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1                                              MMEJ activation was dependent on XRCC1 phosphorylation b
2                                              MMEJ does not require S139-phosphorylated histone H2AX (
3                                              MMEJ has similarities to homology-dependent repair, in t
4                                              MMEJ recombinants showed evidence that Pol delta proofre
5                                              MMEJ repair efficiency increased concomitant with microh
6                                              MMEJ repairs DNA breaks via the use of substantial micro
7                                      Using a MMEJ and HR competition repair substrate, we demonstrate
8 vents DNA end resection in mitosis, allowing MMEJ to take place.
9    Here, we identify the APE2 nuclease as an MMEJ effector.
10 ide (TMZ) resistance display elevated HR and MMEJ activity, suggesting that these pathways contribute
11  This report identifies ATM-dependent HR and MMEJ as targetable resistance mechanisms in TP53-mutant
12 chromosomal gene conversion involving HR and MMEJ at different ends of a duplicated sequence.
13 tem, suggesting a competition between HR and MMEJ for the repair of a DSB.
14 d by C-NHEJ, the relationship between HR and MMEJ is less clear.
15 etween NHEJ (non-homologous end-joining) and MMEJ (microhomology-mediated end-joining).
16 eous functional disruption of both MiDAS and MMEJ pathways upon CIP2A loss provides rationale for the
17              Combined inhibition of NHEJ and MMEJ using two nontoxic, targeted DNA repair inhibitors
18 ed to play a role in both classical NHEJ and MMEJ, but the involvement of the analogous MRE11/RAD50/N
19  profiles into contributions from c-NHEJ and MMEJ.
20  resulted in increased partial resection and MMEJ, thus revealing a functional distinction between th
21 cilitate DNA accumulation, DNA synapsis, and MMEJ.
22 ominant pathway for DSB repair in our assay, MMEJ was significantly enhanced in preirradiated cells,
23 systems and discuss the relationship between MMEJ and 'alternative end joining'.
24 recise creation in a template-free manner by MMEJ repair.
25 ical dependence on the DSB repair pathway by MMEJ.
26 codes the flap endonuclease needed to cleave MMEJ intermediates before DNA synthesis.
27 d its interacting partner, RHINO, as crucial MMEJ factors.
28  co-immunoprecipitate complex (IP) displayed MMEJ activity in vitro, which was significantly elevated
29  By combining knockout screening with a dual MMEJ:NHEJ reporter inserted in 19 different chromatin en
30 delta proofreading function is active during MMEJ-mediated DSB repair.
31      53BP1 supports sequence deletion during MMEJ consistent with a putative role in facilitating end
32 s necessary in generating the near-exclusive MMEJ associated with Lig4 deficiency.
33 totic localisation of Poltheta to facilitate MMEJ.
34  with euchromatin, while proteins that favor MMEJ generally synergize with distinct types of heteroch
35 site substitutions showing isoleucine favors MMEJ and alanine favors primer extension in both enzymes
36 ous recombination in S/G2 phase but also for MMEJ in G1.
37 polymerase delta (Pol delta) is critical for MMEJ, independent of microhomology length and base-pairi
38 2 group genes, and Rad27 are dispensable for MMEJ.
39 eta (POLtheta), the polymerase essential for MMEJ, we investigated the role of POLtheta in EBV-lympho
40           We propose a mechanistic model for MMEJ and highlight important questions for future resear
41 DSBR sites with both monomers positioned for MMEJ.
42 ng of the mechanism and factors required for MMEJ repair.
43 clease activities of MRE11 were required for MMEJ, as has been observed for homology-directed DSB rep
44 d governs its DNA substrate requirements for MMEJ.
45 mal DSBs and is epistatic with Pol Theta for MMEJ activity.
46 at the frequency of deletions resulting from MMEJ repair, characterized as deletions greater than or
47                                 Furthermore, MMEJ efficiency was enhanced with an increase in the len
48                                 Furthermore, MMEJ is used to repair DSBs generated at collapsed repli
49 nase inhibitor, AZD1390, as a potent dual HR/MMEJ inhibitor that suppresses radiation-induced phospho
50 ENTHU, inDelphi, and Lindel - in identifying MMEJ-repaired, homogeneous genotypes (PreMAs) in an inde
51 n impedes replication fork progress, impairs MMEJ-mediated repair of DNA double-stranded breaks, and
52                                           In MMEJ, the repair of DNA breaks is mediated by annealing
53 his previously unappreciated role of APE2 in MMEJ contributes to the addiction of HRD cells to APE2,
54 cate a role for the X. laevis MRN complex in MMEJ.
55 ted in MMEJ, cause a synergistic decrease in MMEJ repair.
56  the DNA polymerase previously implicated in MMEJ, cause a synergistic decrease in MMEJ repair.
57  Although the genetic components involved in MMEJ are largely unknown, those in NHEJ and SSA are char
58 eporter and showed that Fen1 participates in MMEJ, underscoring the importance of MMEJ as a collatera
59 operative involvement of both polymerases in MMEJ.
60           Consistent with a specific role in MMEJ we confirm that 53BP1 status does not affect c-NHEJ
61 ur data support the role of Sae2 and Tel1 in MMEJ and genome integrity.
62 portance of polymerase-helicase tethering in MMEJ and the structural organization of Poltheta.
63           We show that loss of APE2 inhibits MMEJ at deprotected telomeres and at intra-chromosomal D
64 s intrinsic flap-cleaving activity, that its MMEJ function in cells depends on its nuclease activity,
65  through microhomology-mediated end joining (MMEJ) and has emerged as a key synthetic lethal drug tar
66 (cNHEJ), microhomology-mediated end joining (MMEJ) and single strand annealing (SSA).
67 ddition, microhomology-mediated end joining (MMEJ) and single-strand annealing (SSA) provide backup D
68 (cNHEJ), microhomology-mediated end joining (MMEJ) and single-strand annealing (SSA).
69 omology-mediated non-homologous end joining (MMEJ) can also be used but to a lesser extent compared t
70          Microhomology-mediated end joining (MMEJ) can generate more predictable outcomes for functio
71 tations, microhomology-mediated end joining (MMEJ) creates precise deletions based on the alignment o
72          Microhomology-mediated end joining (MMEJ) is a major pathway for Ku-independent alternative
73          Microhomology-mediated end joining (MMEJ) is an intrinsically mutagenic pathway of DNA doubl
74     This microhomology-mediated end joining (MMEJ) is Ku independent, but strongly dependent on Mre11
75          Microhomology-mediated end joining (MMEJ) joins DNA ends via short stretches [5-20 nucleotid
76 HEJ) and microhomology-mediated end joining (MMEJ) massively increases LOH, although the dependence o
77 d by the microhomology-mediated end joining (MMEJ) pathway.
78  through microhomology-mediated end joining (MMEJ) rather than the canonical non-homologous end joini
79 or-prone microhomology-mediated end joining (MMEJ) repair pathway.
80 , robust microhomology-mediated end joining (MMEJ) was observed with DNA substrates bearing 5-, 8-, 1
81 pair via microhomology-mediated end joining (MMEJ), also termed theta-mediated end joining (TMEJ).
82          Microhomology-mediated end joining (MMEJ), an error-prone DNA damage repair mechanism, frequ
83          Microhomology-mediated end joining (MMEJ), an error-prone pathway for DNA double-strand brea
84 HEJ) and microhomology-mediated end joining (MMEJ), and the efficiency of HDR outcomes is not predict
85 pathway, microhomology-mediated end joining (MMEJ), can also be deployed.
86 m, named microhomology-mediated end joining (MMEJ), has received increasing attention.
87 olved in microhomology mediated end joining (MMEJ), one of the characteristics of B-NHEJ.
88 ncreased microhomology-mediated end joining (MMEJ), thus bridging the two different translocation mec
89 (HR) and microhomology-mediated end joining (MMEJ), while non-homologous end joining (NHEJ) has not b
90  (HDR)-, microhomology-mediated end joining (MMEJ)-, and nonhomologous end joining (NHEJ)-based strat
91 (HR) and microhomology-mediated end joining (MMEJ).
92  more on microhomology-mediated end joining (MMEJ).
93  well as microhomology-mediated end joining (MMEJ).
94 epair by Microhomology Mediated End Joining (MMEJ).
95 HR), and microhomology-mediated end joining (MMEJ).
96 m termed microhomology-mediated end joining (MMEJ).
97 ifically microhomology-mediated end-joining (MMEJ) and homology-directed repair (HDR).
98 epair by microhomology-mediated end-joining (MMEJ) and is overexpressed in many cancers.
99  such as microhomology-mediated end-joining (MMEJ) and mitotic DNA synthesis (MiDAS).
100 SBR) via microhomology-mediated end-joining (MMEJ) and that a mobile group II intron-encoded RT has a
101 n in the microhomology-mediated end-joining (MMEJ) component, polymerase theta/mutagen-sensitive 308
102  whereas microhomology-mediated end-joining (MMEJ) has been regarded as a backup mechanism.
103 promotes microhomology-mediated end-joining (MMEJ) of DNA double-strand breaks (DSBs).
104  wherein Microhomology-Mediated End-Joining (MMEJ) or Insertion events predominate during early rapid
105 s in the microhomology-mediated end-joining (MMEJ) pathway are key predictors of sensitivity to DNA-P
106 ates the microhomology-mediated end-joining (MMEJ) pathway of double-strand break (DSB) repair.
107 or-prone microhomology-mediated end-joining (MMEJ) pathway.
108 eloped a microhomology-mediated end-joining (MMEJ) reporter and showed that Fen1 participates in MMEJ
109 otion of microhomology-mediated end-joining (MMEJ), a subtype of alt-NHEJ, in G1-phase.
110 HEJ) and microhomology-mediated end-joining (MMEJ).
111 SBR) via microhomology-mediated end-joining (MMEJ).
112 known as microhomology-mediated end-joining (MMEJ).
113 EJ), and microhomology-mediated end-joining (MMEJ).
114 pathway, microhomology-mediated end-joining (MMEJ).
115 known as microhomology-mediated end-joining (MMEJ).
116 ining or microhomology-mediated end-joining (MMEJ).
117 pendent classical nonhomologous end joining, MMEJ--even with very limited end resection--requires cyc
118 iated HDR effectively outcompetes the longer MMEJ-mediated deletions but not NHEJ-mediated indels.
119 cular mechanisms governing Poltheta-mediated MMEJ remain poorly understood.
120 e final sealing of DSBs during mitochondrial MMEJ.
121 tIP, FEN1, MRE11, and PARP1 in mitochondrial MMEJ.
122  indicate that HR factors suppress mutagenic MMEJ following DSB resection.
123  individual DSB created by CRISPR/Cas9-NHEJ, MMEJ, and HDR-and show its applicability in evaluating t
124 of CtIP in homologous recombination, but not MMEJ, is dependent on the phosphorylation of serine resi
125  allowed measurement of relative activity of MMEJ versus NHEJ.
126 Here, we summarize the genetic attributes of MMEJ from several model systems and discuss the relation
127               We discuss the contribution of MMEJ pathways to genome evolution, subtelomere recombina
128 ggest that radiation-mediated enhancement of MMEJ in cells surviving radiation therapy may contribute
129            Thus, we describe the features of MMEJ in Trypanosoma brucei, which is analogous to micro
130 ates in MMEJ, underscoring the importance of MMEJ as a collateral repair pathway in the context of ho
131    Whether POLQ also operates independent of MMEJ remains unexplored.
132 MRE11, POLQ and PARP, and thus indicative of MMEJ.
133 ere fusions, but the underlying mechanism of MMEJ in mammalian cells is not well understood.
134 ontent all favored repair and the pattern of MMEJ described above was similar at several different lo
135     Here, we review the molecular process of MMEJ as well as new targets and approaches exploiting th
136                  Interestingly, promotion of MMEJ by 53BP1 in G1-phase cells is only observed in the
137 e observations highlight the central role of MMEJ in maintenance of mammalian mitochondrial genome in
138 omplementary DNA ends that rely primarily on MMEJ repair.
139 achieving more predictable and deletion-only MMEJ-mediated mutations in many plant species.
140 les efficient precise editing through HDR or MMEJ while suppressing indels caused by NHEJ in dividing
141 ouble-strand gap in its DNA gene via NHEJ or MMEJ, independently from DNA synthesis.
142      How full-length human Poltheta performs MMEJ at the molecular level remains unknown.
143  that the helicase is essential for Poltheta MMEJ of long ssDNA overhangs which model resected DSBs.
144                         Remarkably, Poltheta MMEJ of ssDNA overhangs requires polymerase-helicase att
145 A-PK/NHEJ inhibitor with a targeted POLtheta/MMEJ inhibitor may provide a rational treatment strategy
146                        Sae2 and Tel1 promote MMEJ but inhibit NHEJ, likely by regulating Mre11-depend
147  end-joining (NHEJ) and promotes error-prone MMEJ, providing a mechanistic rationale for the clinical
148  a complex network of proteins that regulate MMEJ:NHEJ balance in a chromatin context-dependent manne
149 ate varied changes in short-range resection, MMEJ, and translocation, imposed by compromising specifi
150 unexpected function for RHINO in restricting MMEJ to mitosis.
151 dividual DSBR survivors exclusively revealed MMEJ-based deletions but no NHEJ.
152                                           SD-MMEJ explains the locus specificity of interruptions, wh
153  sequence-specific factors that influence SD-MMEJ repair remain to be fully characterized.
154 ndent microhomology-mediated end joining (SD-MMEJ) can account for most, if not all, the dynamic chan
155 ndent microhomology-mediated end joining (SD-MMEJ) explains many of the alt-EJ repair products recove
156 ndent microhomology-mediated end joining (SD-MMEJ), in which de novo synthesis by an accurate non-pro
157 ndent microhomology-mediated end joining (SD-MMEJ), predicts that differences between DNA sequences n
158 NA polymerase theta is necessary for most SD-MMEJ repair at Cas9 breaks.
159 es consistent with the predictions of our SD-MMEJ model.
160 nce characteristics that drive successful SD-MMEJ repair.
161           Genetic analysis indicates that SD-MMEJ is Ku70, Lig4 and Rad51-independent but impaired in
162        Here, we expand the utility of the SD-MMEJ model through computational analysis of repair prod
163      We also obtained evidence for 'trans SD-MMEJ,' involving at least two consecutive rounds of micr
164  deletions were RAD51-independent, one-sided MMEJ was RAD51 dependent.
165 nd annealing; and RAD51 dependent, one-sided MMEJ.
166 ombination (HR), Rad52 and Rad51, suppressed MMEJ in this system, suggesting a competition between HR
167  describe a role for HR genes in suppressing MMEJ in human cells.
168 ic lethal therapeutic approaches that target MMEJ repair.
169                           Although targeting MMEJ has emerged as a powerful strategy to eliminate HR-
170 ition repair substrate, we demonstrated that MMEJ with short end resection is used in mammalian cells
171       Additionally, we provide evidence that MMEJ activity in mitosis repairs persistent DSBs that or
172                            We also find that MMEJ compensates for loss of nonhomologous end joining t
173                                We found that MMEJ requires the nuclease activity of Mre11/Rad50/Xrs2,
174                          We also showed that MMEJ shares the initial end resection step with homologo
175                   These studies suggest that MMEJ not only is a backup repair pathway in mammalian ce
176 gments loss of DNA sequence, suggesting that MMEJ is a highly regulated DSB repair process.
177  rad52Delta yku70Delta strains suggests that MMEJ also contributes to the repair of DSBs induced by i
178                                          The MMEJ also occurs when Rad52 is absent, but the extent of
179 as new targets and approaches exploiting the MMEJ pathway in cancer therapy.
180 nsformed B cell lines abundantly express the MMEJ enzyme POLtheta that likely protects cellular repli
181                             Importantly, the MMEJ pathway is commonly upregulated in cancers, especia
182         Overall, POLQ, a key mediator in the MMEJ pathway, is critical for DSB repair in BRCA2-defici
183 hes within Poltheta-hel that orchestrate the MMEJ process in DSB repair, laying the groundwork for th
184 simplicity, reliability and efficacy of this MMEJ-based therapeutic strategy should permit the develo
185 argeting PARP, an enzyme that contributes to MMEJ, results in the death of EBV-lymphoma cells.
186 ome rearrangement while also contributing to MMEJ in both species.
187 that the use of MENdel helps researchers use MMEJ at scale for reverse genetics screenings and with s
188 trand breaks, to recapitulate DSB repair via MMEJ or nonhomologous end-joining (NHEJ).
189 quent annealing necessary for DSB repair via MMEJ.
190 ingle-stranded DNA after DNA damage, whereas MMEJ remains unaffected.
191                                        While MMEJ is suppressed by C-NHEJ, the relationship between H
192                                        While MMEJ-based deletions were RAD51-independent, one-sided M
193 mbda showed faster kinetics associating with MMEJ substrates following DSB induction than Pol delta.

 
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