ライフサイエンスコーパス: dysfunctional

1 or metabolic resources often renders T cells dysfunctional.

2 ecause the virus-specific immune response is dysfunctional.

3 to major T cell exhaustion pathways and were dysfunctional.

4 nt mice, in which microglia were present but dysfunctional.

5 in the adipocyte as it becomes progressively dysfunctional.

6 ein networks become disturbed and ultimately dysfunctional.

7 d in Q175 heterozygotes can be classified as dysfunctional.

8 1 (ROR1) infiltrate tumors poorly and become dysfunctional.

9 Thus, dysfunctional ACC/HPC signaling to the BLA may be a pred

10 tant failed to rescue reduced expression and dysfunctional activity-dependent trafficking of Syt1 in

11 stemic metabolism, as shown by the fact that dysfunctional adipose tissue in obesity leads to a varie

12 mineralocorticoid receptor (MR) may promote dysfunctional adipose tissue in patients with type 2 dia

13 s play a central role in energy balance, and dysfunctional adipose tissue severely affects systemic e

14 ing the altered transcriptional landscape of dysfunctional adipose tissue, 4) genome-wide studies rev

15 Pericellular fibrosis, a hallmark of dysfunctional adipose tissue, was greater in Om and corr

16 Our findings demonstrate that dysfunctional Ag.pTfh cells with an altered IL-21/IL-2 a

17 environmental-induced lung tumors and of the dysfunctional airway and alveolar epithelial turnover ob

18 Unexpectedly, dysfunctional alloreactive B cells acquired the ability

19 f glycinergic dis-inhibition associated with dysfunctional alpha3GlyRs, our current understanding of

20 the subtle difference between functional and dysfunctional amyloid.

21 ons change when the endothelial cells become dysfunctional and have an impact in diseases such as cer

22 mor microenvironment, which is enriched with dysfunctional and immunosuppressed antigen-presenting ce

23 subcutaneous adipose tissue is metabolically dysfunctional and loses its capacity to expand, leading

24 lar homeostasis, it may lead to a persistent dysfunctional and pathological state.

25 sential protease that selectively eliminates dysfunctional and short-lived regulatory proteins in euk

26 We anticipate that such VSDs become dysfunctional and unable to respond to changes in transm

27 solid tumors, blood vessels are abnormal and dysfunctional and, thus, immune effector cell infiltrati

28 , thereby providing mechanistic insight into dysfunctional antibody responses in patients with PIK3CD

29 d (TCA) cycle flux and glutamate metabolism, dysfunctional arginine and nitric oxide pathways, and in

30 ea that the gating defect is the result of a dysfunctional ATP-binding site 2 in the nucleotide bindi

31 Recent studies have shown that dysfunctional autophagy in endothelial cells, smooth mus

32 nctional autoregulation (ABP above LLA) from dysfunctional autoregulation (ABP below the LLA).

33 e play an important role in the emergence of dysfunctional avoidance behaviors.

34 this infection-type dependence is due to QS-dysfunctional bacteria having a significant survival adv

35 eoarthritis (TMJ-OA) and is promoted through dysfunctional biochemical or biophysical signaling.

36 n, impaired vasodilation, vessel stiffening, dysfunctional blood flow and interstitial fluid drainage

37 e a possible therapeutic approach to control dysfunctional BMP and TGFbeta signaling by regulating HO

38 ent in many idiopathic PAH forms, suggesting dysfunctional BMPR2 signaling to be a key feature of PAH

39 ne regulation program in PAECs downstream of dysfunctional BMPR2 to rehabilitate PAH PAECs, regenerat

40 Taken together, dysfunctional BMPRII responsiveness impairs apoptosis vi

41 e body and the environment in functional and dysfunctional body and brain states.

42 These observations led us to propose a dysfunctional brain-gut communication hypothesis for hyp

43 tion of Hsp70 enhances the ubiquitination of dysfunctional but not native nNOS, and it suggests that

44 tize not only variants that are likely to be dysfunctional but those that are likely involved in the

45 lved in emotional processing may be rendered dysfunctional by chronic exposure to delta-9-tetrahydroc

46 These changes rendered murine neurons dysfunctional by promoting neurite retraction, and we al

47 Associated with this dysfunctional Ca(2+) signaling is destabilization of neu

48 ynaptic vesicle trafficking rates that, when dysfunctional, causes a movement disorder in patients an

49 ity analyses reveal unique features of these dysfunctional CD8(+) T cells, with limited overlap with

50 individuals, the SYMP individuals presented dysfunctional CD8(+) T(EM) cells, expressing major exhau

51 Dysfunctional CD8(+) TILs possess canonical epigenetic a

52 (GR) expression and signaling from naive to dysfunctional CD8(+) tumor-infiltrating lymphocytes (TIL

53 f a molecular pathway in which exhausted or "dysfunctional" CD8+ T cells enhance cellular adhesivenes

54 creasingly recognized as a disease involving dysfunctional cellular metabolism.

55 The elucidation of dysfunctional cellular processes that can induce the ons

56 ) is mutated in CF, and we hypothesized that dysfunctional CFTR in platelets, which are key participa

57 o be a safeguard against the accumulation of dysfunctional CI arising from the inactivation of the N-

58 in the general population is consistent with dysfunctional circuitry commonly found in clinical popul

59 al and psychiatric disorders correlated with dysfunctional circuitry.

60 es in the brain, particularly where treating dysfunctional circuits, versus single brain regions, is

61 with drugs that target the clock, and that a dysfunctional clock ablates this response.

62 s that result in either aberrant proteins or dysfunctional components of the proteolytic machinery th

63 ces of phenotypic variation under normal and dysfunctional conditions, with the aim of identifying ta

64 SSc results in dysfunctional connective tissues with excessive profibro

65 However, the origin of this dysfunctional distal lung epithelium remains unknown due

66 Dysfunctional dopamine (DA) signaling has been associate

67 These results suggest that dysfunctional dopamine autoregulation might precipitate

68 A dysfunctional dopamine system is implicated in most psyc

69 elium in asthma and upper airway diseases is dysfunctional due to disturbed tight junction formation.

70 dipocyte progressively becomes metabolically dysfunctional due to its acquisition of fibrogenic funct

71 ict L1 activity and how this process becomes dysfunctional during aging and in cancer cells is poorly

72 Here, we show that this response is dysfunctional during amyloid beta toxicity and pathology

73 t MAIT cells are highly activated and become dysfunctional during clinical sepsis, and contribute to

74 ional (e.g., as membrane-less organelles) or dysfunctional (e.g., as precursors to pathological prote

75 The dysfunctional eating behavior of VAChTcKO mice was allev

76 wever, no data exist examining the impact of dysfunctional EC signalling on satellite cells.

77 eading to progression to active MM, in which dysfunctional effector lymphocytes, tumor-educated immun

78 -intrinsically protected memory cells from a dysfunctional, effector-like transcriptional program, si

79 provide direct evidence for a key role of a dysfunctional eIF2alpha pathway in the pathogenesis of d

80 chondrial dysfunction are characteristics of dysfunctional endothelial cells in diabetic patients.

81 nical evidence supports a negative impact of dysfunctional energy metabolism on the disease progressi

82 potent stem cell state may effectively erase dysfunctional epigenetic donor cell memory or disease-as

83 Allergic diseases have in common a dysfunctional epithelial barrier, which allows the penet

84 Dysfunctional ER acetylation, as caused by heterozygous

85 These dysfunctional ex-Tfr cells may have roles in modulating

86 xpressing PD-1 and TIGIT were committed to a dysfunctional, exhausted-like lineage.

87 Paradoxically, despite harboring highly dysfunctional fat, transgenic mice display massive beta-

88 5 and FGF21 levels, indicating metabolically dysfunctional fat.

89 Further, cell lines with dysfunctional Fbxw7 are less sensitive to IRF1 overexpre

90 es and in therapies for disorders related to dysfunctional fear memories.

91 onstrate that the endogenous expression of a dysfunctional FIX can deleteriously affect the hemostati

92 roves hemostasis in CRM(+) mice expressing a dysfunctional FIX, FIX(R333Q), that nevertheless compete

93 aRGD tissues and cells assemble abnormal and dysfunctional FNDeltaRGD fibrils in a syndecan-dependent

94 y different, at FIX(WT) < FIX(FC) < FIX(Alb) Dysfunctional forms of FIX, however, circulate in the ma

95 y intein-based toxin reconstitution from two dysfunctional fragments provided their cytoplasmic deliv

96 n of RNA-binding proteins (RBPs), leading to dysfunctional gene splicing and tumor-specific dependenc

97 HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can b

98 DPGK hypomorphic zebrafish further displayed dysfunctional glucose metabolism.

99 of the unfolded protein response (UPR), and dysfunctional glucose-induced Ca(2+) oscillations in tun

100 TCMR was usually found in dysfunctional grafts with an elevation in the serum crea

101 ysbiosis contributes to the development of a dysfunctional gut barrier, facilitating the translocatio

102 a rationale for our emerging hypothesis of a dysfunctional gut-brain axis in hypertension.

103 bolism including increased energy depletion, dysfunctional H(+) regulation, and decreased antioxidati

104 ther with PD-1 as a discriminatory marker of dysfunctional HCV-specific CD4+ T cells.

105 increased lipoprotein dicarbonyl adducts and dysfunctional HDL.

106 in Fanconi anemia (FA) patients results from dysfunctional hematopoietic stem and progenitor cells (H

107 sty for the treatment of stenotic lesions in dysfunctional hemodialysis arteriovenous fistulas during

108 sty is the current recommended treatment for dysfunctional hemodialysis fistulas, yet long-term outco

109 wever, an understanding of the mechanisms of dysfunctional host-microbiome interactions in hypertensi

110 information for the understanding of several dysfunctional human behaviors such as overeating and gam

111 Dysbiosis of the oral biofilm and a dysfunctional immune response drive chronic inflammation

112 and molecular mechanisms contributing to the dysfunctional immune response of the elderly to the vacc

113 ronic hepatitis B (CHB) is associated with a dysfunctional immune response, and therefore a selective

114 munotherapy and those that target a specific dysfunctional immune response, especially within the tum

115 se, resulting in recurrent infections due to dysfunctional immune response.

116 ne system and the subsequent contribution of dysfunctional immune responses to disease progression.

117 g and immune modulatory cytokines that drive dysfunctional immune responses.

118 nhibitors in cancer immunotherapy suggests a dysfunctional immune synapse as a pivotal tolerogenic me

119 Pancreatic cancer is associated with a dysfunctional immune system and poor prognosis.

120 ay gut microbiota profiles characteristic of dysfunctional immunity.

121 we performed electrophysiology to assess the dysfunctional impact of Abeta and tau oligomers as well

122 on normal physiology of somatic tissues and dysfunctional impacts in diseases associated with aging,

123 The airway epithelium is dysfunctional in asthma and epigenetic mechanisms are co

124 ase-driven Parkin ubiquitin ligase, which is dysfunctional in autosomal recessive Parkinson's disease

125 to primary hemostasis, but become profoundly dysfunctional in critically injured patients by an unkno

126 lts show that VIP-INs express Nav1.1 and are dysfunctional in DS, which may contribute to DS pathogen

127 lease channel in the heart, how RYR2 becomes dysfunctional in HF and AF, and its potential as a thera

128 lipoprotein A-I (apoA-I) is cross-linked and dysfunctional in human atheroma.

129 ability and sympathovagal balance, which are dysfunctional in mood and anxiety disorders, are insensi

130 sister chromatids and has been identified as dysfunctional in numerous tumour cell lines.

131 other major cellular process reported to be dysfunctional in part of the ALS/FTD spectrum.

132 etween specific fronto-striatal circuits was dysfunctional in pre-HD, compared with controls, and whe

133 (reg) cells are numerically deficient and/or dysfunctional in several autoimmune diseases that can af

134 y is that tumor-infiltrating lymphocytes are dysfunctional in situ, yet are capable of stem cell-like

135 Recently we have shown that autophagy is dysfunctional in the retinal pigment epithelium (RPE) of

136 trinsic mediators that render CD8(+) T cells dysfunctional in the tumor microenvironment is a require

137 re, we found that TRAF6-deficient Tregs were dysfunctional in vivo; mice with Treg-restricted deletio

138 sterior to prefrontal cortices, resulting in dysfunctional integration of new information about conte

139 Translating to humans, we find analogous dysfunctional interactions between hippocampus and prefr

140 ers are often conceptualized as arising from dysfunctional interactions between neural systems mediat

141 rehensive circuit-based model proposing that dysfunctional interactions between the brain's cognitive

142 Dysfunctional interactions in the IC<->CE/NBM network ma

143 gastrointestinal disease resulting from the dysfunctional interplay between genetic susceptibility,

144 and stemness, unique stromal properties, and dysfunctional intratumoral immune infiltration.

145 lopmental defects of the SV and consequently dysfunctional ion homeostasis and a reduction in the EP,

146 Recent reports have indicated that dysfunctional iron handling in the lungs of COPD patient

147 which, is sequestered within the cell and if dysfunctional leads to Hypogonadotropic Hypogonadism.

148 c remodeling in heart failure contributes to dysfunctional lipid trafficking and lipotoxicity.

149 Despite a dysfunctional locomotor system, patients show normal ada

150 The OcrlY/- mice show muscular defects with dysfunctional locomotricity and present massive urinary

151 pid mediators in conditions characterized by dysfunctional LOX activity, such as obesity.

152 ng lymphatic muscle fatigue in patients with dysfunctional lymphatics.

153 disease sites are genetically susceptible to dysfunctional lysosomal alpha-synuclein processing and m

154 Sensing and clearance of dysfunctional lysosomes is critical for cellular homeost

155 Dysfunctional lysosomes underlie Alzheimer's disease, Pa

156 abolism, likely of mitochondrial origin, and dysfunctional maintenance processes that support axonal

157 l control of diameter and, furthermore, that dysfunctional mechanobiological control can yield lesion

158 contractility are more important in terms of dysfunctional mechanosensing and mechanoregulation of ma

159 ng, reduced smooth muscle contractility, and dysfunctional mechanosensing or mechanoregulation of ext

160 ioral flexibility deficits observed suggests dysfunctional medial prefrontal cortex (mPFC) activity.

161 tand the pathway from normal memory to later dysfunctional memory.

162 This framework relies on targeting specific dysfunctional mental processes by modifying their underl

163 ak-link enzyme, pushing material through the dysfunctional metabolic pathway.

164 SBMA embryonic motor neurons also displayed dysfunctional mitochondria along with DNA damage, possib

165 The importance of understanding how dysfunctional mitochondria and mitophagy contribute to c

166 Cardiomyocytes ejected dysfunctional mitochondria and other cargo in dedicated

167 is late stage, cells have become filled with dysfunctional mitochondria and protein aggregates, which

168 The clearance of damaged or dysfunctional mitochondria by selective autophagy (mitop

169 Molecularly, HSCs carrying dysfunctional mitochondria can re-enter quiescence but f

170 governing the identification and removal of dysfunctional mitochondria from the cell, a process of m

171 alyses illustrated a significant increase of dysfunctional mitochondria in Angpt2-silenced tumor cell

172 activity and in a buildup of fragmented and dysfunctional mitochondria in heart failure.

173 in microglia, thus inhibiting the release of dysfunctional mitochondria into the extracellular milieu

174 during the neurodevelopment and suggest that dysfunctional mitochondria may contribute to the FXS phe

175 athophysiology of disorders characterized by dysfunctional mitochondria or lysosomes.

176 ts underlying oxidative cellular damage from dysfunctional mitochondria remain unresolved.

177 nse and neuronal cell death by extracellular dysfunctional mitochondria suggests a potential new inte

178 iated mitophagy, causing the accumulation of dysfunctional mitochondria that trigger epithelial stres

179 HSCs keep and accumulate dysfunctional mitochondria through asymmetric segregatio

180 Elimination of dysfunctional mitochondria via mitophagy is essential fo

181 Depletion of Mitofusin (dMfn) or Opa1 led to dysfunctional mitochondria, activation of Target of rapa

182 rm coined to describe autophagy that targets dysfunctional mitochondria, has emerged as an important

183 Loss of p62 significantly delayed removal of dysfunctional mitochondria, increased mitochondrial supe

184 Here, we show that dysfunctional mitochondria, linked to down-regulation of

185 was also associated with an accumulation of dysfunctional mitochondria, producing excessive reactive

186 activation could lead to an accumulation of dysfunctional mitochondria, resulting in inflammation an

187 umulation of unfolded protein aggregates and dysfunctional mitochondria, the consequent increased pro

188 mage and nuclear oxidative stress induced by dysfunctional mitochondria, there was a lack of gross nu

189 response seen in preeclampsia is provoked by dysfunctional mitochondria.

190 associated with impaired insulin signaling, dysfunctional mitochondrial energetics and oxidative str

191 le of an immune deficiency that is linked to dysfunctional mitochondrial energy metabolism and caused

192 s without tertiary lymphoid structures had a dysfunctional molecular phenotype.

193 ociated with the disease derives solely from dysfunctional motor neurons that may be efficiently targ

194 must be designed to treat this aspect of the dysfunctional motor unit.

195 ysfunction causes disease phenotypes through dysfunctional multipass membrane protein topogenesis.

196 The wild-type ORF57, but not its N-terminal dysfunctional mutant, inhibits PB formation by interacti

197 more detrimental than homoplasmy even for a dysfunctional mutant, that heteroplasmy distribution (no

198 Our results link the benefit of QS-dysfunctional mutants in vivo to biofilm-mediated immune

199 Current evidence suggests that dysfunctional natural killer (NK) cell responses during

200 mics during motor control in both intact and dysfunctional nervous systems.

201 To identify dysfunctional neuronal subtypes underlying seizure activ

202 Here the effects of linezolid on healthy and dysfunctional neutrophils (modelled by C5a-induced injur

203 id significantly improved killing of MRSA by dysfunctional neutrophils, which was supported by concom

204 shown to enhance the ubiquitination of only dysfunctional nNOS while leaving the native functional n

205 It does not alter their propensity to become dysfunctional, nor does it enhance the capacity of IL-2-

206 Given previous studies suggesting that dysfunctional oligodendrocytes (OLs) may trigger MS, we

207 hlight that not all CTLs expressing PD-1 are dysfunctional; on the contrary, T(RM) cells with PD-1 ex

208 , which are co-expressed and co-regulated on dysfunctional or 'exhausted' T cells in chronic viral in

209 the degradation of specific cargos, such as dysfunctional organelles and protein aggregates.

210 tments maintain cellular fitness by clearing dysfunctional organelles and proteins from cells.

211 pendent degradative pathway that disposes of dysfunctional organelles that are major sources of cellu

212 nery provides selective pressure to identify dysfunctional organelles through the coordinated action

213 adative pathway that clears the cytoplasm of dysfunctional organelles.

214 Dysfunctional p53 formation and activity can result from

215 ping CNS, and may provide new insights about dysfunctional pathways that cause vascular-related CNS d

216 This was due to induction of dysfunctional PD-1(+)CD38(hi) CD8(+) cells by PD-1 block

217 This study suggests that dysfunctional pDCs are a key initial mechanism associate

218 activated this nociceptive ensemble to drive dysfunctional perceptual changes associated with neuropa

219 ranscription factor TCF-1, and inhibited the dysfunctional phenotype, culminating in tumor growth inh

220 Although exhibiting a dysfunctional phenotype, TSA-reactive CD8(+) TILs posses

221 ent memory cell formation, consistent with a dysfunctional phenotype.

222 but that this adaptation fails in the small dysfunctional placenta in FGR [insulin-like growth facto

223 eveals that proliferation-competent cells in dysfunctional populations show a previously unrecognized

224 ution of CPE in betaOGTKO islets rescued the dysfunctional proinsulin-to-insulin ratio.

225 o fusions used in previous studies displayed dysfunctional protein interaction activity.

226 carboxyl truncation that can be augmented by dysfunctional proteostasis, dramatically potentiates the

227 lex, were dramatically reduced, indicating a dysfunctional RalGAP complex.

228 mune dysregulation has been shown to lead to dysfunctional regulatory T lymphocytes and increased pro

229 Whether AMB are dysfunctional remains controversial, as there are also s

230 I and to better understand it effects on the dysfunctional renin-angiotensin-aldosterone system durin

231 With a potential link between dysfunctional repair and immunoreactivity, we investigat

232 nvestigate the immunological consequences of dysfunctional repair examining chronic disease in mouse

233 Lung epithelial cell damage and dysfunctional repair play a role in the development of l

234 effect depends on a complex mechanism, where dysfunctional replication forks lead to recruitment of e

235 ally, alveolar macrophages were depleted and dysfunctional, resembling pulmonary alveolar proteinosis

236 ticipated in the fMRI experiment to identify dysfunctional responses associated with chronic alcohol

237 rtebrate development, organogenesis and when dysfunctional result in pleiotropic human genetic disord

238 Cues can also promote dysfunctional reward-seeking behavior, as in overeating.

239 n patients with major depressive disorder, a dysfunctional reward-system may exist, with blunted temp

240 red a method for treatment for patients with dysfunctional right ventricular outflow tracts.

241 When TRPM2 is inhibited, mitochondria are dysfunctional, ROS levels are increased, and cell viabil

242 Importantly, dysfunctional SBP2 is associated with endocrine disorder

243 Dysfunctional signaling to the amygdala from the ACC or

244 Although dysfunctional signaling transduction is attributed to ai

245 igment epithelium indicating the presence of dysfunctional sphincter muscle.

246 previously considered to be an artifact of a dysfunctional spliceosome.

247 This dysfunctional state involves widespread vasoconstriction

248 hematological malignancies but can acquire a dysfunctional state, which limits antitumor immunity.

249 they enter a hyporesponsive ('exhausted' or 'dysfunctional') state(6-9) triggered by chronic antigen

250 ion between tumor development and the T-cell dysfunctional status seen in this viral oncogenesis huma

251 equire Frizzled 1/2/7 binding to elicit this dysfunctional stem cell state.

252 Strategies to address dysregulated or dysfunctional steps within the heme biosynthetic pathway

253 enges imparted by mutant protein conformers, dysfunctional subcellular organelles, and dysregulated t

254 y hemostatic function is perturbed in type 2 dysfunctional subtypes of von Willebrand disease (VWD) b

255 scuss the recent work on the contribution of dysfunctional SVE to midbrain dopaminergic neurons' sele

256 Previous studies have found dysfunctional T cell responses correlate to severe disea

257 Recent studies in humans have found that dysfunctional T cell responses strongly correlate with d

258 y circuits may help in the future to rectify dysfunctional T cell responses.

259 re neurodegenerative disease associated with dysfunctional tau protein.

260 Dysfunctional telomeres activate DDR signaling, genomic

261 Short/dysfunctional telomeres are at the origin of idiopathic

262 ue to imperfect DDR signaling in response to dysfunctional telomeres creates a preponderance of chrom

263 syndromes, but how microcephaly is linked to dysfunctional telomeres is not known.

264 mage factors and homology directed repair of dysfunctional telomeres lacking POT1-TPP1.

265 our study establishes that relocalization of dysfunctional telomeres to the nuclear periphery is crit

266 buffering senescence stresses due to short, dysfunctional telomeres, and preventing malignant transf

267 DDRNA production at chromosomal DSBs and at dysfunctional telomeres, which in turn promotes 53BP1 ac

268 kers of senescence such as reduced HMGB1 and dysfunctional telomeres, without detectable telomere sho

269 premature cellular senescence in response to dysfunctional telomeres.

270 ions, and inhibits 53BP1-dependent fusion of dysfunctional telomeres.

271 Interestingly, dysfunctional Tfh from HIV infected-individual fail to r

272 and how failure of these mechanisms leads to dysfunctional Tfr cells.

273 ectivity is unknown, but animal models imply dysfunctional theta phase coupling between hippocampus a

274 ractions are generally homeostatic, but when dysfunctional, they can incite food sensitivities and ch

275 as been argued that the p factor may reflect dysfunctional thinking present in serious mental illness

276 However, tumor-associated NK cells become dysfunctional; thus, stimulation of NK cells in cancer i

277 s reveal a previously unappreciated role for dysfunctional tissue repair in local immunomodulation th

278 culture or can be implanted into damaged or dysfunctional tissue to restore normal function.

279 transgenic rabbits had higher frequencies of dysfunctional tissue-resident CD8(+) T(RM) cells.

280 phocytes harboring ubiquitous TCRs display a dysfunctional tissue-resident phenotype.

281 pology during embryonic development leads to dysfunctional tonotopy of the auditory system.

282 A dysfunctional tPA-plasmin system causes defective proteo

283 We show that TOX is highly expressed in dysfunctional TST cells from tumours and in exhausted T

284 The efficacy of chemotherapy is reduced by dysfunctional tumor vasculature, which may limit chemoth

285 ss-induced compensation but downregulated in dysfunctional type 2 diabetic (T2D) human beta cells.

286 s and characterize terminally differentiated dysfunctional UC CD8(+) T cells expressing IL-26, which

287 Tregs may become unstable and dysfunctional under inflammatory conditions, which can e

288 Vma2Delta cells have dysfunctional V-ATPases, rendering their vacuoles nonaci

289 s to a considerable number of patients whose dysfunctional vascular cells preclude TEVG generation vi

290 Aberrant Wnt tone in OPCs mediates their dysfunctional vascular detachment and also leads to OPC

291 In a condition of dysfunctional visceral fat depots, as in the case of obe

292 ophysiology of visual symptoms might involve dysfunctional visual cortex.

293 hronically stimulated adaptive NK cells were dysfunctional when challenged with tumor targets.

294 the abovementioned reward systems are still dysfunctional when patients are in remission.

295 T cells become dysfunctional when they encounter self antigens or are e

296 unophenotype, Tox-deleted TST cells remained dysfunctional, which suggests that the regulation of exp

297 s on "flashbulb" memories, and it can become dysfunctional with age and diseases, such as Alzheimer's

298 become progressively activated and seemingly dysfunctional with age, and genetic studies have linked

299 d the mechanisms by which these cells become dysfunctional with diabetes, there has been a scientific

300 ndings indicate that the platelets in HD are dysfunctional with respect to the release of angiogenic