pDC generation required

108 e coevolution, as more mobile hosts can fuel CLP adaptation to less mobile hosts.

109 Furthermore, CLP associated IRF6 missense mutations disrupt the abili

110 equal groups: US+CLP group, US+saline group, CLP+sham US group, and no treatment group.

111 gen-overexpressing transgenic mice harboring CLP-1 heterozygosity.

112 Furthermore, our results identified CLPs, and not lymphoid-primed multipotent progenitors, a

113 sly administered EPCs are also beneficial in CLP sepsis and that CTCE provides synergistic benefit.

114 ers of EPCs were coadministered with CTCE in CLP mice they synergistically improved survival.

115 microcirculation and severe side effects in CLP induced septic rats, whereas the balanced crystalloi

116 s reveal multiple protective roles of HDL in CLP-induced sepsis.

117 odulating NF-kappaB-mediated inflammation in CLP-induced API.

118 inally, the presence of the p38 inhibitor in CLP mice reduced the development of cardiac dysfunction.

119 s, with a twofold decline in viable LSECs in CLP animals compared with sham controls.

120 However, OVLT neurons in CLP rats were hyperpolarized significantly compared with

121 gh blood TGFBIp levels were also observed in CLP-induced septic mice.

122 T cells underwent Ag-driven proliferation in CLP-treated SFB(+), but not in SFB(-), mice.

123 model of the acute inflammatory response in CLP (cecal ligation and puncture)-induced sepsis in rats

124 r bacterial levels, and improved survival in CLP without antibiotics.

125 er myeloerythroid genes was also enhanced in CLPs and lineage-negative progenitors, with a concurrent

126 Furthermore, FL induced IFN-I expression in CLPs, which in turn induced Flt3 up-regulation that faci

127 he lip, with or without palatal involvement (CLP), is associated with a higher incidence of developme

128 cted to a lethal dose of TNF, or to a lethal CLP procedure.

129 At the molecular level, CLP inhibited the activity of the ubiquitin E3 ligase It

130 ereas depletion of FOXO1 activity in LY6D(+) CLPs ablates EBF1 transcript levels.

131 that depletion of EBF1 expression in LY6D(+) CLPs severely affects FOXO1 mRNA abundance, whereas depl

132 CLP and indicate a direct role for the major CLP gene Irf6 in salivary gland development and a signif

133 nal targeting approach, we ablated the major CLP gene Irf6 only in the late embryonic oral epithelium

134 nditional knockout model involving the major CLP gene, Irf6, that overcomes the previously reported p

135 ApoM was stably associated with bone marrow CLPs, which showed active S1P1 signalling in vivo.

136 he three types of polymers, P(MBL)VAP, P(MBL)CLP, and P(MBL)ROP, can be readily controlled by adjusti

137 s, thus affording cross-linked polymer P(MBL)CLP.

138 Moreover, CLP-treated SFB(+) mice showed resistance to secondary l

139 As most CLP genes are expressed throughout the oral epithelium,

140 ion of IL-17 is an inherent feature of mouse CLPs.

141 and NME2 G71V in a patient with nonsyndromic CLP).

142 In addition, association of CLP with the nucleus was almost absent after 5LO knockdo

143 126 in vivo abolished CpG-ODN attenuation of CLP-induced cardiac dysfunction.

144 ion under the same compression conditions of CLP I and CLP II were observed and characterized quantit

145 However, the effects of CLP on bone metabolism are unknown.

146 authors hypothesized that the expression of CLP genes may persist in the dental epithelium and thus,

147 Expression of CLP increased MM6 cellular 5LO activity for all stimuli

148 associations between VAX1 and human forms of CLP, we find no evidence of a direct role for this trans

149 5LO activity remained in all incubations of CLP knockdown cells.

150 We observed that introduction of CLP-1 haplodeficiency in the transgenic alpha-myosin hea

151 tment in the outcome of a fulminant model of CLP.

152 hology of thousands crystalline particles of CLP I and CLP II before and after compression.

153 into the role of IRF6 in the pathogenesis of CLP, we sought to identify direct IRF6 protein interacto

154 The pDCs of CLP origin showed evidence of past RAG1 expression and h

155 our findings underscore the critical role of CLP-1 in remodeling of the genetic response during hyper

156 In this study, we evaluated the role of CLP-1 in vivo in induction of left ventricular hypertrop

157 To study the roles of CLP and FLAP, we knocked down these proteins in the huma

158 tal forms were all irregular, the surface of CLP II was found to be rougher than CLP I.

159 Next, treatment of CLP mice with exosomes released from miR-223-KO MSCs sig

160 Given the demonstrated ability of CLPs to modify collagens, our results not only provide a

161 requirement for CD11a in the development of CLPs.

162 understanding of the evolutionary ecology of CLPs is essential for the development of effective frame

163 Our studies describe effector functions of CLPs consistent with innate host defense traits of the c

164 at facilitated survival and proliferation of CLPs, as well as their differentiation into pDCs.

165 Effects of TGFBIp knockout on CLP-induced septic mortality and effects of TGFBIp on mu

166 op increased survival after LPS injection or CLP.

167 When subjected to LPS or CLP, compared with sham-operated controls, CKD mice exhi

168 or hardly, protected against a lethal TNF or CLP challenge.

169 e novo deletions among cleft lip and palate (CLP) cases than seen among cleft palate (CP) and cleft l

170 eft lip only (CLO) and cleft lip and palate (CLP).

171 seases, isolated cleft lip and cleft palate (CLP), hypothyroidism and thyroid cancer all map to the F

172 ida, cleft lip with or without cleft palate (CLP), or cleft palate only.

173 Patients with cleft lip/palate (CLP) have been reported, in some studies, to exhibit an

174 and nonsyndromic forms of cleft lip/palate (CLP).

175 Patients with cleft lip and/or palate (CLP), who undergo numerous medical interventions from in

176 Cleft lip with or without palate (CLP) and isolated cleft palate (CP) are common human dev

177 , are caused by complex lifecycle parasites (CLPs): parasites that sequentially infect different host

178 triple-helix-forming collagen-like peptide (CLP) to yield ELP-CLP conjugates that show a remarkable

179 s the consistency of closed-loop perception (CLP) with empirical data and show that it can be synthes

180 ts underwent cecal ligation and perforation (CLP), and serum and brain (hippocampus and prefrontal co

181 und in the calcineurin-like phosphoesterase (CLP) family of metalloenzymes; however, it cleaves a pyr

182 the hippocampus at days 15, 17, and 19 post-CLP reduced Abeta and p-Tau(Ser-202) accumulation, Akt/m

183 hat injection of miR-223-KO MSCs at 1 h post-CLP did not confer protection against CLP-triggered card

184 Six hours post-CLP, both Live-P and Die-P groups have equivalent perito

185 vely decreased during the 30-day period post-CLP, concomitant with a progressive increase in RAGE lig

186 wed a maintenance of cardiac function at pre-CLP levels.

187 Common lymphoid precursors (CLPs) produced only a few cDCs with variable efficiency,

188 CpG-ODN prevented CLP-induced cardiac dysfunction, as evidenced by mainten

189 CpG-ODN prevents CLP-induced cardiac dysfunction, in part through activat

190 C) expansion and common lymphoid progenitor (CLP) depletion in a model of chronic low-dose LPS.

191 arrested in the common lymphoid progenitor (CLP) LY6D(+) cell stage.

192 required in the common lymphoid progenitor (CLP), and was essential for the differentiation of alpha

193 s of MPP-derived common lymphoid progenitor (CLP), common myeloid progenitor (CMP), megakaryocyte-ery

194 PP) switch into common lymphoid progenitors (CLP) or common myeloid progenitors (CMP) during this pro

195 enitors (LMPP), common lymphoid progenitors (CLP), and B/T cell precursors.

196 r generation of common lymphoid progenitors (CLPs) and lymphoid-primed multipotent progenitors.

197 rs develop from common lymphoid progenitors (CLPs) and that E4bp4 must be expressed at the CLP stage

198 ells (LSKs) and common lymphoid progenitors (CLPs) in bone marrow.

199 er, a subset of common lymphoid progenitors (CLPs) that expresses the integrin alpha4beta7 gives rise

200 rentiation into common lymphoid progenitors (CLPs), which decreased lymphopoiesis.

201 tors (MPPs) and common lymphoid progenitors (CLPs).

202 ta1 in HSCs and common lymphoid progenitors (CLPs).

203 evelopment from common lymphoid progenitors (CLPs).

204 ctivity in the crypt-denuded lamina propria (CLP) increased within 24 h postinfection, followed by it

205 accessory proteins, coactosin-like protein (CLP) and 5-lipoxygenase-activating protein (FLAP), can s

206 ymatically inactive chitinase-like proteins (CLPs) such as BRP-39, Ym1 and Ym2 are established marker

207 Both the caecal ligation and puncture (CLP) and lipopolysaccharide models of sepsis induce the

208 ollowing murine cecal ligation and puncture (CLP) at 8 h and 34 +/- 9% following LPS treatment in vit

209 was induced by cecal ligation and puncture (CLP) in 77 male rats.

210 psis induced by cecal ligation and puncture (CLP) in mice.

211 psis induced by cecal ligation and puncture (CLP) in mice.

212 e, we show that cecal ligation and puncture (CLP) in rats impairs the osmoresponsiveness of neurons i

213 ality following cecal ligation and puncture (CLP) in the severely immunodeficient nonobese diabetic (

214 vitro and after cecal ligation and puncture (CLP) in vivo In both cases, C5a in vitro caused activati

215 s, our model of cecal ligation and puncture (CLP) induced sepsis stratifies mice as predicted to Live

216 Using the mouse cecal ligation and puncture (CLP) model of sepsis, the administration of LXA4 (7 mug/

217 cently, using a cecal-ligation and puncture (CLP) model of sepsis, we showed that sepsis induces subs

218 sing the murine cecal ligation and puncture (CLP) model of sepsis.

219 ut (KO) mice in cecal ligation and puncture (CLP) model.

220 endotoxemia and cecal ligation and puncture (CLP) models of sepsis.

221 Here, we used a cecal ligation and puncture (CLP) murine model of prolonged sepsis to show that adopt

222 a model and the cecal ligation and puncture (CLP) peritonitis model.

223 -based model of cecal ligation and puncture (CLP) that standardizes the testing of time-sensitive the

224 Cecal ligation and puncture (CLP) was used as a polymicrobial sepsis model in vivo to

225 thal shock, and cecal ligation and puncture (CLP) were performed in genetically or pharmacologically

226 dy, we employed cecal ligation and puncture (CLP), a clinically relevant septic animal model, and uti

227 eased following cecal ligation and puncture (CLP), an animal model of polymicrobial sepsis, and was c

228 3; or underwent cecal ligation and puncture (CLP), followed by treatment with AB103.

229 crobial sepsis, cecal ligation and puncture (CLP), in C57BL/6J-mMCP-4-deficient mice versus C57BL/6J

230 psis induced by cecal ligation and puncture (CLP), we investigated the role of the NLRP3 inflammasome

231 y in a model of cecal ligation and puncture (CLP), with or without antibiotics.

232 susceptible to caecal ligation and puncture (CLP)-induced peritonitis than wild-type (WT) mice.

233 murine model of cecal ligation and puncture (CLP)-induced polymicrobial sepsis, which transitions fro

234 rotects against cecal ligation and puncture (CLP)-induced sepsis as shown by 75% fatality in Scarb1(I

235 ium (SFB) after cecal ligation and puncture (CLP)-induced sepsis using mice that either contained or

236 Mice undergoing cecal ligation and puncture (CLP)-induced sepsis were treated with neutralizing anti-

237 ibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal g

238 1 hour prior to cecal ligation and puncture (CLP)-induced sepsis.

239 ction following cecal ligation and puncture (CLP)-induced sepsis.

240 ic shock and in cecal ligation and puncture (CLP)-induced septic mice.

241 mouse model of cecal ligation and puncture (CLP)-induced septic shock.

242 was induced by cecal ligation and puncture (CLP).

243 sham surgery or cecal ligation and puncture (CLP).

244 uced in rats by cecal ligation and puncture (CLP).

245 g) or sepsis by cecal ligation and puncture (CLP).

246 psis induced by cecal ligation and puncture (CLP).

247 epsis caused by cecal ligation and puncture (CLP).

248 psis induced by cecal ligation and puncture (CLP).

249 psis induced by cecal ligation and puncture (CLP).

250 on of sepsis by cecal ligation and puncture (CLP).

251 ly the model of cecum ligation and puncture (CLP).

252 psis induced by cecal ligation and puncture (CLP).

253 mice undergoing cecal-ligation-and-puncture-(CLP).

254 linear solver COIN-OR Linear program Solver (CLP).

255 rface of CLP II was found to be rougher than CLP I.

256 Our findings indicate that CLP causes bone loss by enhancing Itch-mediated osteocla

257 These results show that CLP in humanized mice provides a model to study human se

258 polylinker region in Smad3, suggesting that CLP-1-mediated changes in pTEFb activity may trigger Cdk

259 We conclude that CLPs have reached the point where they cannot be a Notch

260 We show that CLPs participate in dynamic host-parasite coevolution, a

261 ere obtained at days 1, 15, and 30 after the CLP.

262 of NF-kappaB activity in the crypts and the CLP regulates crypt hyperplasia and/or colitis, and diet

263 LPs) and that E4bp4 must be expressed at the CLP stage for differentiation toward the NK lineage to o

264 In the CLP mouse sepsis model, L-37pA improved survival from 6

265 Tyr(182)) and p38 (Thr(202)/Tyr(204)) in the CLP preceded increases in the crypts.

266 elevated temperatures upon unfolding of the CLP domain.

267 in the conserved metal-binding motifs of the CLP family greatly inhibit HiLpxH activity, highlighting

268 ooth defects could be considered part of the CLP spectrum in relatives of an affected individual.

269 ture of the ELP domain upon formation of the CLP triple helix.

270 wild-type virulent Listeria), suggesting the CLP-induced polymicrobial sepsis primed for a protective

271 ommon to the Nudix family rather than to the CLP family.

272 Therefore, CLP affects the properties of osmoregulatory neurons in

273 In contrast, Cl-amidine attenuated these CLP and lipopolysaccharide-induced alterations.

274 and analyzed for quantitative comparison to CLP I and CLP II.

275 onfirmed that the direct addition of LXA4 to CLP neutrophils increased phagocytic ability but not CD6

276 estrogen deactivation and sensitizes mice to CLP-induced inflammatory response.

277 pha, and IL-10) and organ damage relative to CLP in wild-type mice.

278 transgenic mice were moderately resistant to CLP-induced septic death compared with B6 mice.

279 e the variability in physiologic response to CLP sepsis and conduct a cost analysis detailing the pot

280 from death in Nlrp3(-/-) mice in response to CLP.

281 Mice were subjected to CLP and administered EPCs at varying doses, CTCE, or a c

282 ched wild-type (n=12) mice were subjected to CLP.

283 ApoA-I-KO mice were more susceptible to CLP-induced septic death as shown by the 47.1% survival

284 were the most effective subset (relative to CLPs).

285 ther tlr2(-/-)or tlr2 4(-/-), that underwent CLP were resistant to the secondary pulmonary infection.

286 , tlr5(-/-), tlr2 4(-/-) mice that underwent CLP were secondarily subjected to P. aeruginosa pulmonar

287 measured plasma biomarkers in the untreated CLP group, comprising 14 pro- and anti-inflammatory cyto

288 %; range 54-95%) compared with the untreated CLP group.

289 randomly divided into four equal groups: US+CLP group, US+saline group, CLP+sham US group, and no tr

290 In vivo, CLP led to a significant increase in splenic cfB express

291 Theory tells us when CLPs should be favoured by selection, but more empirical

292 anencephaly, 123 with spina bifida, 277 with CLP, and 117 with cleft palate only in addition to 785 c

293 hat the rs7850258 allele (G) associated with CLP and hypothyroidism has significantly greater enhance

294 htened caries susceptibility associated with CLP and indicate a direct role for the major CLP gene Ir

295 tudies of postnatal sequelae associated with CLP have been hampered by neonatal lethality.

296 tension, and organ dysfunction compared with CLP WT mice.

297 tations in the NME proteins in patients with CLP (NME1 R18Q in an IRF6 and GRHL3 mutation-negative pa

298 However, as patients with CLP congenitally lack bone in the cleft site with dimini

299 In patients with CLP, the frequency of coding mutations in FOXE1 fails to

300 re, we demonstrate that WT mice treated with CLP for 2 weeks had significantly reduced trabecular bon