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1 age-related macular degeneration and macular telangiectasia.
2 2 and other retinal diseases associated with telangiectasia.
3 leiotropic neurodegeneration disorder ataxia-telangiectasia.
4 athogenic dissection and treatment of ataxia telangiectasia.
5 AH is associated with hereditary hemorrhagic telangiectasia.
6 verall cosmesis and reduces the risk of skin telangiectasia.
7 etinal angiomatous proliferation and macular telangiectasia.
8 se states, including malignancies and ataxia telangiectasia.
9 genetic instability in patients with ataxia-telangiectasia.
10 e most common sequelae after involution were telangiectasias (145, 84.3%), fibrofatty tissue (81, 47.
11 of brain function, in 10 adults with ataxia-telangiectasia, 19 non-affected adult relatives (12 sibl
16 ereditary autosomal recessive disease ataxia telangiectasia (A-T) is caused by mutation in the DNA da
18 on is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation of the A
21 ase mutated in the rare human disease ataxia telangiectasia (A-T), has been the focus of intense scru
24 ns, is substantially reduced in human ataxia-telangiectasia and Atm(-/-) mouse cerebellar Purkinje ce
25 , this pathogenesis appears common to ataxia-telangiectasia and Cockayne syndrome, two other DNA repa
26 e expression of genes involved in ATM/ataxia telangiectasia and Rad-3-related (ATR) signaling, apopto
28 s for the cell cycle checkpoint genes ATAXIA TELANGIECTASIA AND RAD3 RELATED (ATR) and ALUMINUM TOLER
29 manner that is partially dependent on ataxia telangiectasia and Rad3 related (ATR) but not cyclin T o
30 positive correlation between ERH and ataxia telangiectasia and Rad3 related (ATR) expression in live
32 ers homology-directed repair and ATR (ataxia telangiectasia and Rad3 related)-dependent checkpoint ac
33 important for activation of the ATR (ataxia telangiectasia and Rad3 related)-regulated DNA damage si
34 motes PKA-mediated phosphorylation of ataxia telangiectasia and rad3-related (ATR) at Ser435 (ATR-pS4
40 involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to CHK2, w
42 omains, which inhibits recruitment of Ataxia telangiectasia and Rad3-related protein (ATR) and reduce
44 e of UV-induced XPA nuclear import on ataxia telangiectasia and Rad3-related protein (ATR) in S-phase
45 the replication stress sensing kinase ataxia telangiectasia and Rad3-related protein (ATR) reduces th
46 on of a G2 checkpoint mediated by the ataxia telangiectasia and Rad3-related protein (ATR)-checkpoint
47 e stress leading to activation of the ataxia telangiectasia and Rad3-related protein (ATR)-mediated D
48 5C was regulated by activation of the ataxia telangiectasia and Rad3-related protein (ATR)/checkpoint
50 oter region of DNA repair kinase ATR (ataxia-telangiectasia and Rad3-related protein) and acts as a t
51 ing of ataxia telangiectasia mutated, ataxia telangiectasia and Rad3-related protein, and DNA-depende
54 mplexes (Top1ccs) in murine models of ataxia telangiectasia and spinocerebellar ataxia with axonal ne
55 other brain areas in individuals with ataxia-telangiectasia and tested for brain changes in asymptoma
56 ther neurodegenerative disorders (eg, ataxia-telangiectasia), and DNA double-strand breaks are crucia
58 ART-A, moderate or marked breast induration, telangiectasia, and breast oedema were significantly les
61 the type of sequelae classified as residual telangiectasia, anetodermal skin, redundant skin, persis
63 Cells isolated from patients with ataxia telangiectasia are exquisitely sensitive to ionizing rad
65 were used to compare individuals with ataxia-telangiectasia, asymptomatic relatives, and unrelated co
66 Selective laser photocoagulation of retinal telangiectasia at the retinal vasoproliferative tumors'
73 nhibitors of ATM, the gene mutated in ataxia telangiectasia, can sensitize tumor cells to radiation t
74 e-phase disc leakage, central and peripheral telangiectasias, capillary anomalies, and capillary agen
75 (both associated with hereditary hemorrhagic telangiectasia), caveolin-1 (CAV1), and a gene (KCNK3) e
77 scribe a novel mouse model expressing ataxia telangiectasia group D complementing gene (ATDC, also kn
80 ebellar metabolism, participants with ataxia-telangiectasia had widespread changes in metabolic rates
82 st-mortem studies in individuals with ataxia-telangiectasia have reported cerebellar atrophy; but abn
83 F-beta/BMP signaling: hereditary hemorrhagic telangiectasia (HHT) and cerebral cavernous malformation
87 ease, we investigated hereditary hemorrhagic telangiectasia (HHT), which is caused by mutations in TG
90 life in patients with hereditary hemorrhagic telangiectasia (HHT; also known as Osler-Weber-Rendu dis
91 ical manifestations including oculocutaneous telangiectasia, immune disorders, increased susceptibly
92 ne has been extended to patients with ataxia-telangiectasia in whom it seems to reduce slow-phase vel
93 ary density was significantly reduced around telangiectasias in both SCP (P = .021) and DCP (P = .042
94 pre-RT photographs) and clinical assessment (telangiectasia, induration, edema, and pigmentation).
95 that showed increased sensitivity to ataxia telangiectasia inhibition, and a neuroendocrine-associat
96 ent due to concurrent hereditary hemorrhagic telangiectasia: iron deficiency impairs hypoxemia compen
99 A long-standing mystery surrounding ataxia-telangiectasia is why it is mainly cerebellar neurons, P
100 a more lateral distribution of erythema and telangiectasia, less neurogenic mast cell activation, an
101 Mutations throughout MRE11 cause ataxia-telangiectasia-like disorder (ATLD) featuring cerebellar
103 r death, Muller and microglia activation and telangiectasia-like vascular remodelling-features that w
105 T/Myb-like domain of nuclear protein, ataxia-telangiectasia locus (NPAT), a transcriptional co-activa
106 ods were used to study the stages of macular telangiectasia (MACTEL): Power-Doppler optical coherence
107 or the diagnostic criteria of CM, removal of telangiectasia macularis eruptiva perstans from the curr
110 ects, particularly TP53 and biallelic ataxia telangiectasia mutated (ATM) aberrations, are associated
112 phosphorylated at S455 downstream of ataxia telangiectasia mutated (ATM) and AKT following DNA damag
113 naling cascades via activation of the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia-
114 s critical for activating the kinases ataxia-telangiectasia mutated (ATM) and ATM and Rad3-related (A
115 by the DNA damage checkpoint kinases ATAXIA TELANGIECTASIA MUTATED (ATM) and ATM AND RAD3-RELATED (A
116 ng with DNA-damage checkpoint kinases ataxia telangiectasia mutated (ATM) and ATM- and Rad3-related (
117 tions of the key DNA repair molecules ataxia-telangiectasia mutated (ATM) and checkpoint kinase 2 (CH
118 ring V(D)J recombination activate the Ataxia Telangiectasia mutated (ATM) and DNA-dependent protein k
119 tive DDR-associated proteins, such as ataxia telangiectasia mutated (ATM) and H2AX, was induced as ea
120 coordinate recognition of DNA damage, ataxia-telangiectasia mutated (ATM) and PARP-1, were induced.
121 e 1 (Chk1) phosphorylation in an ATR [ataxia-telangiectasia mutated (ATM) and Rad3-related]-dependent
122 duced SMR5/SMR7 expression depends on ATAXIA TELANGIECTASIA MUTATED (ATM) and SUPPRESSOR OF GAMMA RES
123 gatively regulating the expression of ataxia telangiectasia mutated (ATM) and the subsequent DNA dama
124 ine signaling pathways, including the ataxia telangiectasia mutated (ATM) and transforming growth fac
125 suppresses miR-205 expression through ataxia telangiectasia mutated (ATM) and zinc finger E-box bindi
128 ial cell as well as activation of the ataxia telangiectasia mutated (ATM) DNA repair pathway that in
129 caused by biallelic mutations in the ataxia-telangiectasia mutated (ATM) gene, but heterozygous carr
138 monstrated that in replicating cells, ataxia telangiectasia mutated (ATM) is predominantly a nuclear
139 kinases (PI3KKs) involved in the DDR: ataxia telangiectasia mutated (ATM) kinase and ATM and Rad3-rel
143 e DNA damage response mediated by the Ataxia Telangiectasia Mutated (ATM) kinase may affect the relat
145 one Igkappa allele signal through the ataxia telangiectasia mutated (ATM) kinase to feedback-inhibit
146 , we reported that the absence of the ataxia telangiectasia mutated (ATM) kinase, a critical DNA dama
147 sly reported a novel inhibitor of the ataxia-telangiectasia mutated (ATM) kinase, which is a target f
150 that DNA damage signaling through the ataxia telangiectasia mutated (ATM) pathway induces the translo
151 irst time, to our knowledge, that the ataxia telangiectasia mutated (ATM) pathway, involved in DNA da
152 Upon DNA damage, the protein kinase ataxia-telangiectasia mutated (ATM) phosphorylates 53BP1 and re
157 ection of multiple cell lines lacking ataxia telangiectasia mutated (ATM) protein produced wild-type
159 ermediate state activate differential ataxia telangiectasia mutated (ATM) signaling where CHK2 is not
161 ciated feedback loop between DDB2 and ataxia telangiectasia mutated (ATM) was observed in infected ce
162 epair factors histone H2AX (H2AX) and ataxia telangiectasia mutated (ATM) were examined in pancreatic
164 anism: DIM caused rapid activation of ataxia-telangiectasia mutated (ATM), a nuclear kinase that regu
165 EMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM), and ATM- and Rad3-related
166 IDs, autosomal recessive mutations in ataxia-telangiectasia mutated (ATM), autosomal dominant mutatio
167 ment is independent of the DDR sensor ataxia telangiectasia mutated (ATM), but dependent on poly (ADP
168 d by the DNA damage response protein, ataxia telangiectasia mutated (ATM), in cytokine-induced NF-kap
169 TIP damage sites, DDR factors such as ataxia telangiectasia mutated (ATM), MDC1, WRN, and FANCD2 are
170 -regulation and/or phosphorylation of ataxia telangiectasia mutated (ATM), phosphorylated H2AX (gamma
171 lation of the major DNA damage kinase Ataxia telangiectasia mutated (ATM), thereby triggering cellula
172 red DSB-induced checkpoint integrity, Ataxia Telangiectasia Mutated (ATM)-deficient mice harboring th
175 strand breaks (DSBs), as indicated by ataxia telangiectasia mutated (ATM)-mediated H2AX phosphorylati
176 lymphocytic leukemia (CLL) where the ataxia telangiectasia mutated (ATM)-p53 pathway is inactivated
179 e in the bone marrow regulated by the ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and R
180 an up-regulation of components of the ataxia telangiectasia mutated (ATM)/Chek1/p53 pathway in miR-15
181 plication stress), which activate the ataxia telangiectasia mutated (ATM)/p53-dependent tumor barrier
182 BS1 expression and epirubicin-induced ataxia-telangiectasia mutated (ATM)phosphorylation in breast ca
183 amage response marker, phosphorylated ataxia telangiectasia mutated (pATM), were quantified in circul
185 ngle strand DNA, the key platform for ataxia telangiectasia mutated and Rad3-related (ATR) activation
186 nt in PKA-mediated phosphorylation of ataxia telangiectasia mutated and Rad3-related (ATR) at S435, a
187 immediate phosphorylation of Chk1 by ataxia telangiectasia mutated and Rad3-related (ATR) in the pre
189 ATRIP, the regulatory partner of the ataxia telangiectasia mutated and Rad3-related (ATR) kinase, at
190 eta and ISG induction is dependent on ataxia-telangiectasia mutated and Rad3-related (ATR) kinase, bu
192 V also produced maximal activation of ataxia telangiectasia mutated and Rad3-related (Atr)-mediated D
193 e is mediated by additive activity of ATAXIA TELANGIECTASIA MUTATED AND RAD3-RELATED and ATAXIA TELAN
194 chromosomal anomalies (trisomy-12 or ataxia telangiectasia mutated anomaly + del13q14) and negativel
195 hich led to the downregulation of the ataxia-telangiectasia mutated DNA damage pathway and the chemok
196 nases DNA-dependent protein kinase or ataxia-telangiectasia mutated enhanced GDC-0973/GDC-0941-mediat
197 the number of nuclear phosphorylated ataxia telangiectasia mutated foci in the post-LVAD hearts.
198 angiogenesis through the silencing of ataxia telangiectasia mutated in neighboring target cells.
201 lar epithelial cells, as indicated by ataxia telangiectasia mutated kinase (ATM)-dependent phosphoryl
204 because of functional redundancy with ataxia telangiectasia mutated kinase, a protein that also has s
206 IECTASIA MUTATED AND RAD3-RELATED and ATAXIA TELANGIECTASIA MUTATED kinases, which cause postreplicat
209 mediated in part by activation of the ataxia-telangiectasia mutated pathway, which is preliminarily a
210 tric cancer, especially in those with ataxia-telangiectasia mutated protein (ATM)-negative tumours.
211 yocyte nuclear foci of phosphorylated ataxia telangiectasia mutated protein, an upstream regulator of
212 e yeast Ataxia telangiectasia mutated/Ataxia telangiectasia mutated Rad3-related checkpoint regulator
213 nase catalytic subunit (DNA-PKcs) and ataxia-telangiectasia mutated respond primarily to DNA double-s
214 nd break repair is the recruitment of ataxia-telangiectasia mutated serine/threonine kinase (ATM) to
217 ethylation conferred compromised ATM (ataxia telangiectasia mutated) activation, decreased efficiency
220 uced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenua
221 Ai)-based screen that identified ATM (ataxia telangiectasia mutated) as being synthetic lethal with F
223 nteracting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent intera
224 s provided by the protein kinase ATM (ataxia telangiectasia mutated) that is capable of commanding a
226 trol (poly(ADP)-ribose polymerase and ataxia telangiectasia mutated), those within the cell metabolis
227 her systems is known to activate ATM (ataxia telangiectasia mutated)-mediated DNA damage response (DD
229 T3 induces a rapid activation of ATM (ataxia telangiectasia mutated)/PRKAA (adenosine monophosphate-a
231 the master DNA damage response kinase Ataxia telangiectasia mutated, revealing potential mechanistic
232 genes requires ATR and ALT2, but not ATAXIA TELANGIECTASIA MUTATED, thus demonstrating that in respo
234 chanistic links between PALB2 and the Ataxia telangiectasia mutated-dependent DNA damage responses.
235 ine array analysis identified several ataxia-telangiectasia mutated-dependent senescence-associated s
238 ent kinase (CDK), and Mec1, the yeast Ataxia telangiectasia mutated/Ataxia telangiectasia mutated Rad
239 ndent kinase, encoded by PRKDC), ATM (ataxia telangiectasia, mutated), and ATR (ATM and Rad3-related)
240 e DNA damage-activated protein kinase ataxia-telangiectasia-mutated (ATM) and casein kinase1 (CK1) an
241 damage by the coordinated actions of ataxia-telangiectasia-mutated (ATM) and casein kinases (CKs) 1
242 the DNA damage response downstream of ataxia telangiectasia-mutated (ATM) and p38/MK2 and promotes ce
244 eplication stress in malignant cells (ataxia telangiectasia-mutated (ATM) and Rad3-related-checkpoint
245 results in reduced activation of the ataxia telangiectasia-mutated (ATM) checkpoint kinase, ineffici
247 tant for Chaos3 and components of the ataxia telangiectasia-mutated (ATM) double-strand break respons
249 cyclobutane pyrimidine dimers in the ataxia telangiectasia-mutated (ATM) gene in human fibroblasts i
250 y contrast, loss of the DSB signaling ataxia telangiectasia-mutated (ATM) kinase did not significantl
251 lation of KAP1-Serine 824 (Ser824) by ataxia-telangiectasia-mutated (ATM) kinase is necessary for rep
253 colony formation required NF-kappaB, ataxia telangiectasia-mutated (ATM), and the inhibitor of kappa
254 reased levels of p53, but not Hdm2 or ataxia telangiectasia-mutated (ATM), were seen after expression
255 he DNA damage response protein kinase ataxia telangiectasia-mutated (ATM)- and Rad-3-related (ATR) in
256 -cell lymphomas that arise in certain ataxia telangiectasia-mutated (ATM)-deficient compound mutant m
257 int activation involves activation of ataxia telangiectasia-mutated (ATM)/ATM- and rad3-related (ATR)
259 ases p53 stability as demonstrated by ataxia telangiectasia-mutated kinase activation, increased Ser-
261 lication even in the presence of ATM (ataxia telangiectasia-mutated kinase) and Chk2 phosphorylation
262 a-S-phase arrest is regulated by ATM (ataxia telangiectasia-mutated kinase) signaling in a p53-indepe
264 d this was abrogated by inhibition of ataxia-telangiectasia-mutated signaling, suggesting that DNA da
265 Kcs also acts in concert with MRN and ataxia telangiectasia-mutated to regulate resection and thus DN
266 oinositide 3-kinase-like kinases ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad3-related) a
267 ding the DNA-damage signaling kinase, ataxia-telangiectasia-mutated) increase Familial Pancreatic Can
270 mplications included cataract (n = 13), iris telangiectasia (n = 5), corneal epithelial defect (n = 4
271 may therefore be a driving force in macular telangiectasia, neovascular AMD and other retinal diseas
272 hort stature, hearing loss, premature aging, telangiectasia, neurodegeneration, and photosensitivity,
273 l degeneration associated with early retinal telangiectasia, neuronal alterations, and loss of retina
275 nical correlate for the formation of retinal telangiectasia or Coats-like vasculopathy in patients wi
276 68; 95% CI, 0.48 to 0.96; P = .027) and skin telangiectasia (OR, 0.58; 95% CI, 0.36 to 0.92; P = .021
278 cipants with ETR tended to have erythema and telangiectasia primarily on the central face (79%), wher
279 ere calculated inside 100-mum circles around telangiectasias, projected over superficial (SCP) and de
281 the ALK1 gene cause hereditary haemorrhagic telangiectasia type 2 (HHT2), a disabling disease charac
283 Muller glial cells resembling human macular telangiectasia type 2 (MacTel 2), which is a retinal dis
286 two relatively rare clinical units, macular telangiectasia type 2 and solitary astrocytic hamartoma
288 the case of a 69-year-old woman with macular telangiectasia type 2 in whom multimodal fundus imaging
290 cavitation similar in appearance to macular telangiectasia type 2 on spectral-domain optical coheren
293 oveal retinal telangiectasis type 2 (macular telangiectasia type 2; MacTel) is a rare neurovascular d
294 Here we present a model of human ataxia telangiectasia using induced pluripotent stem cells, and
295 lit lamp or during pars plana vitrectomy for telangiectasia visible at the retinal vasoproliferative
298 of capillary changes (dilation, pruning, and telangiectasia) was also substantial (ICC 0.712 for the
300 ding 403 [90.5%] with hereditary hemorrhagic telangiectasia) were recruited to a prospective series.
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