ライフサイエンスコーパス: in resting

1 pharmacological inhibitor of FAK, PF562,271, in resting A549 cells.

2 mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infec

3 cell activation, we compared Pol II profiles in resting and activated B cells.

4 e expression dynamics of nascent transcripts in resting and activated CD4+ T cells.

5 estigated the regulation of SRSF1 expression in resting and activated human T cells.

6 subunit of the CD3 T cell receptor complex, in resting and activated primary human T cells.

7 ty, TF binding, and gene expression patterns in resting and activated subsets of Treg cells, conventi

8 zed glycolysis and mitochondrial respiration in resting and activated T cells, along with markers rel

9 richia coli AcrAB-TolC multidrug efflux pump in resting and drug transport states, revealing a quater

10 gnaling in response to the protein beverages in resting and exercised muscle.

11 able to provoke greater levels of autophagy in resting and fasting cardiomyocytes in vivo.

12 We quantified the change in resting and hyperemic flow velocity after PCI in sten

13 olysaccharide (LPS) induced hemophagocytosis in resting and IFN-gamma-pretreated macrophages, whereas

14 ansgenic (TG) mice showed a marked reduction in resting and in maximal heart rate, whereas cardiac ou

15 GFR dynamics on live CHO-K1 plasma membranes in resting and ligand-bound states.

16 acellularly, with an overall modest increase in resting and odorant-evoked responses during serotoner

17 We found that Hdac3 is highly expressed in resting and prehypertrophic growth plate chondrocytes

18 Mitochondria, which are essential organelles in resting and replicating cells, can vary in number, ma

19 poral regulation of cytokine gene expression in resting and restimulated effector T helper 1 (Th1) ce

20 cis, gene expression in resting B cells, and in resting and stimulated monocytes.

21 osphorylation status of presynaptic proteins in resting and stimulated nerve terminals isolated from

22 affected whole-brain serotonergic signaling in resting and stress-induced conditions, an effect that

23 , open chromatin region, and 3D interactions in resting and TNFalpha-treated human endothelial cells.

24 d oscillatory activity in the 20-40 Hz range in resting and walking states, and increased interhemisp

25 LFPs were recorded in resting and walking states, before and after unilater

26 o constrain the positions of key side chains in resting- and activated-state VS model structures, pro

27 gic signalling and maintained at high levels in resting anergic T cells.

28 a B bind to a wide range of active promoters in resting B and T cells.

29 rly Genes (IEG), which were highly expressed in resting B cell and shifted from non-poised to poised

30 phorylates histone H3S28 at active promoters in resting B cells as well as inhibiting Ring1B-mediated

31 iant that regulates, in cis, gene expression in resting B cells, and in resting and stimulated monocy

32 can be ruled out as direct pro-FD activators in resting blood; however, active MASP-3 is a very likel

33 echanisms for the observed diurnal variation in resting brain activity and the importance of accounti

34 CD) mapping to study alcohol-related changes in resting brain activity and their association with beh

35 of DNase I hypersensitive sites genome wide, in resting but not in activated B cells.

36 ntain a poised state at the Il2 target locus in resting but previously stimulated CD4(+) T cells.

37 the aberrant temperature-dependent increase in resting Ca(2+) in myotubes from an RYR1-RM mouse mode

38 l analysis in astrocytes revealed a decrease in resting calcium signaling.

39 e decreases by ~2-3 degrees C, causing drops in resting capillary blood flow, capillary Po2, hemoglob

40 ular coupling at rest and that the reduction in resting CBF reflected reduction in synchronized spont

41 that a major restriction on HIV-1 infection in resting CD4 T cells resides in the capacity of these

42 studies suggest diminished HIV reactivation in resting CD4 T cells with daily exposure to VOR.

43 ills (SIVrcm/mnd-2), increased HIV infection in resting CD4 T cells, but not in macrophages, and, une

44 With repeat exposure to VOR in resting CD4 T cells, we found similar and consistent

45 fferences in the frequency of persistent HIV in resting CD4 T cells.

46 n is prevalent in polyadenylated transcripts in resting CD4(+) T cells and is significantly reduced u

47 Furthermore, Naf1 knockdown in resting CD4(+) T cells from HIV-1-infected individual

48 ent classes of latency reversal agents (LRA) in resting CD4(+) T cells from HIV-infected individuals

49 quantified the fraction of HIV-1 proviruses in resting CD4(+) T cells from patients on suppressive a

50 A stable latent reservoir for HIV-1 in resting CD4(+) T cells is the principal barrier to a

51 hieved clinically, only 0.079% of proviruses in resting CD4(+) T cells were reactivated to produce vi

52 The latent HIV-1 reservoir primarily resides in resting CD4(+) T cells which are a heterogeneous popu

53 kines suppressed R5 and X4 virus replication in resting CD4(+) T cells, and individually SDF-1beta, C

54 HIV persists in resting CD4(+) T cells, and possibly other cell types

55 owever, HIV-1 persists in a latent reservoir in resting CD4(+) T cells, and rebound viremia occurs fo

56 to quantify replication-competent latent HIV in resting CD4(+) T cells, both increasing accuracy and

57 n is important: in maintaining HIV-1 latency in resting CD4(+) T cells, potentially affect immune fun

58 This property would be important in resting CD4(+) T cells, where dNTP pools are reduced

59 t encode replication-competent virus persist in resting CD4(+) T cells.

60 ts indefinitely in a stable latent reservoir in resting CD4(+) T cells.

61 eases in unspliced cellular HIV-1 RNA levels in resting CD4(+) T cells.

62 infection because latent proviruses persist in resting CD4(+) T cells.

63 A latent reservoir for HIV-1 in resting CD4(+) T lymphocytes precludes cure.

64 ion require the reactivation of latent HIV-1 in resting CD4+ T cells (rCD4s).

65 triphosphohydrolase that depletes dNTP pools in resting CD4+ T cells and macrophages and effectively

66 lular models and increased unspliced HIV RNA in resting CD4+ T cells isolated from HIV-infected indiv

67 HIV persists in a quiescent state in resting CD4+ T cells, where the replicative enzymes t

68 at (Exo-Tat) which can activate latent HIV-1 in resting CD4+ T lymphocytes from antiretroviral treate

69 CD28(-) T cells, and inhibiting its activity in resting CD8(+)CD28(+) T cells enhanced glycolytic cap

70 Biological degradation was investigated in resting cell suspensions of Geobacter metallireducens

71 ors in mediating microglial process dynamics in resting cells and alpha2A receptors in activated cell

72 s sufficient to render MRTF-A inactive, both in resting cells and in cells with exogenously activated

73 ATM exists in an inactive state in resting cells but can be activated by the Mre11-Rad50

74 nase-3 is a Ser/Thr kinase, tonically active in resting cells but inhibited by phosphorylation of an

75 Instead, we made a novel discovery that in resting cells myoferlin was bound to EHD2 protein and

76 We found that in resting cells p53 is present in a mix of oligomeric s

77 nt pathway leading to basal Ly49E expression in resting cells that is induced by Pro2-mediated Ly49e

78 dy-state organization of the plasma membrane in resting cells that is poised to orchestrate assembly

79 pression from integrated proviruses occurred in resting cells that lacked surface CD4, likely resulti

80 The absence of puncta in resting cells was required to prevent spontaneous sto

81 help maintain low levels of cytosolic cavin1 in resting cells, a prerequisite for cavins acting as si

82 In resting cells, AIM2 physically interacted with and li

83 f endoplasmic reticulum Ca(2+) concentration in resting cells, and for the refilling of Ca(2+) stores

84 ble for maintaining TF in an encrypted state in resting cells, and the hydrolysis of SM leads to decr

85 In resting cells, Irbit was sequestered by InsP3 recepto

86 In resting cells, IRF8 was mainly bound to composite sit

87 leted viral sequences formed more frequently in resting cells, likely due to lower deoxynucleoside tr

88 interactions and IRF3 activation, show that, in resting cells, microsome but not mitochondrial fracti

89 In resting cells, Munc18-2, but not STX3, interacted wit

90 In resting cells, RIP of CREB3L1 is blocked by transmemb

91 In resting cells, STIM1 diffusion is Brownian, while Ora

92 In resting cells, these transcription factors remain in

93 n of CD45 exon 4 in the final mRNA; however, in resting cells, TRAP150 binds PSF and prevents access

94 eased the formation of LC3(+) autophagosomes in resting cells, while other isoforms promoted autophag

95 ted at the lower dNTP concentrations present in resting cells.

96 ter in actively growing bacterial cells than in resting cells.

97 in self-clusters that did not associate well in resting cells.

98 e 3 at lysine 27 (H3K27) of the HIV provirus in resting cells.

99 s undetected by existing large-scale studies in resting cells.

100 tate, whereas F57Bpa interacts predominantly in resting channel conformations.

101 ther astroglial Cx43 hemichannels are active in resting conditions and regulate basal synaptic transm

102 that NPY3-36 is the main circulating peptide in resting conditions and that NPY and catecholamines ar

103 al functions, the uniporter must stay closed in resting conditions, becoming open only when stimulate

104 In resting conditions, estrogens have strong regulatory

105 In resting conditions, NK3Rs were predominantly located

106 to inhibit HIV-1 activation and replication in resting conventional T cells in vitro.

107 scle metaboreflex activation on ventilation, in resting COPD patients and healthy participants.

108 Here we show that heterogeneities in resting discharge variability mediate a trade-off bet

109 ation of efferents was linked to an increase in resting discharges of afferents and a decrease in the

110 Finally, we found that ECs in resting endothelial monolayers use lamellipodial prot

111 he energy they contain, a possible increment in resting energy expenditure, and an augmentation of fa

112 to demonstrate that patterns of correlation in resting fMRI are closely aligned with functional arch

113 al activity induced a long-lasting reduction in resting free astrocyte Ca(2+) and that this phenomeno

114 We suggest that reduction in resting GABAergic inhibition triggers homeostatic pla

115 raphe stimulation elicited a strong increase in resting GCaMP fluorescence with only a slight enhance

116 We found increased ADP content in resting Glu(-) cells, a condition that counteracts th

117 port fear of terror-induced annual increases in resting heart rate (pulse), a notable risk factor of

118 hat ADHD medications cause modest elevations in resting heart rate and blood pressure.

119 ased on the occurrence of extreme elevations in resting heart rate relative to the individual baselin

120 is demonstrated that for 1 beat/min increase in resting heart rate, there was a 4% greater adjusted r

121 idues [S-nitrosothiol (SNO)] on 491 proteins in resting hearts from a mouse model of DMD (dmd(mdx):ut

122 ers showed consistent individual differences in resting HRV across years.

123 r classes of drug transporters, SLC and ABC, in resting human blood neutrophils.

124 ophilin A, and 12-kDa FK506-binding protein, in resting human Jurkat T cells.

125 that LFA-1 has a low ligand-binding activity in resting human NK cells, but it can be stimulated by t

126 Importantly, SLC1A5 failed to be upregulated in resting human T cells kept under low tryptophan condi

127 Telomerase activity is not readily detected in resting human T lymphocytes, however upon antigen pre

128 ton has been reported to restrict signalling in resting immune cells.

129 ICP elevation and correlated with increases in resting IOP.

130 ute to the increased reliance on fatty acids in resting KO animals.

131 The rise in resting levels of Ca(2+) may not alter the processes

132 M but not Ca(2+)-free CaM were preassociated in resting live cells, while capsaicin activation induce

133 re, the anabolic function of PTEN deficiency in resting liver is transformed into catabolic activitie

134 Monocytes in resting lung and LN had similar gene expression profi

135 to -3.0 mm Hg]; P = 0.020), and mean change in resting LVEF was -6% (CI, -10% to -1%).

136 Mer acted as a tolerogenic receptor in resting macrophages and during immunosuppression.

137 lpha, AS-IL1alpha is expressed at low levels in resting macrophages and is induced following infectio

138 promoter-proximal RNA polymerase II pausing in resting macrophages is marked by co-localization of t

139 TDB/TDM caused only weak Syk-phosphorylation in resting macrophages, consistent with low basal Mincle

140 In resting macrophages, GAPDH binds to and suppresses tr

141 Although TRPML2 expression was negligible in resting macrophages, TRPML2 mRNA and protein levels d

142 While the receptors exist as monomers in resting macrophages, two distinct populations were di

143 omoted phagocytosis of apoptotic neutrophils in resting macrophages, whereas immobilized HC-HA promot

144 itutive interaction between STAT2 and IFNAR2 in resting MEFs, an interaction that is dependent on the

145 regions of IFNAR1 and IFNAR2, respectively, in resting MEFs.

146 A transwall gradient in resting membrane potential (RMP) exists across the ci

147 commodation response mode induced by changes in resting membrane potential (RMP) or added neurotrophi

148 iculum via IP3Rs contributes to the decrease in resting membrane potential, prolongation of the actio

149 osite response dynamics are due to the shift in resting membrane potential.

150 ifetime, benign, persistent latent infection in resting memory B cells in vivo, where the virus is qu

151 deficiency virus type 1 (HIV-1) DNA persists in resting memory CD4(+) T cells despite antiretroviral

152 The latent reservoir for HIV-1 in resting memory CD4(+) T cells is the major barrier to

153 The latent reservoir (LR) of HIV-1 in resting memory CD4(+) T cells serves as a major barri

154 rge the persistent reservoir of latent virus in resting memory CD4(+) T cells, but the degree of rese

155 remarkably stable reservoir of latent HIV-1 in resting memory CD4(+) T cells.

156 ists in a stable latent reservoir, primarily in resting memory CD4(+) T cells.

157 viremia or depletion of the latent reservoir in resting memory CD4(+) T cells.

158 s transcriptionally silent latent infections in resting memory T cells and hematopoietic stem and pro

159 nt effects on body composition or any change in resting metabolic rate (stable within 8 kcal/d).

160 overall dietary energy intake but no change in resting metabolism.

161 bserved no significant extrinsic sialylation in resting mice, suggesting that extrinsic sialylation i

162 rrow (BM) produces the majority of serum IgM in resting mice.

163 In resting microglia, butaprost induced cAMP formation a

164 PO, which is expressed in activated, but not in resting, microglia.

165 hibits growth of L. braziliensis amastigotes in resting monocytes, and that classical monocytes are p

166 Interestingly, this occurs in resting MPhis through tempering of steady-state mitoc

167 ciency severe enough to impair fat oxidation in resting muscle causes an increase, not a decrease, in

168 drial peroxide generation was also increased in resting muscle from old (26 month) mice compared with

169 We propose that the increase in resting muscle metabolism contributes to these positi

170 , myosin heads were extended closer to actin in resting muscle.

171 In resting muscles, there was no difference between geno

172 p expression quantitative trait loci (eQTLs) in resting myeloid cells and CD4(+) T cells from cord bl

173 The primary efficacy end point was change in resting myocardial perfusion over 6 months.

174 Mean iodine concentration in resting myocardium was 2.19 mg/mL +/- 0.57.

175 In resting myocytes, RyR2s can also open spontaneously g

176 d by that OM induces a continuous activation in resting myosin ATPase.

177 OH)(4)(-) did not induce significant changes in resting [Na(+)(i)] or the amplitude and rate of acidi

178 molecular signature was already established in resting naive cells and was dominated by enrichment o

179 ces accumulation of depolarized mitochondria in resting neonatal rat cardiac myocytes, as well as in

180 ause larger changes in transmembrane voltage in resting neurons with low membrane conductances than i

181 It populates ER-PM contacts in resting neurons, but elevations of cytosolic Ca(2+) m

182 owed a decrease in activated and an increase in resting NK cells in both lesional and nonlesional ski

183 We found that TRIM29 was not expressed in resting NK cells, but was readily upregulated followi

184 e cytokine production and cytolytic activity in resting NK cells.

185 (2+) chelator BAPTA caused smaller increases in resting open probability in Bth mutant OHCs than in w

186 No difference was found in resting or sleeping energy expenditure, normalised to

187 oes not colocalize preferentially with ORAI1 in resting or stimulated cells, assemble stably at ER-PM

188 hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes p

189 in linear and nonlinear age-related changes in resting oscillatory power and network synchrony were

190 he basal activity of the NF-kappaB signaling in resting peripheral T cells.

191 JAM-A associates with integrin alphaIIbbeta3 in resting platelets and dissociates upon platelet activ

192 TYMP-associated Lyn was inactive in resting platelets, and TYMP trapped and diminished ac

193 ript-1, which is localized to alpha-granules in resting platelets, binds fibrinogen, and acts as a po

194 The results show that, in resting platelets, free RGS18 levels are relatively l

195 A recruits Csk to the integrin-c-Src complex in resting platelets.

196 itotic catastrophe, but the function of MDM2 in resting podocytes has not been explored.

197 Instructive signals mediated by changes in resting potential control proliferation, differentiat

198 re, we report excessive NF-kappaB signalling in resting primary bronchial epithelial cells from ZZ pa

199 In resting primary CD4(+) T cells, where levels of P-TEF

200 , LRRC8A channels are key cGAMP transporters in resting primary human vasculature cells and universal

201 howed low levels of tyrosine phosphorylation in resting primary mouse CD4(+) T cells; the levels of t

202 We find that Orai1 is a dimer in resting primary mouse embryonic fibroblasts but displ

203 We show that CLEC3A is present in resting, proliferating, and hypertrophic growth-plate

204 d approximately 9% to 10% of total variation in resting QTc in EA individuals and approximately 12% t

205 agonist association is slower than diffusion in resting receptors but nearly diffusional in active re

206 tization on this timescale within LBD dimers in resting receptors.

207 in labeling to measure IN-OT-induced changes in resting regional cerebral blood flow (rCBF) in 32 hea

208 access to its binding site is extremely slow in resting RyR2 but is accelerated by promoting RyR open

209 ter-hemispheric symmetry, typically observed in resting sensorimotor networks, depends on coordinated

210 PE caused robust vasoconstriction in resting skeletal muscle during control vasodilator in

211 alpha-adrenoceptors elicits vasoconstriction in resting skeletal muscle that is blunted during exerci

212 to blunt alpha1 -adrenergic vasoconstriction in resting skeletal muscle would be independent of KIR ,

213 This conformation is present in resting skeletal muscle, but it is not known how exit

214 s involved in maintaining tissue homeostasis in resting skin and hint at their contribution to signal

215 TR1 knockout mice had a normal phenotype in resting skin, whereas GPx4 loss in the epidermis caus

216 en brain states have been well characterised in resting state acquisitions, the remodelling of these

217 ilar optimum at a timescale of around 200 ms in resting state and in task data.

218 Correlations between fluctuations in resting state BOLD fMRI signals are interpreted as me

219 This study aimed to investigate changes in resting state brain activity in remissive Crohn's Dis

220 rate that the global directionality patterns in resting state brain networks can be predicted solely

221 e found that human peripheral blood Th cells in resting state do not show surface expression of IL-3R

222 r (ASD) has been associated with a reduction in resting state functional connectivity, though this as

223 Despite advances in resting state functional magnetic resonance imaging i

224 amework for analysing effective connectivity in resting state functional MRI with strong a priori hyp

225 Here we assess LRTCs in resting state human EEG data during a 40-hour sleep d

226 Our findings identify large-scale changes in resting state network interactions that are a physiol

227 standard deviation of BOLD signal amplitude) in resting state networks (RSNs) associated with cogniti

228 on the organization of synchronous activity in resting state networks.

229 nt and dose-dependent longitudinal increases in resting state rCBF in brain regions intrinsic to memo

230 clusterin gene (CLU) on longitudinal changes in resting state regional cerebral blood flow (rCBF) dur

231 heorized that topological network alignments in resting state scans predict psychologically condition

232 ctional connectivity and cerebral blood flow in resting state).

233 e-producing adenomas conducts omega-currents in resting state, but not during voltage-sensing domain

234 shift that is observed in depressed subjects in resting-state activities between the perigenual anter

235 have reported functionally localized changes in resting-state brain activity following a short period

236 highlight both state and trait abnormalities in resting-state brain activity in MDD.

237 Although changes in resting-state brain connectivity are a transdiagnosti

238 he results suggest that individual variation in resting-state brain dynamics offer a neural explanati

239 Using ICA, we investigated the differences in resting-state brain networks in patients with MDD who

240 ns are associated with widespread reductions in resting-state CBF.

241 Differences in resting-state connectivity may be false-negative resu

242 PTSD differences in resting-state connectivity of BLA complex could be bi

243 n tumors, tumor characteristics, and changes in resting-state connectivity, to explore neurovascular

244 Mean HEP amplitudes in resting-state electroencephalograms and their correla

245 synchrony of the low-frequency fluctuations in resting-state fMRI (rs-fMRI), known as "functional co

246 paper, topological organisation was examined in resting-state fMRI data obtained from 32 ASPD patient

247 In resting-state fMRI, hemodynamic fluctuations have bee

248 of functional connectivity networks detected in resting-state fMRI.

249 aimed at characterizing age-related changes in resting-state functional brain organization from mid-

250 ssion (PPD) is associated with abnormalities in resting-state functional connectivity (RSFC) but the

251 Alterations in resting-state functional connectivity (rsFC) have bee

252 s (HC) and specifically compared differences in resting-state functional connectivity (RSFC) within t

253 we have demonstrated age-related decrements in resting-state functional connectivity across most par

254 of day was associated with marked decreases in resting-state functional connectivity across the whol

255 ratings was also correlated with an increase in resting-state functional connectivity between the mid

256 We found that post-learning increases in resting-state functional connectivity between the SN/

257 s in the head of the caudate predict changes in resting-state functional connectivity between this st

258 Capitalizing on recent advances in resting-state functional connectivity magnetic resona

259 Fluctuations in resting-state functional connectivity occur but their

260 Changes in resting-state functional connectivity, focusing on th

261 ehavioral impairment was mirrored in changes in resting-state functional magnetic resonance imaging (

262 Major advances in resting-state functional magnetic resonance imaging (

263 We observed reduced effective connectivity in resting-state functional magnetic resonance imaging b

264 studies suggest circumscribed abnormalities in resting-state functional magnetic resonance imaging c

265 d healthy control (HC) subjects participated in resting-state functional magnetic resonance imaging.

266 Here, we examined variation in resting-state functional MRI (fMRI) in around 900 ind

267 sychopathology groups in age-related changes in resting-state functional MRI amygdala-to-whole brain

268 The global signal in resting-state functional MRI data is considered to be

269 Increases in resting-state heart rate and decreases in its variabi

270 tionships between interregional correlations in resting-state measures of activity, neuronal function

271 l tissue, sequential spatiotemporal patterns in resting-state MEG data, and large-scale waves in huma

272 In resting-state MEG recordings from healthy participant

273 ons in brain intrinsic activity-as organized in resting-state networks (RSNs) such as sensorimotor ne

274 ults demonstrate that intrinsic fluctuations in resting-state variability exhibit unique maturation t

275 ession based on the local-level similarities in resting-state whole-brain connectivity between partic

276 the activity of astroglial Cx43 hemichannels in resting states regulates basal excitatory synaptic tr

277 Further, there is a marked increase in resting sympathetic nervous system (SNS) activity wit

278 We found that basal ZAP70 activation in resting T cell lines reduced the threshold ("primed")

279 ng that PAG is constitutively phosphorylated in resting T cells and rapidly dephosphorylated once the

280 In resting T cells cholesterol keeps TCRs in the resting

281 l lines and primary CTCL cells but is absent in resting T cells from healthy donors and B-cell lympho

282 ssfully produce infectious offspring virions in resting T cells that become activated after infection

283 In resting T cells treated with the intrinsic apoptosis

284 CTPS1 expression was found to be low in resting T cells, but rapidly upregulated following TC

285 We report that, in resting T cells, FOXO1 inhibition impaired autophagy

286 In resting T cells, the CD3epsilon cytoplasmic tail asso

287 In resting T cells, the TCR is largely unphosphorylated

288 HDAC11 at the Eomes and Tbet gene promoters in resting T cells, where it rapidly disassociated follo

289 Because miR-28-3p is highly expressed in resting T cells, which are resistant to HTLV-1 infect

290 the balance between active and inactive Lck in resting T cells, which guarantees operative T cell ef

291 vivo, Zap70 is bound to phosphorylated ITAMs in resting T cells.

292 The extent of VM-PM contact areas in resting terminals correlated with eccentricity in ves

293 sed at the TNF locus and other related genes in resting Th1 cells and released in a myosin VI-depende

294 ehavior superimposed on drift, whereas cells in resting tissue did not show significant displacements

295 cle is blunted relative to that which occurs in resting tissue; however, the mechanisms underlying th

296 ulatory elements in DNA by Foxp3 was similar in resting Treg cells and those activated in vivo, Foxp3

297 we can achieve almost 50% average reduction in resting tremor amplitude and in so doing form the bas

298 y regions of genes involved in TLR signaling in resting UCB monocytes.

299 rocaspase-3 and -9 are basally persulfidated in resting (unstimulated) cells and become depersulfidat

300 es and lymphotoxin (LT) alphabeta dependency in resting versus TCR-activated intraepithelial gammadel