ライフサイエンスコーパス: SCN

1 SCN neurons define circadian time using transcriptional/

2 SCN of three genetic backgrounds-wild-type, short-period

3 SCN timekeeping is sustained by a cell-autonomous transc

4 SCN-enriched transcripts identified in this study provid

5 A total of 79 microarrays were used (24 SCN and 55 WB samples, 4 different microarray platforms)

6 oisy circadian rhythms in the isolated E14.5 SCN and most show reliable, self-sustained, synchronized

7 sustained, synchronized rhythms in the E15.5 SCN.

8 not disrupt circadian synchrony in the E15.5 SCN.

9 atforms), alongside 17 RNA-Seq data files (7 SCN and 10 WB).

10 sults, we transformed five WRKY genes into a SCN-susceptible soybean cultivar and generated transgeni

11 ogic SCN ligands were sufficient to activate SCN antibacterial activity against Escherichia coli In t

12 tral phase wave of PER2 typical of the adult SCN appears approximately P2, indicating that multiple s

13 opeptide critical for synchrony in the adult SCN, and its receptor, VPAC2R, reached detectable levels

14 n clock gene expression typical of the adult SCN.

15 r how alterations in CRY1/2 stability affect SCN neurophysiology.

16 transfer the nitride group to CS2 to afford SCN(-) and uranium(IV) disulfide.

17 s are governed by dynamic interactions among SCN neurons, with neuroadaptations in network function d

18 emporally reorganize circadian phasing among SCN neurons, which in turn changes the period length of

19 We thereby identify Gpr176 as an SCN-enriched orphan GPCR that sets the pace of circadian

20 protein response and apoptosis induced by an SCN-derived NE mutant, which was associated with sustain

21 that a G-CSFR mutant, d715, derived from an SCN patient inhibited G-CSF-induced expression of NE in

22 te because a sufficient amount of Gnd(+) and SCN(-) partitioned to the polymer surface to prevent cro

23 l variation in both BK current magnitude and SCN firing, and disrupting behavioural rhythmicity.

24 The vSPVZ integrates retinal and SCN input and, when activated, suppresses locomotor acti

25 autonomous circadian activity in arrhythmic SCN-lesioned (SCNX) C3H/HeN mice.

26 nary catechols that were able to function as SCN ligands of which pyrogallol in particular was positi

27 ons correspond to functional Fe(III)-binding SCN ligands, we devised a biophysical protein binding sc

28 isms are known to be capable of biodegrading SCN(-); however, little is known regarding the potential

29 iring or by physical cutting suppresses both SCN reorganization and period changes.

30 naling was activated in Arabidopsis early by SCN infection.

31 Gpr176 is expressed in a circadian manner by SCN neurons, and molecular characterization reveals that

32 rk are preferentially located in the central SCN, with sparsely connected shells surrounding these co

33 Stability of BeB11 (X)12(3-) (X=CN, SCN, BO) trianions is demonstrated in the gas phase, wit

34 In contrast, SCN astrocytes are active during circadian nighttime, wh

35 , and cellular desynchrony in Lhx1-deficient SCN largely results from Vip loss [17, 18].

36 heat application to cultured Lhx1-deficient SCN.

37 For degus SCN c-Fos activation by light was stronger with RGB-ligh

38 oscillations in gene expression that direct SCN electrical activity and thence behavior.

39 Disrupting SCN circadian rhythms is sufficient to cause helplessnes

40 mRNA population analysis revealed a distinct SCN transcript profile that includes multiple novel Rbfo

41 idnight triggered c-Fos expression in dorsal SCN.

42 nsmission is sensed by neurons of the dorsal SCN via specific pre-synaptic NMDA receptor assemblies c

43 The transcription factor LHX1 drives SCN Vip expression, and cellular desynchrony in Lhx1-def

44 d circadian rhythms from the whole embryonic SCN.

45 st screened soybean WRKY genes for enhancing SCN resistance when over-expressed in transgenic soybean

46 ers originating from ipRGCs cover the entire SCN, physiological evidence suggests that only vasoactiv

47 e innervation patterns throughout the entire SCN.

48 anxiety-like behavior in mice, establishing SCN-Bmal1-KD mice as a new animal model of depression.

49 hloride regulation in AVP and VIP-expressing SCN neurons and found evidence suggesting that [Cl(-)]i

50 s in Fbxl3(Afh/Afh) compared with Fbxl3(+/+) SCN slices.

51 e that endogenous daily rhythms in the fetal SCN begin with few noisy oscillators on E14.5, followed

52 We found that a few SCN cells developed circadian periodicity in PER2 by 14.

53 GmSNAPs indicates a co-regulation following SCN infection.

54 However, not all genes critical for SCN function are rhythmically expressed.

55 nsity, spectra, and timing are important for SCN synchronisation.

56 en various anions and shows a preference for SCN(-) and Cl(-).

57 We map spatial receptive fields (RFs) for SCN neurons and find that only a minority are excited (o

58 myeloid leukemia (AML), and progression from SCN to AML is accompanied by mutations in CSF3R encoding

59 tion and perform patch-clamp recordings from SCN brain slices across the projected day/night cycle.

60 od CK1epsilon tau mutation specifically from SCN astrocytes resulted in lengthened rhythms in the SCN

61 emonstrate the functionality of the GmSHMT08 SCN resistance gene in a transgenic soybean plant.

62 ophysical protein binding screen to identify SCN ligands through direct analysis of human urine.

63 Electrophysiological and calcium imaging SCN recordings demonstrated changes in the response to g

64 In SCN neurons, auto-regulatory feedback on core clock gene

65 nah exon 12, all consistent with a change in SCN RBFOX activity.

66 racellular molecular clock drives changes in SCN neuronal excitability, but it is unclear how mutatio

67 ic re-programming of intracellular clocks in SCN astrocytes was capable of remodeling circadian behav

68 e also demonstrated functional correlates in SCN gene transcripts; inclusion of Cacna1c exon 7, and a

69 for circadian function, we expressed CRY in SCN of Cry-deficient mice using adeno-associated virus (

70 r, the novel gain of function of GmSHMT08 in SCN resistance remains to be characterized.

71 Cs are the primary regulators of [Cl(-)]i in SCN neurons.

72 comprehensive regulatory network involved in SCN resistance and provided insights into the complex mo

73 CN(-) reactor expressed proteins involved in SCN(-) degradation, sulfur oxidation, carbon fixation, a

74 Of eleven isoforms in SCN and cerebral cortex that exhibit exon variation acro

75 e proapoptotic activity of the NE mutants in SCN patients.

76 ean, to understand its regulatory network in SCN defense.

77 o alongside cellular molecular pacemaking in SCN slices in vitro demonstrated that such chimeric circ

78 are rare in de novo AML, are so prevalent in SCN/AML.

79 NKCC1 contributes to [Cl(-)]i regulation in SCN neurons, but that the KCCs are the primary regulator

80 s and network-level circadian rhythmicity in SCN never previously exposed to CRY.

81 e GmSNAP18 is performing a different role in SCN resistance than PI 88788-type GmSNAP18.

82 ctions aside from its main enzymatic role in SCN resistance.

83 dentifying genes which may play key roles in SCN physiology or provide SCN-specific drivers.

84 e essential clock gene Bmal1 specifically in SCN astrocytes lengthened the circadian period of clock

85 The distribution of functional molecules in SCNs provides insight into the information flow and the

86 NV exists within Fayette, a released, inbred SCN-resistant soybean cultivar with a high copy number a

87 ity of a microbial community over increasing SCN(-) loadings, we established and operated a continuou

88 ed in this study provide novel insights into SCN function, including identifying genes which may play

89 SCN and WB samples) reliably detected known SCN markers.

90 Although similarly enriched in known SCN(-)-degrading strains of thiobacilli, this consortium

91 imately Br(-) approximately NO3(-) <ClO4(-) <SCN(-) series.

92 Many SCN neurons express vasopressin, and it has been assumed

93 ompletely degraded up to approximately 10 mM SCN(-) to ammonium and sulfate, with some evidence of ni

94 ain-of-function mutant ein4-1 attracted more SCN than the wild-type, there were no significant differ

95 recordings we show that neurons in the mouse SCN are responsive to stimuli with these characteristics

96 ns during embryonic development in the mouse SCN.

97 Escherichia coli In the presence of multiple SCN ligands, native mass spectrometry demonstrated that

98 ample, FDA of the CK1epsilon(Tau/Tau) mutant SCN treated with the CK1epsilon-specific inhibitor PF-48

99 bles ultra-high selectivity for CO2 over N2 (SCN approximately 40 000) and CH4 (SCM approximately 330

100 Soybean cyst nematode (SCN) is the most damaging pest of soybean worldwide.

101 s that contributes to soybean cyst nematode (SCN) resistance in the Peking-type resistance of soybean

102 confers resistance to soybean cyst nematode (SCN), is a CNV of multiple 31.2-kb genomic units each co

103 erodera glycines, the soybean cyst nematode (SCN), quickly migrated to soybean roots in Pluronic F-12

104 ysis in resistance to soybean cyst nematode (SCN), the most important soybean pathogen.

105 mediate resistance to soybean cyst nematode (SCN).

106 e widely used against soybean cyst nematode (SCN, Heterodera glycines Ichinohe).

107 mediate resistance to soybean cyst nematode (SCN; H. glycines), the most economically damaging pathog

108 lobe network (TLN), and subcortical network (SCN), and sensorimotor network (SMN) were selected as re

109 ific cell type, the Shepherd's crook neuron (SCN), extends dendrites in both input regions.

110 Severe congenital neutropenia (SCN) and Shwachman-Diamond syndrome (SDS) are congenital

111 patients with severe congenital neutropenia (SCN).

112 omplexity of the axonal arborizations in non-SCN regions are less elaborate than those in the SCN.

113 expression comparable to that of nonchimeric SCN, demonstrating that this circuit-level property is i

114 tion of rod/cone and suprachiasmatic nuclei (SCN) by light was paradoxically greatly reduced, while t

115 are regulated by the suprachiasmatic nuclei (SCN) in the hypothalamus, which are primarily entrained

116 Suprachiasmatic nuclei (SCN) neurons contain an intracellular molecular circadia

117 ck is located in the suprachiasmatic nuclei (SCN) of the hypothalamus and it regulates circadian osci

118 Neurons in the suprachiasmatic nuclei (SCN) of the hypothalamus are described as master pacemak

119 rcadian clock in the suprachiasmatic nuclei (SCN) of the hypothalamus regulates physiology and behavi

120 ls is located in the suprachiasmatic nuclei (SCN) which regulate physiology and behaviour, as well as

121 etworking within the suprachiasmatic nuclei (SCN), the circadian "master clock," which is DNA methyla

122 adian pacemaker, the suprachiasmatic nuclei (SCN).

123 master clock in the suprachiasmatic nuclei (SCNs) and/or reduce the synchronizing effects of light i

124 circadian pacemaker (Suprachiasmatic Nuclei, SCN) maintains the phase relationship with the external

125 jection targets the suprachiasmatic nucleus (SCN) (an important hypothalamic control center).

126 The suprachiasmatic nucleus (SCN) defines 24 h of time via a transcriptional/posttran

127 cadian clock of the suprachiasmatic nucleus (SCN) encodes time-of-day information that allows mammals

128 The suprachiasmatic nucleus (SCN) is the central circadian clock in mammals.

129 The suprachiasmatic nucleus (SCN) is the master circadian clock controlling daily beh

130 rangely depleted in suprachiasmatic nucleus (SCN) neurons, and may be compensated by a change in Rbfo

131 In mammals, the suprachiasmatic nucleus (SCN) of the hypothalamus coordinates daily rhythms inclu

132 The suprachiasmatic nucleus (SCN) of the hypothalamus has an essential role in orches

133 nal activity in the suprachiasmatic nucleus (SCN) of the hypothalamus of mice that displayed contagio

134 The suprachiasmatic nucleus (SCN) of the hypothalamus orchestrates daily rhythms of p

135 hese project to the suprachiasmatic nucleus (SCN) of the hypothalamus to entrain circadian rhythms th

136 k in mammals is the suprachiasmatic nucleus (SCN) of the hypothalamus.

137 The suprachiasmatic nucleus (SCN) receives direct retinal input from the intrinsicall

138 mic hamsters in the suprachiasmatic nucleus (SCN) that paralleled changes in the medial septum and hi

139 dian pacemaker, the suprachiasmatic nucleus (SCN), determine the period of wheel-running activity.

140 ircadian clock, the suprachiasmatic nucleus (SCN), is vital in allowing animals to optimize physiolog

141 The suprachiasmatic nucleus (SCN), the brain's circadian pacemaker, governs daily rhy

142 transmission in the suprachiasmatic nucleus (SCN), the master pacemaker of circadian physiology.

143 The suprachiasmatic nucleus (SCN)-often referred to as the master circadian clock-is

144 ological clock, the suprachiasmatic nucleus (SCN).

145 coordinated by the suprachiasmatic nucleus (SCN).

146 area (VTA) and the suprachiasmatic nucleus (SCN).

147 strongly and competitively by N3(-), OCN(-), SCN(-), NO2(-), and NO3(-), whereas CO2 reduction is inh

148 Activation of SCN GRP/GRPR neurons evoked scratching behavior.

149 evidence links the antibacterial activity of SCN in human urine to iron sequestration and metabolomic

150 ighttime, when they suppress the activity of SCN neurons by regulating extracellular glutamate levels

151 ght entrainment, synchrony, and amplitude of SCN cellular clocks and organizes circadian behavior [5-

152 Binding of SCN-, however, eliminates the water wires altogether.

153 (-) reactor, Thiobacillus strains capable of SCN(-) degradation were highly abundant, whereas the amm

154 provides a new perspective on the concept of SCN pacemaker cells.

155 roteins influence the temporal expression of SCN neuronal state or intercellular communication within

156 irradiance increased time averaged firing of SCN neurons (typically considered to encode background l

157 recapitulated by chemogenetic inhibition of SCN GRP neurons.

158 s-flow bioreactor fed increasing loadings of SCN(-).

159 The molecular mechanism of SCN resistance remains largely unknown.

160 hts into the complex molecular mechanisms of SCN resistance in wild soybean.

161 ructure of the PER2 PAS core and the pace of SCN circadian timekeeping.

162 onium sulfate to mimic breakdown products of SCN(-).

163 cadian changes in the membrane properties of SCN neurons, but it is unclear how alterations in CRY1/2

164 Electrophysiological responses of SCN neurons to light steps are well established, but res

165 ssin release contributes to the responses of SCN neurons to light, and enhances expression of the imm

166 asopressin release enhances the responses of SCN neurons to light.

167 The robustness of SCN timekeeping is further enhanced by interneuronal, ci

168 Seepage of SCN(-)-contaminated waters into aquifers can occur from

169 the brain and illuminate a subpopulation of SCN neurons as a focal point for future studies aimed at

170 l unclear, therefore, which subpopulation of SCN neurons receives synaptic input from the retina and

171 ,7-triazacyclononane-1,4,7-triacetic acid (p-SCN-Bn-NOTA) allows the incorporation of radiometals for

172 ,7-triazacyclononane-1,4,7-triacetic acid (p-SCN-Bn-NOTA) and labeled with (64)Cu ((64)Cu-NOTA-FVIIai

173 ,7-triazacyclononane-1,4,7-triacetic acid (p-SCN-Bn-NOTA) and labeled with (64)Cu.

174 The chelator p-SCN-Bn-DFO was conjugated to AMG102, radiolabeling with

175 By postnatal day 2 (P2), SCN oscillators displayed the daily, dorsal-ventral phas

176 d, defined culture system, these physiologic SCN ligands were sufficient to activate SCN antibacteria

177 play key roles in SCN physiology or provide SCN-specific drivers.

178 rom differential expression between relevant SCN and WB samples) reliably detected known SCN markers.

179 Approximately 75% of light-responsive SCN units modulate their firing according to simple spat

180 fore, post-translational modification shapes SCN neuronal state and network properties.

181 subthreshold membrane properties that shift SCN neurons into the daytime 'upstate'.

182 lease the antimicrobial protein siderocalin (SCN; also known as lipocalin-2, neutrophil gelatinase-as

183 n the present study, we recorded from single SCN neurons in urethane-anaesthetized rats, categorized

184 tion may be the principal barrier to in situ SCN(-) biodegradation in mine tailing waters and also yi

185 ironmentally realistic assessment of in situ SCN(-) biodegradation potential.

186 the potential of native microbes for in situ SCN(-) biodegradation, a remediation option that is less

187 sights into the microbial ecology of in situ SCN(-) bioremediation involving autotrophic sulfur-oxidi

188 vation of GHT neurons selectively suppresses SCN responses to retinal input, and also that this effec

189 , native mass spectrometry demonstrated that SCN may preferentially combine different ligands to coor

190 The SCN also receives input from other retinorecipient brain

191 The SCN expresses many functionally important neuropeptides,

192 The SCN receives input from intrinsically photosensitive ret

193 The SCN-Bmal1-KD mice also showed greater weight gain, an ab

194 expression that progresses daily across the SCN.

195 monstrating that cholinergic activity at the SCN is necessary for arousal-induced phase shifting.

196 in GHT output, indicating modulation at the SCN level.

197 with an activated carbon (AC) electrode, the SCN/AC asymmetric supercapacitor delivered a specific en

198 Our findings highlight the SCN's ability to encode naturalistic temporal modulation

199 s synaptic input from the retina and how the SCN receives equal inputs from both eyes.

200 ptide receptor (GRPR) or GRPR neurons in the SCN abolished contagious scratching behavior, which was

201 ocytes resulted in lengthened rhythms in the SCN and behavior.

202 adian period of clock gene expression in the SCN and in locomotor behavior.

203 ed, possibly by coordinating activity in the SCN and septohippocampal pathway.

204 then inferred functional connections in the SCN by applying the maximal information coefficient stat

205 lue light evokes higher Fos induction in the SCN compared to the sleep-promoting ventrolateral preopt

206 conditions in which the central clock in the SCN is dampened, peripheral oscillators in the hippocamp

207 orting that paternal UBE3A expression in the SCN is often of neuronal origin.

208 peptide (GRP) cells located ventrally in the SCN receive retinal input.

209 assumed that the role of vasopressin in the SCN reflects the activity of these cells.

210 an cycling and intercellular coupling in the SCN remains poorly understood.

211 Paternal UBE3A-positive cells in the SCN show partial colocalization with the neuropeptide ar

212 Key organisms in the SCN(-) reactor expressed proteins involved in SCN(-) deg

213 In the SCN(-) reactor, Thiobacillus strains capable of SCN(-) d

214 orphan GPCRs with enriched expression in the SCN, (ii) generate mutant animals deficient in candidate

215 erficial changes in Rbfox2 expression in the SCN, but mRNA population analysis revealed a distinct SC

216 well as the immediate-early gene Fos in the SCN, dorsal hippocampus, and olfactory bulb.

217 ion of the immediate early gene c-fos in the SCN, which is involved in photic entrainment of circadia

218 e genes that are selectively enriched in the SCN.

219 Per1 and Fos expression is attenuated in the SCN.

220 nsmitting contagious itch information in the SCN.

221 ation of excitatory GABA transmission in the SCN.

222 regions are less elaborate than those in the SCN.

223 -40') C-terminal domain (CTD)-variant in the SCN.

224 a single ipRGC can bilaterally innervate the SCN.

225 Interestingly, the SCN is the only brain region that receives equal inputs

226 In this work, we investigated the SCN network at a single-cell resolution through a chemic

227 Here we launch the SCN orphan GPCR project to (i) search for murine orphan

228 Here, we examined the transcriptome of the SCN and whole brain (WB) of mice using meta-analysis of

229 ted elasticity and temporal structure of the SCN circadian oscillation.

230 at neurons constitute only one "half" of the SCN clock, the one metabolically active during circadian

231 lasticity, resilience, and robustness of the SCN clock.

232 e required for temperature resistance of the SCN clockworks and demonstrate that acute light control

233 and physiological systems downstream of the SCN could respond to visual images [5].

234 When isolated at E13.5, the anlagen of the SCN expresses high, arrhythmic PER2.

235 The cells of the SCN harvested at E15.5 expressed sustained, synchronous

236 Investigating the function of the SCN has often focused on the identification of rhythmica

237 The time-averaged firing rate of the SCN is modestly increased under these conditions, but in

238 actively modulates specific features of the SCN light response, indicating that GHT cells are primar

239 The cells of the SCN must synchronize to each other to drive these circad

240 , we assessed the temporal elasticity of the SCN network.

241 ds and differential phase sensitivity of the SCN to genetic and pharmacological manipulations.

242 cond harmonic generation measurements of the SCN(-) ion, a prototypical chaotrope, determined a free

243 contacts with major peptidergic cells of the SCN, including VIP, GRP, and arginine vasopressin (AVP)

244 ipRGC innervating specific subdomains of the SCN.

245 rcadian synchrony during the ontogeny of the SCN.

246 In the learned helplessness paradigm, the SCN-Bmal1-KD mice were slower to escape, even before exp

247 ogical and genetic manipulations to push the SCN clockwork toward its limits and, by doing so, probe

248 Here, we report that it also renders the SCN responsive to visual images.

249 Loss of Cry1 and Cry2 stops the SCN clock, whereas individual deletions accelerate and d

250 mbient light (irradiance) to synchronize the SCN's endogenous circadian clock with local time and dri

251 Our data indicate that the SCN contains information about irradiance and spatial pa

252 Given that the SCN is a prototypical example of oscillating neural syst

253 light control of sleep is routed through the SCN and its immediate output regions.

254 activity can help gate retinal input to the SCN according to time of day.

255 ght input and glutamatergic signaling to the SCN were concomitantly assessed through behavioral assay

256 e pretreated with atropine injections to the SCN, demonstrating that cholinergic activity at the SCN

257 tion retains intact optic projections to the SCN, thalamus and pretectum and a functional GHT.

258 also blocked by infusions of atropine to the SCN.

259 ical mimic of the light input pathway to the SCN.

260 ed in many retinal cells that project to the SCN.

261 results indicate that astrocytes within the SCN communicate to neurons to determine circadian rhythm

262 opamine receptor (Drd1) signaling within the SCN is necessary for properly timed resynchronization of

263 PERIOD2 (PER2), a clock protein, within the SCN isolated from embryonic and postnatal mice of undete

264 te or intercellular communication within the SCN network.

265 Within the SCN, interconnected individual neurons are oscillators t

266 cadian rhythms that are generated within the SCN.

267 Without the SCN, these peripheral clocks rapidly become desynchroniz

268 cotransporters to setting [Cl(-)]i in these SCN neurons and found that the chloride uptake transport

269 Thiocyanate (SCN(-)) is a contaminant requiring remediation in gold m

270 on-deuterium (C-D), cyano (CN), thiocyanate (SCN), and azide (N3) "transparent window vibrational pro

271 for one industrial contaminant, thiocyanate (SCN(-)), relies upon microbial hydrolysis, but this proc

272 In addition to N3(-), thiocyanate ((-)SCN) and cyanate ((-)OCN) anions were also studied.

273 suggests, and experiments confirm, that this SCN reorganization depends upon GABAergic signaling.

274 Thus, SCN circuit-level timekeeping arises from interdependent

275 xyvinylglycine (AVG) were more attractive to SCN than untreated roots, and significantly more nematod

276 sponse mutant ctr1-1, was less attractive to SCN.

277 aling pathway reduces root attractiveness to SCN in a way similar to that reported for root-knot nema

278 rize the principal biogeochemical barrier to SCN(-) biodegradation for an autotrophic microbial conso

279 ype GmSNAP18 is sufficient for resistance to SCN in combination with Rhg4.

280 RKY genes that promote soybean resistance to SCN, we first screened soybean WRKY genes for enhancing

281 transgenes displayed increased resistance to SCN.

282 oybean cultivars with enhanced resistance to SCN.

283 a novel minor gene conferring resistance to SCN.

284 P11 contributes to an additive resistance to SCN.

285 was positively associated with high urinary SCN activity.

286 ht and enhances hyperpolarization of ventral SCN neurons at this time.

287 ythm in membrane excitability in the ventral SCN (vSCN) was enhanced in amplitude and delayed in timi

288 of hypoexcited neuronal state in the ventral SCN at night and enhances hyperpolarization of ventral S

289 in calbindin-containing cells of the ventral SCN in early and late night.

290 ight-induced c-Fos expression in the ventral SCN.

291 clock protein (PERIOD2) output from ex vivo SCN revealed no deficits in Myk/+ molecular clock functi

292 specific ligand combinations affects in vivo SCN antibacterial activity.

293 eding can improve cognitive performance when SCN timing has been compromised, possibly by coordinatin

294 Thus, the truncated G-CSFRs associated with SCN/AML may protect myeloid precursor cells from apoptos

295 athways were affected in both genotypes with SCN infection.

296 tics to create temporally chimeric mice with SCN containing dopamine 1a receptor (Drd1a) cells with a

297 collapsed state of the ELP when paired with SCN(-), which is a strong binder for the ELP.

298 y controls (0/17, P < .001) or patients with SCN (0/40, P < .001).

299 Patients with SCN are predisposed to acute myeloid leukemia (AML), and

300 ations of CSF3R was present in patients with SCN but was not detected in healthy controls or patients

301 e was identified in HSPCs from patients with SCN compared with 3.9 +/- 0.4 for healthy controls (P =