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1       We report the cloning of fission yeast mcm3 +.
2  associate with Mcm2-7 via interactions with Mcm3.
3 whose action is mediated by interaction with MCM3.
4 n bind to chromatin through interaction with MCM3.
5    We have characterized two mutant alleles, mcm3-1 and mcm3-10, in Saccharomyces cerevisiae and show
6                                              Mcm3-1 contains a G246E mutation that diminishes the eff
7 t Mcm3-10 is defective in a step before, and Mcm3-1 is defective in a step after the recruitment of t
8 ynthetically lethal with orc2-1, mcm2-1, and mcm3-1.
9                                              Mcm3-10 contains a P118L substitution that compromises i
10             These observations indicate that Mcm3-10 is defective in a step before, and Mcm3-1 is def
11 characterized two mutant alleles, mcm3-1 and mcm3-10, in Saccharomyces cerevisiae and showed that the
12  ubiquitination by uba1-165, a suppressor of mcm3-10, restored the interaction of Mcm3-10p with subun
13 ssor of mcm3-10, restored the interaction of Mcm3-10p with subunits of the MCM complex and its recrui
14  dimer of the Mcm4/6/7 heterotrimer, and the Mcm3/5 heterodimer.
15 ic core of the Mcm complex and that Mcm2 and Mcm3/5 may be involved in the regulation of the activity
16 e results, the interaction of either Mcm2 or Mcm3/5 with the Mcm4/6/7 complex resulted in the disasse
17  suggested that Mcb1 interacts robustly with Mcm3-7 but not Mcm2.
18 R-Cas9-mediated PrL->VTA projection-specific Mcm3/7 knockdown attenuated ESI-potentiated heroin-seeki
19                                 Study of the Mcm3/7p ATPase shows that an essential arginine in Mcm3p
20 s connects the remaining MCM proteins to the Mcm3/7p pair.
21 of the minichromosome maintenance protein 3 (MCM3), a component of the hexameric MCM DNA helicase.
22 perm chromatin but do prevent association of MCM3, a protein essential for replication.
23 fect MCM2-7 dynamics or function rather than MCM3 abundance.
24                                              MCM3 acetylase (MCM3AP) and germinal-centre associated n
25                  These results indicate that MCM3 acetylase activity of MCM3AP is required to inhibit
26  therefore confused in databases because the MCM3 acetylase DNA sequence is contained entirely within
27                                              MCM3 acetylating protein, MCM3AP, binds and acetylates M
28  mRNA export factor Sac3p, and the mammalian MCM3 acetyltransferase.
29                                      Second, MCM3 acts as a negative regulator of the MCM2-7 helicase
30 ation of KEAP1-interacting proteins revealed MCM3, an essential subunit of the replicative DNA helica
31                                              MCM3 and -4 of the MCM complex specifically bound to the
32                   All three DNA polymerases, Mcm3 and Cdc45, but not Orc2, still formed complexes in
33  include several proteins (Sld2, Cdc6, Orc6, Mcm3 and Cdh1) involved in early S-phase events.
34 lating protein, MCM3AP, binds and acetylates MCM3 and inhibits cell cycle progression.
35 racts directly with MCM5 and MCM6; MCM5 with MCM3 and MCM2; and MCM6 with MCM2 and MCM4.
36        We also show that interaction between MCM3 and MCM3AP is essential for nuclear localization an
37 m5-bob1) strengthens the interaction between Mcm3 and Mcm5 and allows cells to enter S phase independ
38 n of Sld3 that is specifically defective for Mcm3 and Mcm5 interaction (sld3-m10), and also identifie
39  bind to a common site on CMG, including the MCM3 and MCM5 zinc-finger domains.
40 ing cell cycle and DNA damage response, with Mcm3 and Mcm7 (minichromosome maintenance proteins 3/7)
41 interaction with Mcm5 and the recruitment of Mcm3 and Mcm7 to a replication origin.
42                 In "semi-attached OCCM," the Mcm3 and Mcm7 WHDs latch onto ORC-Cdc6 while the main bo
43 ow that members of the replicative helicase (Mcm3 and Mcm7) play a role in silencing and physically i
44                                        Orc2, Mcm3, and DUE-B were also bound at an ectopic c-myc repl
45             In this work, we show that Mcm2, Mcm3, and Mcm5 self-interact and interact with one anoth
46                                        Mcm2, Mcm3, and Mcm5/Cdc46 are conserved proteins essential fo
47 leotide reductase 2, thymidylate synthetase, MCM3, and MCM7 genes, but actin RNA was not affected.
48            Similarly, the signals from Orc1, Mcm3, and Mcm7 were at background levels in cells arrest
49 rofiles of the licensing factors Orc2, Orc3, Mcm3, and Mcm7 with gene expression, replication timing,
50 f Rb-E2F-regulated genes cyclin A, cyclin E, MCM3, and PCNA are also elevated.
51 e sites of KEAP1-dependent ubiquitylation in MCM3, and these sites are on predicted exposed surfaces
52  of the origin recognition complex, ORC, and MCM3, another member of the MCM family.
53                           Intriguingly, both MCM3 apo and dsDNA bound structures exhibit left-handed
54                                     Mcm2 and Mcm3 are abundant proteins, present in approximately 4 X
55 ns for KEAP1 within the nucleus and identify MCM3 as a novel substrate of the KEAP1-CUL3-RBX1 E3 liga
56 The results reported establish that MCM2 and MCM3 assemble into homohexamers and exhibit DNA binding,
57  we now demonstrate that CDK1 phosphorylates MCM3 at Ser-112, Ser-611, and Thr-719.
58 treatment, the inhibitory phosphorylation of MCM3 at Ser-205 was reduced, and this reduction was acco
59 -tagged dsDNA to selectively enrich a stable MCM3-ATP-dsDNA complex for cryoEM structure determinatio
60 lteration of chromatin structure and loss of Mcm3 binding.
61  minichromosome maintenance complex protein, MCM3, bound TR in late-G(1)/S-arrested cells, which coin
62 el qualitative change in the distribution of Mcm3, but not Orc2, across the c-myc replicator.
63 ivation through the novel phosphorylation of MCM3 by Chk1.
64 forms and that distinct isoforms of Mcm2 and Mcm3 can be detected at specific stages of the cell cycl
65 on in cells, and impaired recruitment of the MCM3 complex to the oriP Surface conservation analysis r
66                                              Mcm3-deficient erythroblasts display aberrant DNA replic
67 3 + is essential and spores carrying a Delta mcm3 disruption arrest with an apparently replicated DNA
68        In vitro binding assays indicate that MCM3 does not interact directly with Stat1, suggesting t
69 , preferentially controls the sumoylation of Mcm3 during DNA replication.
70 g them MCM5 (minichromosome maintenance) and MCM3, for transcription activation.
71 iability, but all attempts to delete TK1620 (MCM3) have been unsuccessful arguing that that MCM3 is e
72 conserved in macroH2A2 and the C-terminus of Mcm3 helicase subunit.
73  with Stat1, suggesting that the presence of MCM3 in the group of Stat1TAD-interacting proteins is du
74 ated the carboxyl termini of mMCM3 and human MCM3 in vivo and the phosphorylated form of MCM3 retaine
75 ntain a cohesin-interaction motif from human MCM3 induce cohesin pausing, indicating that MCMs are 'a
76                                              MCM3 inhibits transactivation domain function, whereas M
77              We also show that S. cerevisiae Mcm3 is a phosphoprotein that exists in multiple isoform
78  KEAP1 targeting motif in MCM3 suggests that MCM3 is a point of direct contact between KEAP1 and the
79                                              Mcm3 is a subunit of the hexameric MCM2-7 complex requir
80 M3) have been unsuccessful arguing that that MCM3 is essential and is likely the replicative helicase
81                                 We show that MCM3 is ubiquitylated by the KEAP1-CUL3-RBX1 complex in
82                                              mcm3 + is essential and spores carrying a Delta mcm3 dis
83 but that ATM is the predominant UV-activated MCM3 kinase in vivo.
84 osome remodeling, histone deacetylation, and MCM3 loading at DS.
85 1, coinciding with nucleosome remodeling and MCM3 loading, and preceding the onset of DNA replication
86 at the carboxyl terminus of chromatin-loaded MCM3 may be sequestered from ATM-dependent checkpoint si
87                   Here, we report that MCM2, MCM3, MCM4, and MCM6 (MCM2/3/4/6) are elevated in human
88                    P118 is conserved between Mcm3, Mcm4, Mcm5, and Mcm7.
89 and diverted sideways by OB hairpin-loops of Mcm3, Mcm4, Mcm6, and Mcm7.
90  prereplication complex proteins Orc1, Orc2, Mcm3, Mcm7, and Cdc6 and the novel DNA unwinding element
91                 In G(1)-arrested HeLa cells, Mcm3, Mcm7, and DUE-B were prominent near the DUE, while
92  Ser-732) in the carboxyl terminus of murine MCM3 (mMCM3) and that ATM phosphorylates both sites in v
93        Remarkably, the Mcm2-Mcm3 NLS and the Mcm3 NES are sufficient to form a transport module that
94                         Remarkably, the Mcm2-Mcm3 NLS and the Mcm3 NES are sufficient to form a trans
95  nuclear export signal (NES) adjacent to the Mcm3 NLS.
96 id maintenance and increase EBNA1, ORC2, and MCM3 occupancy at OriP.
97                    First, ATM phosphorylates MCM3 on S535 in response to ionizing radiation.
98 ensis mini-chromosome maintenance complex 3 (MCM3) on cryoEM grids through biotinylation and resolved
99 x undergoes dephosphorylation, and the Mcm2, Mcm3, or Mcm6 subunits are then actively phosphorylated
100 horylation sites are conserved in vertebrate MCM3 orthologs suggesting that this motif may serve impo
101         These data reveal that CDK-dependent MCM3 phosphorylation contributes to the regulated format
102 d ATR jointly contribute to UV light-induced MCM3 phosphorylation, but that ATM is the predominant UV
103 romotes net export by phosphorylation of the Mcm3 portion of this module and that nuclear export of t
104 etermined that KEAP1 does not regulate total MCM3 protein stability or subcellular localization.
105                     The rest of the Mcm2 and Mcm3 proteins are disturbed to both the cytoplasm and nu
106  was related to the time when Orc1, Orc2 and Mcm3 proteins became stably bound to hamster chromatin.
107 s redundancy, we see multiple sites bound to MCM3 (representative of the helicase) in the region flan
108  MCM3 in vivo and the phosphorylated form of MCM3 retained association with the canonical MCM complex
109 t a specific serine/threonine residue in the MCM3 subunit of CMG, which has been previously linked to
110  Here we report that Chk1 phosphorylates the MCM3 subunit of the MCM complex at Ser-205 under normal
111   Our analysis of a KEAP1 targeting motif in MCM3 suggests that MCM3 is a point of direct contact bet
112 lear localization signals (NLSs) on Mcm2 and Mcm3 that are each necessary, but not sufficient, for nu
113 ential, conserved carboxy-terminal domain of Mcm3 that interacts with and stimulates the ATPase activ
114                    Importantly, we find that MCM3 that is prebound to chromatin does not dissociate w
115 ffect steady-state levels of chromatin-bound MCM3, the ATM-phosphorylated form of MCM3 was preferenti
116                                  9 degrees N MCM3, the proposed replicative helicase, unwinds DNA at
117 icate that only a small fraction of Mcm2 and Mcm3 tightly associates with chromatin, from late M phas
118                      Mutating the Ser-205 of MCM3 to Ala increased the length of DNA replication trac
119                          Strikingly, loss of MCM3 triggers the destabilization of other MCM proteins,
120 n-bound MCM3, the ATM-phosphorylated form of MCM3 was preferentially localized to the soluble, nucleo
121                                     Orc1 and Mcm3 were easily eluted from chromatin during mitosis an
122                                     MCM7 and MCM3 were identified as cyclin D1-binding proteins.
123 emporally correlated with that of endogenous MCM3 when cells were released from mitosis.
124 and further examine one replication protein, Mcm3, where a cluster of consensus sites near a nucleocy
125 complexes with the same kinetics as MCM7 and MCM3, where they associated specifically with MCM7.
126 acting proteins is due to the association of MCM3 with MCM5.
127 rylation of Ser-112 triggers the assembly of MCM3 with the remaining MCM subunits and subsequent chro

 
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