ライフサイエンスコーパス: TEN

1 TEN had a significantly higher number of cases with mild

2 TEN PATIENTS WHO REQUIRED two or more anterior teeth ext

3 A total of 20 SJS and 12 TEN cases were included.

4 /TEN: 16.5 +/- 1.0 days, $58,954 +/- $5,238; TEN: 16.2 +/- 1.0 days, $53,695 +/- $4,037) were observe

5 A TEN domain physically separate from the TERT core can ca

6 Suppression of a TEN-domain mutation with a compensatory charge-swap muta

7 cally confirmed cases of SJS/TEN overlap and TEN.

8 HLA-B*1502 and carbamazepine-induced SJS and TEN and that reported sufficient data for calculating th

9 502 allele and carbamazepine-induced SJS and TEN in Han-Chinese, Thai, and Malaysian populations.

10 tay, comorbidities, and mortality of SJS and TEN in US adults.

11 HLA-B*1502 and carbamazepine-induced SJS and TEN was 79.84 (95% CI, 28.45-224.06).

12 ry outcome was carbamazepine-induced SJS and TEN.

13 ommon during the acute phase in both SJS and TEN.

14 acute ocular manifestations between SJS and TEN.

15 f the acute ocular manifestations of SJS and TEN.

16 fication codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564, respectively).

17 SJS, SJS/TEN, and TEN pose a substantial health care burden.

18 an estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million adults per year,

19 thies(13,14) are located at the TERT-TER and TEN-TRAP-TPP1 interfaces, highlighting the importance of

20 To investigate the conservation of TRAP and TEN across species, we performed multiple sequence align

21 holoenzyme reconstitution in vitro to assess TEN domain sequence requirements in the physiological en

22 Here, we present BB-TEN: Big Bird - TNM staging Extracted from Notes, a gene

23 an affirmative finding for any of the 3 BCDR TEN-4-FACESp components in children younger than 4 years

24 diated by a cryptic adhesion complex between TENs and LPHNs regulates synapse specificity.

25 Both TEN and TRAP are absent in the putative Tribolium TERT t

26 9 months and younger, or patterned bruising (TEN-4-FACESp).

27 ase and tensin homolog deleted on chromosome TEN) is a delayed step causatively leading to excitotoxi

28 e and tensin homologue deleted on chromosome TEN) is the major negative regulator of phosphatidylinos

29 e and TENsin homologue deleted on chromosome TEN) mutations predispose to phenotypically diverse diso

30 failed to interact strongly with the cognate TEN domains.

31 Under resting conditions, TEN significantly suppressed basal sympathetic tone comp

32 ical interaction assays pinpoint a conserved TEN domain surface required for holoenzyme subunit assoc

33 Collectively these observations demonstrate TEN can dampen basal sympathetic tone and attenuate symp

34 prim-sulfamethoxazole exposure who developed TEN in a photodistributed pattern 1 day after prolonged

35 ted with mortality after hospital discharge (TEN vs SJS: AHR, 0.95; 95% CI, 0.60-1.47), but acute com

36 ique telomerase essential N-terminal domain (TEN) and the telomerase RAP motif (TRAP) that are unique

37 in vitro in a manner dependent on the Est2p TEN domain interaction.

38 8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

39 known, and there is no effective therapy for TEN(4-6).

40 Ileal bacteria from TEN and TPN piglets were also examined for their ability

41 igh expression of RIP3 in keratinocytes from TEN patients potentiates MLKL phosphorylation/activation

42 is highly upregulated in skin sections from TEN patients and may therefore contribute to the patholo

43 Histologically, the skin from TEN patients exhibits separation at the dermo-epidermal

44 hosphorylation was observed in the skin from TEN patients, indicating the presence of RIP3-dependent

45 the cucurbit-specific tendril identity gene TEN originated from a paleo-polyploidization event at th

46 GO-TEN and ResolveOME analyses confirmed that pathogenic va

47 ptomes enhanced with nanopore sequencing (GO-TEN) that combines targeted cDNA long-read sequencing wi

48 an-fish telomerases that contained the human TEN domain were active but not stimulated by POT1-TPP1,

49 IFD-TEN interactions are not disrupted by multiple amino aci

50 hus highlighting a complex regulation of IFD-TEN interactions as suggested by recent cryo-EM structur

51 ring between the moderate (15% in SJS, 0% in TEN) and severe groups (20% in SJS, 33% in TEN).

52 n TEN) and severe groups (20% in SJS, 33% in TEN).

53 ses with mild involvement (5% in SJS, 42% in TEN, p = 0.01), while no statistically significant diffe

54 ore contribute to the pathological damage in TEN through activation of programmed necrotic cell death

55 associated bacteria (100 colonies tested) in TEN ileal samples grew on mucin.

56 ndrome (SJS) and toxic epidermal necrolysis (TEN) among carbamazepine users, especially in some racia

57 Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome (SJS) are rare, acute,

58 ndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening disorders.

59 ndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening mucocutaneous adverse drug rea

60 ndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening conditions that initi

61 ndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening mucocutaneous disease

62 ndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but potentially life-threatening cutaneous

63 ndrome (SJS) and toxic epidermal necrolysis (TEN) are severe drug reactions associated with a high ra

64 n syndrome (SJS)/toxic epidermal necrolysis (TEN) as a model to study the pathologic role of HLA in d

65 ndrome (SJS) and toxic epidermal necrolysis (TEN) cause diffuse epidermal detachment and necrosis.

66 ndrome (SJS) and toxic epidermal necrolysis (TEN) have been infrequently reported since the first doc

67 Toxic epidermal necrolysis (TEN) is a fatal drug-induced skin reaction triggered by

68 Toxic epidermal necrolysis (TEN) is a severe adverse drug reaction involving extensi

69 ronic ocular SJS/toxic epidermal necrolysis (TEN) were included in the study.

70 syndrome (SJS), toxic epidermal necrolysis (TEN), and graft-versus-host disease (GVHD) are distinct

71 ndrome (SJS) and toxic epidermal necrolysis (TEN), could be life-threatening.

72 syndrome (SJS), toxic epidermal necrolysis (TEN), drug rash with eosinophilia and systemic symptoms

73 syndrome (SJS), toxic epidermal necrolysis (TEN), or drug rash with eosinophilia and systemic sympto

74 Syndrome (SJS), toxic epidermal necrolysis (TEN), or SJS/TEN was performed.

75 ndrome (SJS) and toxic epidermal necrolysis (TEN), varies across studies.

76 ndrome (SJS) and toxic epidermal necrolysis (TEN).

77 ndrome (SJS) and toxic epidermal necrolysis (TEN).

78 syndrome (SJS) or toxic epidermal necrosis (TEN) is even rarer and not well studied.

79 The transmural extent of necrosis (TEN) (%) was measured by triphenyltetrazolium chloride s

80 this transdermal electrical neurosignaling (TEN) method on sympathetic physiology under different ex

81 ques such as the threshold-equalizing noise (TEN) test.

82 s of piglets fed by total enteral nutrition (TEN; n = 6) or TPN (n = 5) were compared with the use of

83 Overall, 40% of SJS and 75% of TEN patients had acute ocular surface inflammation.

84 of the epidermis, leading to a diagnosis of TEN.

85 alling pathways as key pathogenic drivers of TEN and demonstrates the potential of targeted JAKi as a

86 ique to TERT, and conformational dynamics of TEN-TRAP are damped upon TPP1 binding, defining the requ

87 tructure was equally complex in the ileum of TEN and TPN piglets, but profiles clustered according to

88 t significantly different in skin lesions of TEN.

89 Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-me

90 ase severity in two distinct mouse models of TEN.

91 The roles of TEN domain surface residues in primer binding and produc

92 presents a potential target for treatment of TEN.

93 by multiple amino acid changes in the IFD or TEN, thus highlighting a complex regulation of IFD-TEN i

94 SJS (<30% body surface area involvement) or TEN (> = 30% involvement), who were treated at one terti

95 T cells in patients with ALP-induced SJS or TEN and, in particular, there are no reports examining p

96 The studies included 227 SJS or TEN cases, 602 matched control subjects, and 2949 popula

97 nese race/ethnicity, no patients with SJS or TEN were carriers of the HLA-B*1502 allele.

98 exposures who subsequently developed SJS or TEN with photodistribution.

99 In addition, P-TEN exhibited a high degree of substrate specificity, sh

100 thermore, we demonstrate that mutations in P-TEN, identified from primary tumors, tumor cells lines,

101 , demonstrating that enzymatic activity of P-TEN is necessary for its ability to function as a tumor

102 Here we show that recombinant P-TEN dephosphorylated protein and peptide substrates phos

103 didate tumor suppressor from 10q23, termed P-TEN, was isolated, and sequence homology was demonstrate

104 ne, and tyrosine residues, indicating that P-TEN is a dual-specificity phosphatase.

105 Photodistributed TEN has been increasingly described in the literature an

106 WE RECOGNISE TEN SPECIES IN THIS GROUP: S. aureitomentosum Bitter, S.

107 How alternative-splicing regulates TEN-LPHN interaction remains unclear.

108 , 1.81; 95% CI, 1.24-2.64), and EN severity (TEN vs SJS: AHR, 2.14; 95% CI, 1.49-3.07).

109 Ocular involvement in SJS, TEN, and Overlap syndrome is common and the ocular manif

110 ick Children between 2001 and 2011 with SJS, TEN, and Overlap syndrome were reviewed.

111 alysing each particular clinical entity: SJS-TEN (62.5% vs 87.5%), MPE (15% vs 47.4%) and AGEP (33% v

112 SJS/TEN mostly manifest as a reaction to new drug use, but l

113 SJS/TEN serum induced significant MMP9 expression and collag

114 SJS/TEN was associated with nonwhite race, particularly Asia

115 The IHD cohort included 11 084 SJS/TEN survivors (mean [SD] age, 56.6 [18.6] years; 5561 fe

116 affected skin, and blister fluid from 15 SJS/TEN patients.

117 (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hypersensitivity syndrome, and 46 nevirapine-ind

118 The CVA cohort included 10 571 SJS/TEN survivors (mean [SD] age, 56.1 [18.5] years; 5358 fe

119 we calculated an incidence rate of 5.76 SJS/TEN cases per million person-years between 1995 and 2013

120 SJS: 9.8 +/- 0.3 days, $21,437 +/- $807; SJS/TEN: 16.5 +/- 1.0 days, $58,954 +/- $5,238; TEN: 16.2 +/

121 Nine of 48 patients (18 eyes) had acute SJS/TEN from 2000 to 2007 and did not receive protocol care

122 -nine of 48 patients (78 eyes) had acute SJS/TEN from 2008 to 2017 and received protocol care (Group

123 r mortality risks peaked at 1 year after SJS/TEN and persisted for 4 to 7 years.

124 A) or ischemic heart disease (IHD) after SJS/TEN survival.

125 VA and IHD morbidity and mortality after SJS/TEN survival.

126 Causality assessment for DILI and SJS/TEN was carried out with the Roussel Uclaf Causality Ass

127 Prevalence of antibiotic-associated SJS/TEN was presented as pooled proportions with 95% CIs.

128 Among antibiotic-associated SJS/TEN, the sulfonamide class was associated with 32% (95%

129 view has described antibiotic-associated SJS/TEN.

130 rs admitted to an intensive care unit at SJS/TEN diagnosis had significantly higher cardiovascular mo

131 tically significant associations between SJS/TEN and pre-existing depression, lupus erythematosus, re

132 cytotoxicity in in vitro models of both SJS/TEN (elicited by drug-specific antigen) and GVHD (elicit

133 mphocytes of patients with carbamazepine-SJS/TEN, with its expression showing drug/phenotype-specific

134 ify the tear fluid proteins from chronic SJS/TEN patients (n = 22 eyes) and age- and gender-matched c

135 ntly differentially regulated in chronic SJS/TEN.

136 Concomitantly, SJS/TEN displayed a reduced Treg signature compared with MDE

137 and observational studies that described SJS/TEN risks since database inception to February 22, 2022.

138 dentified as risk factors for developing SJS/TEN with severe ocular complications (SOC).

139 ed effector molecules are known to drive SJS/TEN pathophysiology, but the contribution of innate immu

140 alpha inhibitor etanercept, an effective SJS/TEN treatment.

141 ipts in formalin-fixed paraffin-embedded SJS/TEN skin biopsies.

142 were penicillins and cephalosporins for SJS/TEN and AGEP; glycopeptides for DRESS.

143 possible immunomodulating treatments for SJS/TEN and estimate their effects on mortality compared wit

144 national experts, a case report form for SJS/TEN has been created to help standardize the collection

145 differences in treatment strategies for SJS/TEN in Europe; the findings suggest the need for prospec

146 lating therapies or supportive care) for SJS/TEN were selected.

147 with epilepsy and gout, odds ratios for SJS/TEN were significantly increased only in the presence of

148 ed mortality was 4.8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

149 No eyes in Group I received AMT for SJS/TEN, compared to 87% of qualifying eyes in Group II (P <

150 systemic immunomodulating treatments for SJS/TEN, which is of great relevance for treating physicians

151 ages looking for treatment proposals for SJS/TEN.

152 systemic immunomodulating therapies for SJS/TEN.

153 phocytes (CTL) in blister cells from ICI-SJS/TEN skin lesions.

154 approaches to identify culprit drugs in SJS/TEN are associated with overlabeling patients allergic t

155 Serum inflammatory profiles in SJS/TEN patients were notably characterized by massive upreg

156 ing system of chronic ocular features in SJS/TEN sequelae is a useful tool to grade all levels of sev

157 9 expression was significantly higher in SJS/TEN skin (70.6%) than in healthy control skin (0%) (P =

158 ee SJS/TEN patients and was confirmed in SJS/TEN tears and eyelid margins by ELISA and IHC, respectiv

159 In SJS/TEN, HLA class I-restricted oligoclonal CD8(+) T-cell re

160 ecific protocol for acute ocular care in SJS/TEN, including aggressive use of AMT, was highly success

161 y are a putative pathogenic mechanism in SJS/TEN, which is limited by etanercept.

162 on the systemic inflammatory response in SJS/TEN, which may not correlate with clinical outcome diffe

163 f cytotoxic CD8+ T cells into skin as in SJS/TEN, yet a pro-Treg signature as in MDE.

164 d its associated ocular complications in SJS/TEN.

165 d nonexpanded cytotoxic CD8+ skin TRM in SJS/TEN.

166 heir effects on systemic inflammation in SJS/TEN.

167 e 69 cases of PPI-related DHR, including SJS/TEN (n=27) and DRESS (n=10).

168 es (CTLs) from patients with CBZ-induced SJS/TEN and analyzed the interaction between HLA-B and CBZ a

169 isolated from both resolved ALP-induced SJS/TEN cases and drug-naive healthy donors, we show that OX

170 pic profile in both resolved ALP-induced SJS/TEN cases and drug-naive healthy donors.

171 as a risk factor for nevirapine-induced SJS/TEN in a Malawian HIV cohort.

172 ecialist-adjudicated allopurinol-induced SJS/TEN or DRESS (collectively allopurinol-induced severe cu

173 amine 6 cohorts including 25 ICI-induced SJS/TEN patients and conduct single-cell RNA sequencing (scR

174 c corticosteroids treatment, ICI-induced SJS/TEN patients treated with biologic TNF blockade showed a

175 orrelations for CBZ-related drug-induced SJS/TEN.

176 Patients who survive the initial SJS/TEN episodes are affected by various sequelae.

177 syndrome and toxic epidermal necrolysis (SJS/TEN) and drug reaction with eosinophilia and systemic sy

178 Syndrome and Toxic Epidermal Necrolysis (SJS/TEN) are part of a disease continuum of vesiculobullous

179 syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe adverse reactions with high mor

180 syndrome and toxic epidermal necrolysis (SJS/TEN) are severe cutaneous adverse drug reactions charact

181 syndrome or toxic epidermal necrolysis (SJS/TEN) group, whereas glaucoma was found not to significan

182 syndrome and toxic epidermal necrolysis (SJS/TEN) is a rare but life-threatening cutaneous drug react

183 son syndrome/toxic epidermal necrolysis (SJS/TEN) is a severe hypersensitivity reaction.

184 son syndrome/toxic epidermal necrolysis (SJS/TEN) is known to cause multiple end-organ complications

185 syndrome and toxic epidermal necrolysis (SJS/TEN), although a detailed description is lacking in the

186 on syndrome, toxic epidermal necrolysis (SJS/TEN), and drug reaction with eosinophilia and systemic s

187 son syndrome/toxic epidermal necrolysis (SJS/TEN), hindering continuous ICI therapy.

188 syndrome and toxic epidermal necrolysis (SJS/TEN), which are the most severe types of drug hypersensi

189 son syndrome/toxic epidermal necrolysis (SJS/TEN).

190 TEN were identified and matched with non-SJS/TEN participants by age, sex, and Charlson Comorbidity I

191 sion model showed that compared with non-SJS/TEN participants, patients with SJS/TEN had higher risks

192 The use of AMTs in severe ocular SJS/TEN greatly mitigates long-term complications and improv

193 To date, ocular SJS/TEN risk altering alleles have not been widely investiga

194 patients underwent AMT for severe ocular SJS/TEN.

195 The OR for absolute risk of SJS/TEN associated with carriage of HLA-C*04:01 was 5.17 (95

196 associated with more than one-quarter of SJS/TEN cases described worldwide, and sulfonamide antibioti

197 servational study on the epidemiology of SJS/TEN contributes to the understanding of this still under

198 ality based on an international panel of SJS/TEN experts who performed a Delphi consensus-building ex

199 Initiation and progression of SJS/TEN keratinocyte necroptosis appear to involve a cascade

200 ly and histologically confirmed cases of SJS/TEN overlap and TEN.

201 ystemic and cutaneous immune profiles of SJS/TEN patients and to investigate whether/how intravenous

202 ved in the keratinized eyelid margins of SJS/TEN to validate the presence of neutrophils.

203 servational study on the epidemiology of SJS/TEN using data from the UK-based Clinical Practice Resea

204 Survivors of SJS/TEN were identified and matched with non-SJS/TEN partici

205 1992 and December 2016 with a history of SJS/TEN were reviewed.

206 Asian patients were at a 2-fold risk of SJS/TEN when compared with white patients.

207 d 86 patients (167 eyes) with history of SJS/TEN who underwent PROSE treatment from January 1, 2006,

208 f these alleles in the susceptibility of SJS/TEN with or without severe ocular complications in patie

209 By contrast, the incidence of SJS/TEN with SOC in European countries is relatively low.

210 After remission of SJS/TEN, a complete ENT mucosal healing occurred in 36 patie

211 Demographics, etiology of SJS/TEN, age at treatment milestones, best-corrected visual

212 ate and useful" for documenting cases of SJS/TEN, making it more reliable and valuable for future res

213 yspnea is observed at the acute stage of SJS/TEN.

214 therapeutic target for the treatment of SJS/TEN.

215 and may represent a distinct variant of SJS/TEN.

216 ered inflammation during early phases of SJS/TEN.

217 15, 36 (4.8%) had associated features of SJS/TEN.

218 y findings to improve prognostication of SJS/TEN.

219 S), toxic epidermal necrolysis (TEN), or SJS/TEN was performed.

220 w of published cases of photodistributed SJS/TEN.

221 ical Modification codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564, respectiv

222 SJS, SJS/TEN, and TEN pose a substantial health care burden.

223 The mean estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million adults p

224 In this cohort study, SJS/TEN had a lasting association with cardiovascular functi

225 Fatality was more frequent in the SJS/TEN group.

226 36gamma (p < .01) was expressed in three SJS/TEN patients and was confirmed in SJS/TEN tears and eyel

227 hronic ocular surface disease related to SJS/TEN and results in significant improvement in vision tha

228 riptively analyzed potential culprits to SJS/TEN, patients' allergy lists, and currently used approac

229 hronic ocular surface disease related to SJS/TEN, PROSE treatment offers sustained and significant la

230 ting that this was a process specific to SJS/TEN.

231 tion, and long-term sequelae relevant to SJS/TEN.

232 f highly cited manuscripts pertaining to SJS/TEN.

233 Among 551 validated SJS/TEN patients, we calculated an incidence rate of 5.76 SJ

234 n and South East Asian populations where SJS/TEN is prevalent, numerous human leukocyte antigen (HLA)

235 HLA class I associations with SJS/TEN and drug reaction with eosinophilia and systemic sym

236 e US evaluated 121 adults diagnosed with SJS/TEN by inpatient consultive dermatologists between Janua

237 s who developed DILI in association with SJS/TEN from a registry of DILI patients from a single cente

238 non-SJS/TEN participants, patients with SJS/TEN had higher risks of cardiovascular morbidity (CVA: H

239 Retrospective study of 49 patients with SJS/TEN hospitalized in a referral care center from 2005 to

240 iation of HLA -A, -B and -C alleles with SJS/TEN in 33 patients residing in the UK with age matched c

241 ce of DILI occurring in association with SJS/TEN including the etiologic agents, clinical and biochem

242 DILI associated with SJS/TEN is rare and associated with a high death rate, parti

243 himera on CTL responses in patients with SJS/TEN or GVHD.

244 temic inflammation seen in patients with SJS/TEN or GVHD.

245 roportion of antibiotics associated with SJS/TEN was 28% (95% CI, 24%-33%), with moderate certainty o

246 A total of 212 adults with SJS/TEN were included between January 1, 2015, and December

247 All patients with SJS/TEN with chronic (more than 1 year) ocular sequelae were

248 vity, such as that seen in patients with SJS/TEN, as well as the alloreactivity seen in patients with

249 In patients with SJS/TEN, higher mortality was associated with old age and un

250 ety appear to be common in patients with SJS/TEN, with implications for health and well-being.

251 ce of single antibiotics associated with SJS/TEN.

252 counseling, and support to patients with SJS/TEN.

253 t when subjects were experimentally stressed TEN produced a significant suppression of heart rate var

254 s three hypothetical consensus motifs (SVTK, TEN, and KTG) that typically form the active center of o

255 lishes the TEN-LPHN interaction and switches TEN function to specify inhibitory synapses.

256 on of the cell-adhesion molecules teneurins (TENs) with latrophilins (LPHNs/ADGRLs) promotes excitato

257 thyl ether (AME), altenuene (ALT), tentoxin (TEN), and tenuazonic acid (TeA), five alternaria toxins

258 ping in the telomerase essential N-terminal (TEN) and insertions in fingers domain (IFD)-TRAP regions

259 ns with the telomerase essential N-terminal (TEN) domain and roles in telomerase activity.

260 We demonstrate that the TERT N-terminal (TEN) domain determines active-site use of the atypically

261 The telomerase essential N-terminal (TEN) domain is a conserved region of TERT proposed to me

262 he purified telomerase essential N-terminal (TEN) domain of Est2p in vitro.

263 1, with the telomerase essential N-terminal (TEN) domain of the human telomerase reverse transcriptas

264 ranscriptase (TERT) core, a TERT N-terminal (TEN) domain, and additional subunits of the telomerase h

265 thesis does not require the TERT N-terminal (TEN) domain, but RNA-dependent positioning of the TEN do

266 alysis on all identified TERTs and find that TEN and TRAP have coevolved as telomerase-specific domai

267 We find that TEN domain sequence substitutions in the Tetrahymena tel

268 ions are consistent with the hypothesis that TEN modulates noradrenergic signaling to suppress sympat

269 The TEN method involved delivering high-frequency pulsed ele

270 ely-spliced region within TENs abolishes the TEN-LPHN interaction and switches TEN function to specif

271 he docked state is further buttressed by the TEN domain and mutations within the TEN domain substanti

272 However, the TEN test, although fast and easy to perform, requires pa

273 tation of a conserved glycine, Gly100 in the TEN (telomerase essential N-terminal) domain of TERT, ab

274 tify separation-of-function mutations in the TEN-domain of human telomerase reverse transcriptase (hT

275 ate and telomeric DNA handling-including the TEN domain and the TRAP-thumb helix channel-are largely

276 s how domains of TER and TERT, including the TEN-TRAP complex, can interact in a conserved manner to

277 is screen focused on surface residues of the TEN and IFD regions, we identified TERT residues that ar

278 domain, but RNA-dependent positioning of the TEN domain captures substrate and allows repeat synthesi

279 meric DNA complex and the G100 region of the TEN domain of TERT is necessary for high-processivity te

280 nked to telomeric DNA in the presence of the TEN domain.

281 ng assays to investigate the function of the TEN domain.

282 determinants of processivity lie outside the TEN domain.

283 n 0 and 15 dB, in 3 dB steps relative to the TEN level.

284 requency dead regions, as assessed using the TEN(HL) test.

285 We propose a model in which the TEN domain stabilizes short RNA-DNA duplexes in the acti

286 pure tone presented simultaneously with the TEN at SNRs between 0 and 15 dB, in 3 dB steps relative

287 find that the IFD domain interacts with the TEN domain but is not essential for intramolecular hTERT

288 t3 homologues form stable complexes with the TEN domain of telomerase reverse transcriptase.

289 We propose that interaction with the TEN domain unmasks a functionally important nucleic acid

290 r intramolecular hTERT interactions with the TEN domain.

291 d by the TEN domain and mutations within the TEN domain substantially alter the DNA substrate structu

292 p molecular changes that are associated with TEN and identify potential druggable targets, we utilize

293 positive IVC velocity correlated better with TEN (r = -0.94, p < 0.0001) than it did S (r = -0.70, p

294 ak negative velocity) highly correlated with TEN, during ischemia (r = -0.78, p < 0.001) and during r

295 lar involvement, including all patients with TEN (n = 7).

296 Patients with TEN undergo severe and sudden epidermal detachment cause

297 nd keratinocyte compartment of patients with TEN, as well as phosphorylated STAT1 activation.

298 lization and recovery in seven patients with TEN.

299 different experiment, subjects treated with TEN reported significantly lower levels of tension and a

300 IVC velocity was zero in ischemic walls with TEN >20%.

301 a short alternatively-spliced region within TENs abolishes the TEN-LPHN interaction and switches TEN