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 led to decreased miR-145a expression in lung pericyt

9 CLP promoted OC formation and bone resorption and expres

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

11 CLP-induced markers of mitochondrial biogenesis and mito

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

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

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

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

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

17 longer and suffered less organ damage after CLP.

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

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

20 injury with higher serum amylase 24 h after CLP.

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

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

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

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

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

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

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

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

29 Samples were harvested 20 hours after CLP.

30 by echocardiography before and 6 hours after CLP.

31 on was significantly decreased 6 hours after CLP.

32 nd in renal AMPK activation 6-24 hours after CLP/IM.

33 1(+) CD11b(+) MDSCs gradually increase after CLP, reaching approximately 88% of the bone marrow myelo

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

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

36 tly reduced in basophil-deficient mice after CLP.

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

38 Moreover, after CLP, mice whose basophils could not produce TNF, exhibit

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

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

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

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

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

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

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

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

47 o significant differences between FACETS and CLP.

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

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

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

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

52 retion by macrophages in response to LPS and CLP, ultimately resulting in increased survival.

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

54 in patients taking antidepressants, such as CLP.

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

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

57 Because CLP-induced inflammation involves response to fecal cont

58 nic (2D2) CD4 T cells after, but not before, CLP led to EAE disease equivalent to sham mice.

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

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

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

62 fy the polymorphs of clopidogrel bisulphate (CLP).

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

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

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

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

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

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

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

70 lenged with gram-negative bacterium E. coli, CLP, or E. coli derived lipopolysaccharide.

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

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

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

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

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

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

77 As for HBV, DHBV CLPs consist of a dimeric alpha-helical frame-work with

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

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

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

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

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

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

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

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

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

87 Jax mice had 7-d mortality of 90% following CLP, whereas CR mice had a mortality of 53%.

88 6a, miR-122, miR-210) in the blood following CLP.

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

90 inase (ERK) phosphorylation levels following CLP.

91 ohoused mice had improved survival following CLP compared to Jax mice and had similar survival regard

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

93 d dithiocarbamates-methyl isothiocyanate for CLP.

94 spina bifida; and trifluralin and maneb for CLP.

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

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

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

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

99 Direct ex vivo analysis of CD8 TILs from CLP hosts showed decreased proliferation, IFN-gamma prod

100 I significantly impeded pDC development from CLPs.

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

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

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

104 Furthermore, CLP associated IRF6 missense mutations disrupt the abili

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

106 Our results implicate CLP-EGFR-Pyk2-MEK-ERK as a key intrinsic pathway control

107 In CLP-induced sepsis, pericytes lacking miR-145a exhibited

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

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

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

111 oint blockade did not reduce tumor growth in CLP hosts when therapy was administered after PD-1(hi) C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 nes of the single gene for the mitochondrial CLP protease subunit, CLPP2, in Arabidopsis (Arabidopsis

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

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

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

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

136 Notably, CLP mice have delayed onset and reduced disease severity

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

138 126 in vivo abolished CpG-ODN attenuation of CLP-induced cardiac dysfunction.

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

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

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

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

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

144 After 20 h of CLP induction, NETs in the lungs of WT and CIRP(-/-) mic

145 After 20 h of CLP, NETosis in the lungs was significantly decreased in

146 5LO activity remained in all incubations of CLP knockdown cells.

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

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

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

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

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

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

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

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

155 line (n = 14; P < 0.027); 4) LR treatment of CLP-induced sepsis reduced proinflammatory cytokine expr

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

157 requirement for CD11a in the development of CLPs.

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

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

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

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

162 op increased survival after LPS injection or CLP.

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

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

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

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

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

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

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

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

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

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

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

174 tures of several DHBV capsid-like particles (CLPs) determined by electron cryo-microscopy.

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

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

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

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

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

180 llel with proinflammatory cytokines; 2) post-CLP survival rates of Hca2(-/-) knockout mice (n = 22) w

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

182 nous dosing of AVR-25 (10 mg/kg, 6-12 h post-CLP) alone and in combination with antibiotic imipenem p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 enitors (CMPs), common lymphoid progenitors (CLPs), granulocyte-macrophage progenitors (GMPs), megaka

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

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

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

201 evelopment from common lymphoid progenitors (CLPs).

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

203 Although chitinase-like proteins (CLPs) form part of this microenvironment, their function

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

205 mice underwent cecal ligation and puncture (CLP) and human proximal tubule epithelial cells (TEC; HK

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

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

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

209 human sepsis is cecal ligation and puncture (CLP) in mice.

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

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

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

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

217 ortality in the cecal ligation and puncture (CLP) model of sepsis.

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

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

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

221 Following the cecal ligation and puncture (CLP) procedure, intravenous dosing of AVR-25 (10 mg/kg,

222 , rats received cecal ligature and puncture (CLP) surgery and fluid therapy with or without NButGT.

223 study, we show cecal ligation and puncture (CLP) surgery renders mice permissive to increased B16 me

224 sepsis model of cecal ligation and puncture (CLP) that provides additional daily chronic stress (DCS)

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

226 roups underwent cecal ligation and puncture (CLP) to induce peritonitis, while control groups had a s

227 ed the model of cecal ligation and puncture (CLP) to investigate the role of LXR activation during se

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

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

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

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

232 3; or underwent cecal ligation and puncture (CLP), followed by treatment with AB103.

233 have undergone cecal ligation and puncture (CLP), hydroxycarboxylic acid receptor 2 (HCA2) expressio

234 odel of sepsis, cecal ligation and puncture (CLP), we compared sepsis-induced changes in platelet gen

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

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

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

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

239 urvival rate in cecal ligation and puncture (CLP)-induced sepsis by inhibiting lung inflammation, leu

240 , the impact of cecal ligation and puncture (CLP)-induced sepsis on the development of experimental a

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

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

243 1 hour prior to cecal ligation and puncture (CLP)-induced sepsis.

244 of miR-145a in cecal ligation and puncture (CLP)-induced sepsis.

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

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

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

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

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

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

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

252 lyzed following cecal ligation and puncture (CLP).

253 RP(-/-) mice by cecal ligation and puncture (CLP).

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

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

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

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

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

259 olding-proficient extension produced regular CLPs in bacteria but failed to form stable nucleocapsids

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

261 wed strong genetic interactions with stromal CLP protease system mutants, resulting in reduced growth

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

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

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

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

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

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

268 elevated temperatures upon unfolding of the CLP domain.

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

270 are and contrast the mouse microbiome of the CLP model to the emerging science of the microbiome of h

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

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

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

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

275 Therefore, CLP affects the properties of osmoregulatory neurons in

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

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

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

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

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

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

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

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

284 for HCA2 in sepsis; 3) WT mice subjected to CLP-induced sepsis and treated with lactated Ringer's so

285 etween septic patients and mice subjected to CLP.

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

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

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

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

290 %; range 54-95%) compared with the untreated CLP group.

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

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

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

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

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

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

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