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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
12                                       Ataxia-telangiectasia (A-T) is a cerebellar neurodegenerative d
13                                       Ataxia-telangiectasia (A-T) is a rare multi-system disorder cau
14                                       Ataxia telangiectasia (A-T) is a syndrome associated with loss
15                                       Ataxia-telangiectasia (A-T) is an autosomal recessive neurodege
16 ereditary autosomal recessive disease ataxia telangiectasia (A-T) is caused by mutation in the DNA da
17      Germline ATM inactivation causes ataxia-telangiectasia (A-T) syndrome with severe lymphocytopeni
18 on is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation of the A
19  for the autosomal recessive disease ataxia- telangiectasia (A-T) was localized to 11q22.3-23.1.
20                                       Ataxia telangiectasia (A-T), a rare autosomal recessive disorde
21 ase mutated in the rare human disease ataxia telangiectasia (A-T), has been the focus of intense scru
22                     Participants with ataxia-telangiectasia also had higher metabolism in globus pall
23                     The treatment of retinal telangiectasia and areas of retinal nonperfusion identif
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
27                                  ATR (ataxia telangiectasia and Rad-3-related) is a protein kinase th
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
31 G2-M checkpoints mediated by the ATR (ataxia telangiectasia and Rad3 related) and Chk1 kinases.
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
35        The DNA damage response kinase ataxia telangiectasia and Rad3-related (ATR) coordinates much o
36                 Both exposures induce ataxia telangiectasia and Rad3-related (ATR) kinase and poleta
37 e ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and Rad3-related (ATR) kinases.
38                                       Ataxia telangiectasia and Rad3-related (ATR) mediates response
39                                       Ataxia-telangiectasia and RAD3-related (ATR) signals the accumu
40 involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to CHK2, w
41 le-stranded telomeric DNA and prevent ataxia telangiectasia and Rad3-related kinase activation.
42 omains, which inhibits recruitment of Ataxia telangiectasia and Rad3-related protein (ATR) and reduce
43           PKA directly phosphorylates ataxia telangiectasia and Rad3-related protein (ATR) at Ser435,
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
49                   Further analysis of ataxia telangiectasia and Rad3-related protein (ATR)/Chk1 signa
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
52                      Mutations in ATR(ataxia telangiectasia and RAD3-related) cause Seckel syndrome (
53           Both compounds also lead to ataxia telangiectasia and Rad3-related- (ATR-) dependent produc
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
57                In START-B, breast shrinkage, telangiectasia, and breast oedema were significantly les
58 ART-A, moderate or marked breast induration, telangiectasia, and breast oedema were significantly les
59 axia-telangiectasia mutated (ATM) and ataxia-telangiectasia- and rad3-related (ATR) kinases.
60  protein kinase catalytic subunit and ataxia telangiectasia- and Rad3-related kinase.
61  the type of sequelae classified as residual telangiectasia, anetodermal skin, redundant skin, persis
62                          Facial erythema and telangiectasia are commonly associated with the erythema
63     Cells isolated from patients with ataxia telangiectasia are exquisitely sensitive to ionizing rad
64  interaction with the development of retinal telangiectasia are identified.
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'
67 own etiology are commonly observed in ataxia telangiectasia (AT) and Artemis deficiency.
68                                       Ataxia telangiectasia (AT) is a multisystem DNA-repair disorder
69                                       Ataxia-telangiectasia (AT) is a pleiotropic multisystem disorde
70                                       Ataxia telangiectasia (AT) is a progressive multisystem disorde
71      Biallelic mutations in ATM cause ataxia-telangiectasia (AT), a rare inherited disease with a hig
72  cause the neurodegenerative disorder ataxia-telangiectasia (AT).
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
76                                   The ataxia telangiectasia group D complementing gene (ATDC, also ca
77 scribe a novel mouse model expressing ataxia telangiectasia group D complementing gene (ATDC, also kn
78                                       Ataxia-telangiectasia group D-associated gene (ATDC) mediated r
79       We found that participants with ataxia-telangiectasia had lower metabolism in cerebellar hemisp
80 ebellar metabolism, participants with ataxia-telangiectasia had widespread changes in metabolic rates
81              So far, murine models of ataxia telangiectasia have failed to accurately recapitulate ma
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
84                       Hereditary hemorrhagic telangiectasia (HHT) is a highly debilitating and life-t
85                       Hereditary hemorrhagic telangiectasia (HHT) is a potentially life-threatening g
86                       Hereditary hemorrhagic telangiectasia (HHT), the most common inherited vascular
87 ease, we investigated hereditary hemorrhagic telangiectasia (HHT), which is caused by mutations in TG
88 ALK1; ACVRL1), causes hereditary hemorrhagic telangiectasia (HHT).
89 ling manifestation of hereditary hemorrhagic telangiectasia (HHT).
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
97                                       Ataxia telangiectasia is a devastating neurodegenerative diseas
98                                       Ataxia-telangiectasia is a recessive genetic disorder (ATM is t
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
102 editary cancer-susceptibility disease ataxia-telangiectasia-like disorder (ATLD).
103 r death, Muller and microglia activation and telangiectasia-like vascular remodelling-features that w
104                      Nuclear protein, ataxia-telangiectasia locus (NPAT) and FLICE-associated huge pr
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
108                              Using an ataxia-telangiectasia mouse model, we compared lymphoma inciden
109                                       Ataxia telangiectasia mutant (ATM) is an S/T-Q-directed kinase
110 ects, particularly TP53 and biallelic ataxia telangiectasia mutated (ATM) aberrations, are associated
111               Nuclear PKR antagonizes ataxia-telangiectasia mutated (ATM) activation by a mechanism d
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
126                                   The ataxia telangiectasia mutated (ATM) checkpoint is the central s
127                              TP53 and ataxia telangiectasia mutated (ATM) defects are associated with
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
130                      Mutations in the ataxia telangiectasia mutated (ATM) gene, which encodes a kinas
131 r disorder caused by mutations in the ataxia telangiectasia mutated (ATM) gene.
132 , is caused by a defective or missing ataxia telangiectasia mutated (ATM) gene.
133       Involvement of tumor suppressor ataxia telangiectasia mutated (ATM) in the TGF-beta1 pathway re
134                                       Ataxia telangiectasia mutated (ATM) is a protein kinase and a m
135                                       Ataxia telangiectasia mutated (ATM) is activated upon DNA doubl
136                    The protein kinase ataxia telangiectasia mutated (ATM) is an important proximal re
137                                       Ataxia telangiectasia mutated (ATM) is an important signaling m
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
140                      Here we identify ataxia-telangiectasia mutated (ATM) kinase as a modulator of th
141                         Inhibitors of ataxia telangiectasia mutated (ATM) kinase decreased manganese-
142                                   The ataxia telangiectasia mutated (ATM) kinase is involved in the r
143 e DNA damage response mediated by the Ataxia Telangiectasia Mutated (ATM) kinase may affect the relat
144         Strikingly, we found that the ataxia telangiectasia mutated (ATM) kinase regulates the intera
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
148 imized as selective inhibitors of the ataxia telangiectasia mutated (ATM) kinase.
149 sible for the efficient activation of ataxia-telangiectasia mutated (ATM) kinase.
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
153                                       Ataxia-telangiectasia mutated (ATM) plays a unique yet incomple
154                                   The ataxia-telangiectasia mutated (ATM) protein is an apical kinase
155                                   The ataxia-telangiectasia mutated (ATM) protein kinase is a master
156                                       Ataxia-telangiectasia mutated (ATM) protein kinase regulates th
157 ection of multiple cell lines lacking ataxia telangiectasia mutated (ATM) protein produced wild-type
158                                       Ataxia-telangiectasia mutated (ATM) regulates the DNA damage re
159 ermediate state activate differential ataxia telangiectasia mutated (ATM) signaling where CHK2 is not
160 dependent protein kinase (DNA-PK) and Ataxia telangiectasia mutated (ATM) signaling.
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
163                                       Ataxia-telangiectasia mutated (ATM), a member of the phosphatid
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
173                 These 3 responses are ataxia telangiectasia mutated (ATM)-dependent and promote quies
174                                   The ataxia telangiectasia mutated (ATM)-interacting protein ATMIN m
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
177 e of the DNA damage response mediator ataxia telangiectasia mutated (ATM).
178 howed a synergistic relationship with ataxia telangiectasia mutated (ATM).
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
184               Under these conditions, ataxia-telangiectasia mutated activation and accumulation of DN
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
188                                   The ataxia telangiectasia mutated and Rad3-related (ATR) kinase is
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
191                                   The ataxia telangiectasia mutated and Rad3-related (ATR)-checkpoint
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.
199 ancer cells, comparable to effects of Ataxia Telangiectasia Mutated inhibition.
200                   Here we report that ataxia-telangiectasia mutated kinase (ATM) plays a major role i
201 lar epithelial cells, as indicated by ataxia telangiectasia mutated kinase (ATM)-dependent phosphoryl
202         Upon IR, CHK2 is activated by ataxia telangiectasia mutated kinase and regulates the S-phase
203 erase activity, but is independent of ataxia-telangiectasia mutated kinase function.
204 because of functional redundancy with ataxia telangiectasia mutated kinase, a protein that also has s
205 cle checkpoints via activation of the ataxia-telangiectasia mutated kinase.
206 IECTASIA MUTATED AND RAD3-RELATED and ATAXIA TELANGIECTASIA MUTATED kinases, which cause postreplicat
207          To further investigate this, ataxia telangiectasia mutated KO (Atm(-/-)) mice, which develop
208           The association of Tcl1 and Ataxia Telangiectasia Mutated leads to activation of the NF-kap
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
215                         Knock down of ataxia telangiectasia mutated suppressed gammaH2AX and CHK2 pho
216                                       Ataxia telangiectasia mutated was activated but not its 53BP1 a
217 ethylation conferred compromised ATM (ataxia telangiectasia mutated) activation, decreased efficiency
218 on of proteins (H2AX, protein 53, and ataxia telangiectasia mutated) after SPECT.
219                                  ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-related) a
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
222 ere it interacted with activated ATM (ataxia-telangiectasia mutated) at sites of DNA repair.
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
225 by the consecutive activation of ATM (ataxia telangiectasia mutated), Chk2, and p53.
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
228 aks, as well as in activation of ATM (ataxia telangiectasia mutated).
229 T3 induces a rapid activation of ATM (ataxia telangiectasia mutated)/PRKAA (adenosine monophosphate-a
230                 However, silencing of ataxia telangiectasia mutated, ataxia telangiectasia and Rad3-r
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
233                   Both 1 and 3 induce ataxia telangiectasia mutated- (ATM-) and DNA-dependent protein
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
236  damage, and this dissociation may be ataxia telangiectasia mutated-dependent.
237 a novel interaction between Tcl1 with Ataxia Telangiectasia Mutated.
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
243 neration process critically involving ataxia telangiectasia-mutated (ATM) and p53.
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
246 translocations that are a hallmark of ataxia telangiectasia-mutated (ATM) deficiency.
247 tant for Chaos3 and components of the ataxia telangiectasia-mutated (ATM) double-strand break respons
248 is process in cells deficient for the ataxia telangiectasia-mutated (ATM) DSB response factor.
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
252                                   The Ataxia Telangiectasia-Mutated (ATM) protein kinase is recruited
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)
258  replication damage checkpoint kinase ataxia telangiectasia-mutated and rad3-related homolog.
259 ases p53 stability as demonstrated by ataxia telangiectasia-mutated kinase activation, increased Ser-
260                                       Ataxia telangiectasia-mutated kinase activity can compensate fo
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
263                Activation of the ATM (ataxia telangiectasia-mutated kinase)-dependent DNA damage resp
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
268             Following UV irradiation, ataxia telangiectasia-mutated- and Rad3-related protein phospho
269                         The ATR (ATM [ataxia telangiectasia-mutated]- and Rad3-related) checkpoint is
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
274                         Examination revealed telangiectasias on the labial mucosa and nail folds.
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
277 or both overall cosmesis (P = .038) and skin telangiectasia (P = .031).
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
280 , such as lentigines, hyperpigmentation, and telangiectasias, should be considered.
281  the ALK1 gene cause hereditary haemorrhagic telangiectasia type 2 (HHT2), a disabling disease charac
282                                      Macular telangiectasia type 2 (MacTel 2) is a rare disease in wh
283  Muller glial cells resembling human macular telangiectasia type 2 (MacTel 2), which is a retinal dis
284                                      Macular Telangiectasia Type 2 (MacTel) is an uncommon, late-onse
285 chloroquine retinopathy (n = 1), and macular telangiectasia type 2 (n = 4).
286  two relatively rare clinical units, macular telangiectasia type 2 and solitary astrocytic hamartoma
287          To present a coincidence of macular telangiectasia type 2 and solitary retinal astrocytic ha
288 the case of a 69-year-old woman with macular telangiectasia type 2 in whom multimodal fundus imaging
289                                      Macular telangiectasia type 2 is a bilateral disease with charac
290  cavitation similar in appearance to macular telangiectasia type 2 on spectral-domain optical coheren
291 safe and well tolerated in eyes with macular telangiectasia type 2.
292 he clinical features of this case of macular telangiectasia type 2.
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
296 veally in both eyes, leakage from parafoveal telangiectasia was apparent.
297 ns, direct endolaser photocoagulation of the telangiectasia was required.
298 of capillary changes (dilation, pruning, and telangiectasia) was also substantial (ICC 0.712 for the
299                           In MT1 eyes, fewer telangiectasias were identified with OCTA than with FA (
300 ding 403 [90.5%] with hereditary hemorrhagic telangiectasia) were recruited to a prospective series.

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