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1 MMS is an autosomal recessive condition described thus f
2 MMS is known to inhibit replication though activation of
3 MMS plus low glucose (2 mm) or pyruvate (5 mm) gave 11-
4 MMS sensitivity of these mutants was contingent on the s
5 MMS-induced DNA lesions include base damages such as 3-m
6 r show that PRR pathway preference in 0.001% MMS depends on timing and context; cells preferentially
7 nts in their exquisite sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive
12 attend three appointments for the screen (72 MMS, 757 USS), and participant changing their mind (483
14 e subunits Rnr1 and Rnr3, thereby abrogating MMS-induced mutagenesis and enhancing cell lethality.
20 ncreased sensitivity to the alkylating agent MMS and hyper-recombination in an oligonucleotide-mediat
23 es, as measured by SE (r=0.642, P<.0001) and MMS (r=0.443, P<.04), and with post-OLT changes (for SE:
28 ay between initial physician examination and MMS predicted defect size (p = 0.0004), with greater tha
29 lele exhibited significant filamentation and MMS sensitivity in this background whereas mutations tha
31 ic increase in sensitivity to chronic HU and MMS treatment; however, these double mutants were not ch
32 ogue, but when added together KIC (2 mm) and MMS stimulated insulin release 7-fold (versus 12-fold fo
33 tag recBCD) were more sensitive to MNNG and MMS than the single mutants suggesting that homologous r
36 cells against cell killing by BCNU, TMZ, and MMS, which is consistent with the possibility that mitoc
38 ltaddc1 dpb11-1 double mutant is more UV and MMS sensitive than the Deltaddc1 or the dpb11-1 single m
40 is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protect
42 can be readily conjugated to magnetic beads, MMS-based SELEX provides a general platform for rapid ge
49 to ovarian cancer by Dec 31, 2014, comparing MMS and USS separately with no screening, ascertained by
50 t analysis identified seven highly connected MMS-toxicity modulating proteins associated with transla
53 A-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, trans
54 te sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive opportunity to stud
57 cs and antibiotics and sterile gloves during MMS were associated with modest reduction of risk for ad
61 show that, upon incubation in egg extracts, MMS-treated DNA activates a diffusible inhibitor that bl
63 (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to
65 tive values were 89.5%, 99.8%, and 35.1% for MMS, and 75.0%, 98.2%, and 2.8% for USS, respectively.
66 bal cancers were 89.4%, 99.8%, and 43.3% for MMS, and 84.9%, 98.2%, and 5.3% for USS, respectively.
67 exists in the number of stages per case for MMS for head and neck, genitalia, hands, and feet skin c
69 hysicians who received Medicare payments for MMS from any practice performing MMS on the head and nec
71 ned as those whose mean number of stages for MMS was 2 standard deviations greater than the mean numb
78 ete replication fork arrest and lethality in MMS, demonstrating that Rad53 deactivation is a key mech
81 in pph3Delta cells slows fork progression in MMS, whereas deactivation of Rad53, through expression o
82 increased and prolonged gamma-H2AX signal in MMS-treated BRCA1/2 cells suggested an aberrant processi
84 ydroxyurea (HU) and methyl methanesulfonate (MMS) activates DNA integrity checkpoints; in checkpoint-
85 ersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deoxyuridine, agents that in
87 DNA-damaging agents methyl methanesulfonate (MMS) and hydroxyurea by a mechanism(s) that requires the
88 of cells exposed to methyl methanesulfonate (MMS) and in the absence of Mag1, Rad30 and Rev3, human p
89 ng reagents such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU), while expression
91 el of resistance to methyl methanesulfonate (MMS) and temozolomide (TMZ) but simultaneous overexpress
92 ause sensitivity to methyl methanesulfonate (MMS) and/or ionizing radiation, along with follow-up cha
94 DNA damaging agent methyl methanesulfonate (MMS) in comparison to responses to acute heat shock, loo
95 mined the repair of methyl methanesulfonate (MMS) induced DNA damage in haploid G1 yeast cells, so th
96 he alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (damage resistance pro
97 ptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-deficient mre11-3 and sae2D
99 ng with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a function of a particular
100 he alkylating agent methyl methanesulfonate (MMS) was also observed for siRNA-mediated ATR silencing.
102 s were sensitive to methyl methanesulfonate (MMS), and rev1 rad30 or rev3 rad30 double mutant cells w
103 spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces more base substit
104 ydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferating cell nuclear a
105 DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fitness profiling of
106 mitomycin C (MC) or methyl methanesulfonate (MMS), as well as homologous recombination in Hfr mating
107 the genotoxic agent methyl methanesulfonate (MMS), but the molecular basis of genotoxic stress is unc
108 ing agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint.
109 V)-C radiation, and methyl methanesulfonate (MMS), indicating the broad relevance of HRR to genotoxic
111 ing UV irradiation, methyl methanesulfonate (MMS), mitomycin C, phleomycin, hydrogen peroxide, and hy
113 1-oxide (4-NQO) and methyl methanesulfonate (MMS), or when an HO endonuclease-induced DSB was introdu
114 DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell survival required a functional
115 DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimensional gel analyses of rep
116 irs the response to methyl methanesulfonate (MMS)-induced DNA lesions and disrupts telomeric silencin
129 eplication forks in methyl-methanesulfonate (MMS)-damaged cells, under different conditions of Rad53
133 ing agents such as methyl methanesulphonate (MMS), absence of the full-length form of Translation Ini
134 hypersensitive to methyl methanesulphonate (MMS), suggesting that PARP activity and DNA repair respo
137 rates the molecular mass range of the micro-MMS can be, in principle, tuned from less than 10(2) g/m
140 ameters are important to interpret the micro-MMS output: the radius of the interrogating light probe
142 EMS; point mutations required 1.25 microg/mL MMS and 1.40 microg/mL EMS before a mutagenic effect was
143 f chromosomal aberrations was 0.85 microg/mL MMS and 1.40 microg/mL EMS; point mutations required 1.2
145 esolution, NASA's Magnetospheric Multiscale (MMS) mission has found direct evidence for electron dema
146 ields with NASA's Magnetospheric Multiscale (MMS) mission, we utilize Earth's magnetosphere as a plas
149 ), non-ovarian cancer or other disease (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), rel
150 ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to attend three appointments for t
155 mstances in which the additional benefits of MMS outweigh its higher cost are needed, still lacking,
156 Shu complex promotes high-fidelity bypass of MMS-induced alkylation damage, such as N3-methyladenine,
157 ied analysis of death from ovarian cancer of MMS versus no screening with exclusion of prevalent case
161 ng fibroblasts treated with a combination of MMS and 4-AN, a complete inhibition of DNA synthesis is
162 Much of the data regarding complications of MMS are anecdotal or report findings from single centers
163 e able to abrogate the stimulatory effect of MMS, indicating that Elk-1 and C/EBP are both involved i
164 are as sensitive to the cytotoxic effects of MMS and MNNG as the most base excision repair (BER)-defi
165 ighly sensitized to the cytotoxic effects of MMS by 4-amino-1,8-naphthalimide (4-AN), an inhibitor of
167 of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising duri
169 tant when cells replicate in the presence of MMS, and that double deletions lead to a greater reducti
170 H3 N-tails are important for the removal of MMS-induced DNA lesions due to their role in regulating
171 find that REV3 is required for the repair of MMS-induced lesions when recombinational repair is compr
173 s Snail and vimentin, and a subpopulation of MMS-treated cells displayed an elongated fibroblast-like
174 e that RTP801 is a transcriptional target of MMS in human keratinocytes and that C/EBP is implicated
175 ind, randomized, placebo-controlled trial of MMS in 17- to 45-y-old Gambian women who were menstruati
179 60 mg of iron and 400 mug of folic acid, or MMS containing a daily allowance of 15 micronutrients, i
186 ayments for MMS from any practice performing MMS on the head and neck, genitalia, hands, and feet reg
187 nsulin release in fresh islets, and KIC plus MMS gave synergistic insulin release in cultured human i
188 r RNR3 were hypersensitive to rapamycin plus MMS, providing the first demonstration that Rnr3 contrib
190 ins of Sgs1 directly required for processing MMS-induced DNA damage, most notably the helicase domain
191 efined by ATP-dependent DNA Helicase RECQ4A, MMS and UV-sensitive protein81, REV3, and the ATPase Rad
196 f these proteins function together to resist MMS-induced DNA damage and promote gene conversion at bl
199 eta, iota and kappa are capable of restoring MMS-resistance to the normally MMS-sensitive strain.
200 ndom numbers to annual multimodal screening (MMS) with serum CA125 interpreted with use of the risk o
201 as a second-line test (multimodal screening [MMS]; n=50 640); or annual screening with transvaginal u
203 A FACS-based shRNA screen identified several MMS genes as essential for the epithelial-mesenchymal tr
205 nnon entropy (SE) and median mobility shift (MMS) values derived from the heteroduplex mobility assay
207 or the Shu complex in the repair of specific MMS-induced DNA lesions and elucidate the interplay betw
208 screening by using the multimodal strategy (MMS) in which annual serum cancer antigen 125 (CA-125) w
209 havior, we measured the male mating success (MMS) of 12 hypomorphic y mutants and matched-outbred-bac
212 anidine (MNNG) and methyl methane sulfonate (MMS) produce a wide variety of N- and O-methylated bases
213 cells treated with methyl methane sulfonate (MMS), hydroxyurea (HU) or camptothecin (CPT), we show th
214 e alkylating agent methyl-methane sulfonate (MMS), we obtained approximately 2 x 10(5) active mutants
216 tion-blocking agent methylmethane sulfonate (MMS) in smc6 mutants, with double deletions conferring s
217 on and DNA targets: methylmethane sulfonate (MMS), methylnitrosourea (MNU), ethylmethane sulfonate (E
219 O2) and alkylation (methylmethane sulfonate, MMS) stresses induced nearly identical patterns of up- a
222 rrence rates with Mohs micrographic surgery (MMS) are modestly better than those for excision surgery
230 re, a gel mobility shift assay revealed that MMS was able to initiate rapid formation of a protein co
231 thyl methanesulfonate (MMS), and showed that MMS also induces more base substitution mutations in BRC
236 ila ortholog of the yeast snm1 gene, and the MMS- and HN2-sensitive mus301 mutant defines the Drosoph
238 bination, which is a phenotype shared by the MMS-hypersensitive DNA repair mutants rad2, rhp55 and NE
239 x 10(5) active mutants that complemented the MMS sensitivity of AP endonuclease-deficient E. coli.
240 ar of diagnosis was 2008 (1986-2013) for the MMS group vs 2003 (1978-2013) for the WLE group (P < .00
242 clease activity, and the main reason for the MMS sensitivity of nth1 cells appears to be their lack o
244 d a repeat test, and 167 (0.3%) women in the MMS group and 1894 (3.9%) women in the USS group require
245 verall recurrence rates were 5 (1.8%) in the MMS group and 22 (5.7%) in the WLE group (P = .07).
247 Overall, 4355 of 50 078 (8.7%) women in the MMS group and 5779 of 48 230 (12.0%) women in the USS gr
248 Of these women, 148 (0.29%) women in the MMS group, 154 (0.30%) in the USS group, and 347 (0.34%)
249 ncer in 1282 (0.6%) women: 338 (0.7%) in the MMS group, 314 (0.6%) in the USS group, and 630 (0.6%) i
250 e for analysis: 50,624 (>99.9%) women in the MMS group, 50,623 (>99.9%) in the USS group, and 101,299
251 flexible parametric model showed that in the MMS group, this mortality effect was made up of 8% (-20
253 4 results in a 6- to 14-fold increase in the MMS-induced mutation frequency and in a significant incr
256 age analysis (GENEHUNTER version 2.1) of the MMS factor was conducted in the combined marker set samp
257 atients on the GUG, 19.0% of patients on the MMS, 44.0% of patients on the GDS15, and 64.9% of patien
259 eckpoint-defective mrc1 alleles suppress the MMS sensitivity and the checkpoint recovery defect of di
261 y allocated 202,638 women: 50,640 (25.0%) to MMS, 50,639 (25.0%) to USS, and 101,359 (50.0%) to no sc
262 identify chromosomal regions contributing to MMS-related traits represented by composite factors deri
264 yeast, the response of the Rad53 pathway to MMS is compromised due to a loss of Sod1 activity, consi
265 s modest capacities to provide resistance to MMS and to resolve recombination-dependent X-shaped mole
266 mouse cells were slightly more resistant to MMS than wild-type cells, probably due to the production
268 n even after S phase, and normal response to MMS damage correlates with the maintenance of intact Dfp
269 d Rtt107 with Dpb11 (hTopBP1) in response to MMS-induced DNA alkylation, suggesting that Slx4 and Rtt
272 -chromosome mutants were solely sensitive to MMS and define 8 new mutagen-sensitive genes (mus212-mus
276 of PARP activity results in sensitization to MMS through maintenance of an ATR and Chk1-dependent S-p
278 main reasons for withdrawal were death (two MMS, 28 USS), non-ovarian cancer or other disease (none
279 renders tel1-Delta cells (but not wild type) MMS-sensitive, demonstrating that, under certain conditi
281 nd ENU showed linear dose-responses, whereas MMS and EMS had nonlinear curves containing a range of n
283 stone H4; this event is also associated with MMS- or phleomycin-induced DSBs but not with UV-induced
284 e kinetic simulation and its comparison with MMS observations, we show for the first time that ion-sc
290 nsecutive sample of patients presenting with MMS for 35 weeks at each center, with staggered start ti
292 functional categories over-represented with MMS-toxicity modulating proteins and demonstrate that, i
297 sisted of 662 patients with MIS treated with MMS or WLE per standard of care in dermatology and surge
298 UV-irradiated cells or in cells treated with MMS requires Huwe1 and is associated with release of Cdc
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