ライフサイエンスコーパス: MCM7

1 mis using the keratin 14 (K14) promoter (K14.MCM7).

2 ed with tumorigenesis through BMI1, MCM4 and MCM7.

3 ic exclusion mechanism, similar to Mcm4/Mcm6/Mcm7.

4 omosome maintenance (MCM) proteins, Mcm2 and Mcm7.

5 teracting protein (ATRIP)-ATR interacts with MCM7.

6 CM3, where they associated specifically with MCM7.

7 8 is conserved between Mcm3, Mcm4, Mcm5, and Mcm7.

8 b-related proteins, p107 and p130, also bind MCM7.

9 ining of CA9, BMI1, cyclin E, Ki67, MCM4 and MCM7.

10 d in the N terminus (amino acids 221-248) of MCM7.

11 otif was identified in the NH(2)-terminus of MCM7.

12 sion of ITGA7 induced the phosphorylation of MCM7.

13 genomic amplification and overexpression of MCM7.

14 ouble mutant containing both the mcm10-1 and mcm7-1 (cdc47-1) alleles restores interaction between Mc

15 Transcription of MCM7 is increased in the mcm7-1 mutant and decreased in the mcm1-1 mutant, sugges

16 mcm7-98 and both cdc23ts alleles arrest with damaged chr

17 Unlike other mcm mutants or cdc23, mcm7-98 is synthetically lethal with checkpoint mutants

18 We find that mcm7-98 is synthetically lethal with the other mcmts mut

19 olated a novel temperature-sensitive allele, mcm7-98, and also characterized two temperature-sensitiv

20 nds with miniature chromosome maintenance 7 (MCM7), a DNA replication licensing protein.

21 ogue of the DNA replication licensing factor Mcm7, a highly conserved protein found in all eukaryotes

22 p56(Lyn), at Y32, which then phosphorylates MCM7, a licensing factor critical for DNA replication, a

23 code the carboxy-terminal 137 amino acids of MCM7, a member of a family of proteins that comprise rep

24 Immunohistochemical analysis of MCM7, a protein marker for DNA replication, reveals a la

25 re, diminished interaction between Mcm10 and Mcm7, a subunit of the MCM2-7 complex, by a mutation in

26 in D1-dependent kinase did not phosphorylate MCM7, active cyclin D1/CDK4, but not cyclin E/CDK2, did

27 entify minichromosome maintenance protein 7 (MCM7), an E2F-induced cellular DNA replication factor, a

28 ssing and several microRNA host genes, e.g., MCM7 and C9orf5, were significantly up-regulated in pros

29 ked further DNA replication, indicating that MCM7 and Cdc45 are required throughout replication elong

30 pus egg extracts to investigate the roles of MCM7 and Cdc45 in DNA replication.

31 However, the association between Mcm7 and Cdc45 in the chromatin fraction was inhibited i

32 leles restores interaction between Mcm10 and Mcm7 and corrects all of the defects exhibited by each o

33 uces expression of the E2F-responsive genes, Mcm7 and cyclin E, in the absence of the E7 oncogene.

34 an increase in the DNA licensing activity of MCM7 and higher levels of cell proliferation.

35 MCM7 and its clamp-loading partner Cdc6 are highly speci

36 MCM7 and MCM3 were identified as cyclin D1-binding prote

37 protein complexes with the same kinetics as MCM7 and MCM3, where they associated specifically with M

38 The Mcm4/Mcm7 and Mcm4/Mcm6/Mcm7 assemblies can open to load onto

39 We conclude that ILK interaction with MCM7 and MCM7 phosphorylation may be a critical event in

40 ChIP and Re-ChIP colocalizes MCM7 and ORC1 to the same segment specifically in late G

41 high levels of tethered replication factors, MCM7 and PCNA, indicating that DNA replication occurs in

42 may suppress TamR cell growth by inhibiting MCM7 and Rb and subsequently inducing DNA damage.

43 t nuclear export of a fusion protein between Mcm7 and the green fluorescent protein (Mcm7-GFP), where

44 We cloned fission yeast mcm7(+) and showed it is essential for viability; spores

45 inichromosome maintenance complex component (MCM7) and DNA polymerase delta hindering replication for

46 entify minichromosome maintenance protein 7 (MCM7) and p16 as potentially useful biomarkers for HPV-p

47 a protein, Rb(1-400), was used to neutralize MCM7, and antibodies were used to neutralize Cdc45.

48 ower levels of the replication factors Mcm4, Mcm7, and Cdc45 at replication origins in met30 mutants

49 plication complex proteins Orc1, Orc2, Mcm3, Mcm7, and Cdc6 and the novel DNA unwinding element (DUE)

50 In G(1)-arrested HeLa cells, Mcm3, Mcm7, and DUE-B were prominent near the DUE, while Orc1

51 isolates through several steps with MCM6 and MCM7, and MCM8 co-immunoprecipitates with MCM4, MCM6 and

52 -106b-25 cluster, which maps to intron 13 of MCM7, and miR-32, which maps to intron 14 of C9orf5, at

53 ring late G(1) via a direct interaction with Mcm7, and TGF-beta1 blocks their dissociation at G(1)/S.

54 These studies implicate MCM7, and the DNA replication licensing gene family, in

55 efect in loading of initiator proteins Mcm4, Mcm7, and to a lesser degree, Mcm2 onto chromatin during

56 complex isolated by immunoprecipitation with MCM7 antibodies in vitro.

57 In addition, the MCM7/AR interaction down-regulated MCM7 expression.

58 nichromosome maintenance (MCM) proteins MCM2-MCM7 are conserved eukaryotic replication factors that a

59 We also show that MCM5 and MCM7 are topologically constrained on DNA and that the M

60 Here, we identify Mcm7 as a novel cofactor of Mcm1 in the regulation of MC

61 cell cycle box upstream of the promoters of MCM7 as well as CDC6 and MCM5.

62 k1 co-immunoprecipitates with basal forms of Mcm7 as well as with slower migrating forms of Mcm7, ind

63 The Mcm4/Mcm7 and Mcm4/Mcm6/Mcm7 assemblies can open to load onto circular DNA to in

64 ication complex (pre-RC) components Cdc6 and Mcm7 associate with ARS1 in the mcm10-1 mutant, suggesti

65 tory effects of BPDE on DNA synthesis, Cdc45/Mcm7 associations, and interactions between Cdc45 and th

66 show that the association between Cdc45 and Mcm7 at origins of replication is negatively regulated b

67 y of AR is dependent on its interaction with MCM7 because either a mutant AR defective in its interac

68 t is essential for viability; spores lacking mcm7(+) begin S phase later than wild-type cells and arr

69 ynthetic androgen R1881 led to a decrease in MCM7 binding to genomic DNA, a reduction of DNA synthesi

70 or the c-myc replicator DUE allowed Orc2 and Mcm7 binding, but eliminated origin activity, indicating

71 comprised of amino acids 221 to 248, and the MCM7-binding motif for the AR, comprised of amino acids

72 In this report, we show that MCM7 binds SF3B3.

73 Taken together, our data suggest that MCM7 can be a potential prognostic marker and a novel th

74 The phosphorylation of MCM7 reduced MCM7 chromatin association and inhibited cell growth.

75 Knocking down RACK1 significantly reduced MCM7 chromatin association, DNA synthesis, and cell cycl

76 The Mcm4-Mcm7 complex forms a ringed-shaped hexamer that unwinds

77 The Mcm4-Mcm7 complex has a high level of ATPase activity that is

78 y a direct role in altering an inhibitory RB.MCM7 complex possibly allowing for setting of the origin

79 We studied the mechanism of the Mcm4-Mcm6-Mcm7 complex, a useful model system because this complex

80 CDK2, did catalyze the dissociation of an RB.MCM7 complex.

81 We identified the AR-binding motif for MCM7, comprised of amino acids 221 to 248, and the MCM7-

82 We observed that lower levels of MCM7 correlate with reduced cell proliferation, lower au

83 DNA replication, which include cdc6, cdc25A, MCM7, cyclin E, and Cdk2.

84 chromatin recruitment of replication factor Mcm7, demonstrating that JADE1 is required for cell prol

85 130 strongly inhibited DNA replication in an MCM7-dependent fashion in a Xenopus in vitro DNA replica

86 d homologous recombination are necessary for Mcm7-depleted cells to progress to metaphase.

87 heterohexamer, loading of Mcm2-, Mcm4-, and Mcm7-depleted complexes is likely to underlie the S phas

88 largely degradation-independent mechanism of MCM7 deubiquitylation.

89 oylphorbol-13-acetate dramatically decreased MCM7 DNA replication licensing and induced cell growth a

90 Here, six genomic regions (LSU rRNA, mtSSU, MCM7, EF-1alpha, Act and ITS) were used for reconstructi

91 its transactivation domain function, whereas MCM7 enhances HIF-1alpha ubiquitination and proteasomal

92 on marker, our data suggest that deregulated MCM7 expression actively contributes to tumor formation,

93 rimary cell cultures revealed 10-fold higher MCM7 expression in MYCN-amplified versus nonamplified tu

94 determined that siRNA-mediated knockdown of MCM7 expression reduced GBM cell proliferation and also

95 we generated a mouse model with deregulated MCM7 expression targeted to the basal layer of the epide

96 ers including BMI1, cyclin E, ki67, MCM4 and MCM7 expression.

97 itutively to the MCM7 promoter and regulates MCM7 expression.

98 novel cofactor of Mcm1 in the regulation of MCM7 expression.

99 sociated with BMI1, cyclin E, Ki67, MCM4 and MCM7 expression.

100 tion, the MCM7/AR interaction down-regulated MCM7 expression.

101 dy reveals a novel mechanism by which AR and MCM7 facilitate each other's function, suggesting that A

102 We found that Mcm4 and Mcm7 form an active unwinding assembly.

103 Full-length Rb and MCM7 form protein complexes in vitro, and the amino term

104 the prostate cancer specimens studied showed MCM7 gene amplification, and 60% of the aggressive prost

105 In parallel, VDR binding to the MCM7 gene induced H3K9ac enrichment associated with rapi

106 variation at the miR-106b-25 polycistron and MCM7 gene locus on chromosome 7q22.1.

107 we found that the genomic region containing MCM7 gene was amplified in more than 80% of the present

108 by down-regulating the promoter of the host MCM7 gene.

109 ductase 2, thymidylate synthetase, MCM3, and MCM7 genes, but actin RNA was not affected.

110 ween Mcm7 and the green fluorescent protein (Mcm7-GFP), whereas inactivation of these kinases at the

111 sis coincided with the net nuclear import of Mcm7-GFP.

112 ults in the formation of an active Mcm4/Mcm6/Mcm7 helicase assembly.

113 1 or HBO1 coordinated the recruitment of the Mcm7 helicase subunit, the DNA unwinding element (DUE)-b

114 Constitutive expression of MCM7 in a human prostate cancer cell line, DU145, result

115 Fourth, reducing the amount of MCM7 in cells disrupts checkpoint signaling and causes a

116 Residual ubiquitylation of Mcm7 in dia2-DeltaTPR cells is still CMG specific, highl

117 tly reduces the interaction between Cdt1 and MCM7 in G(1) phase cells.

118 therefore we wanted to identify the role of MCM7 in GBM progression.

119 The multiple roles of Mcm7 in replication initiation, replication elongation,

120 To further investigate the general role of MCM7 in tumorigenesis, we generated a mouse model with d

121 of ILK, also blocked the phosphorylation of MCM7 induced by ITGA7.

122 m7 as well as with slower migrating forms of Mcm7, induced in response to DNA damage.

123 -7 complex, by a mutation in either Mcm10 or Mcm7 inhibits replication initiation.

124 hat NCOA4 is a minichromosome maintenance 7 (MCM7)-interacting protein that is able to control DNA re

125 In this study, we found that MCM7 interacts with the androgen receptor (AR) with high

126 In this study, we identified that MCM7 interacts with the receptor for activated protein k

127 se (comprising six related subunits, Mcm2 to Mcm7) into pre-replicative complexes at multiple replica

128 MCM7 is a critical component of the DNA replication lice

129 ge, this is the first report suggesting that MCM7 is a critical RNA splicing factor, thus giving sign

130 Recent studies indicate that MCM7 is amplified and overexpressed in a variety of huma

131 MCM7 is an essential component of DNA replication licens

132 Our previous studies have indicated that MCM7 is both amplified and overexpressed in metastatic p

133 ately expressed during development, although MCM7 is expressed at a higher level in the egg cell.

134 Transcription of MCM7 is increased in the mcm7-1 mutant and decreased in

135 The RACK1 binding motif in MCM7 is located at the amino acid 221-248.

136 In the absence of CRL2(Lrr1), Mcm7 is not ubiquitylated, CMG unloading is inhibited, a

137 MCM7 is not visualized by immunohistochemistry on metaph

138 MCM7 is one of the pivotal DNA replication licensing fac

139 s Mcm1 binds these promoters constitutively, Mcm7 is recruited during late M phase, consistent with M

140 MCM7 is recruited to multiple sites in chromatin in S an

141 matin and that interaction between Mcm10 and Mcm7 is required for proper replication initiation and p

142 Whereas previous studies have shown that MCM7 is useful as a proliferation marker, our data sugge

143 Miniature chromosome maintenance 7 (MCM7) is an essential component of DNA replication licen

144 Minichromosomal maintenance protein 7 (MCM7) is an essential component of the replication helic

145 e maintenance (MCM) family of proteins (MCM2-MCM7) is evolutionarily conserved from yeast to human.

146 These results suggest that Mcm10, like Mcm7, is a critical component of the prereplication chro

147 P construct was also identified in SF3B3 and MCM7 knockdown PC3 and DU145 cells.

148 defective in its interaction with MCM7 or a MCM7 knockdown primarily eliminated AR effects on gene e

149 under minichromosome maintenance protein 7 (MCM7) knockdown in phospho Ser807/811-retinoblastoma pro

150 Knockdown of SF3B3 and MCM7 leads to an increase of cell death of both PC3 and

151 polyubiquitylation of a replisome component (Mcm7) leads to its disassembly at the converging termina

152 tern and strong signal for MCM7 suggest that MCM7 may be a highly informative biomarker for cervical

153 suggesting that AR-independent activation of MCM7 may be a mechanism by which prostate cancers bypass

154 The chromatin association of Mcm7, Mcm10, and proliferating cell nuclear antigen was

155 e, within 40 weeks of treatment over 45% K14.MCM7 mice exhibited tumors that had converted to squamou

156 radecanoylphorbol-13-acetate promotion), K14.MCM7 mice showed significantly increased incidence and p

157 in more than 90% of tumors isolated from K14.MCM7 mice.

158 reased in the mcm1-1 mutant, suggesting that Mcm7 modulates its own expression in conjunction with Mc

159 esults in increased expression of endogenous MCM7 mRNA and a 3-fold increase in protein levels.

160 The MCM7 mutant that does not bind RACK1 has no DNA replicat

161 A MCM7 mutant that does not bind with ILK did not respond

162 nt with a role in the egg cell, heterozygous mcm7 mutants resulted in frequent ovule abortion, a phen

163 ulation, and behaved similarly to a dominant MCM7-negative mutant and neutralized the effect of ITGA7

164 l analysis in the Walker A motif of MCM6 and MCM7 of MCM2-7, we show that ATP binding and/or hydrolys

165 o by preventing loading of the RLFs Mcm2 and Mcm7 onto chromatin.

166 mutant AR defective in its interaction with MCM7 or a MCM7 knockdown primarily eliminated AR effects

167 oupling during elongation with inhibitors of MCM7 or Cdc45, a putative helicase cofactor, results in

168 Loss of Rb or overexpression of Mcm7 or its Rb-binding domain alone abrogates late-G(1)

169 The MCM7 or SF3B3 depleted cell extract failed to splice rep

170 Knockdown of MCM7 or SF3B3 significantly increased unspliced RNA of e

171 the minichromosome maintenance complex (Mcm2-Mcm7, or Mcm2-7).

172 Indeed, MCM7 overexpression produced primary tumors 12 times lar

173 ypercholesterolemia treatment, activated the MCM7/p-RB/gammaH2AX axis and induced DNA damage in TamR

174 se involves K48-linked polyubiquitylation of MCM7, p97-mediated extraction of CMG, and a largely degr

175 h a signaling cascade in which EGFR enhances MCM7 phosphorylation and DNA replication through Lyn pho

176 conclude that ILK interaction with MCM7 and MCM7 phosphorylation may be a critical event in ITGA7 si

177 Knocking down of ILK abrogated ITGA7-induced MCM7 phosphorylation.

178 embers of the replicative helicase (Mcm3 and Mcm7) play a role in silencing and physically interact w

179 cruited during late M phase, consistent with Mcm7 playing a direct role in modulating the periodic ex

180 showed that Mcm1 binds constitutively to the MCM7 promoter and regulates MCM7 expression.

181 Specific electrophoretic mobility shifts of MCM7 promoter sequences are detected in extracts of MYCN

182 In addition, luciferase activity from MCM7 promoter/luciferase gene reporter constructs was si

183 sive prostate cancer specimens had increased MCM7 protein expression.

184 The Saccharomyces cerevisiae Mcm7 protein is a subunit of the presumed heteromeric MC

185 We show that endogenous MCM5 and MCM7 proteins are localized in the nucleus during G1, S,

186 In Xenopus eggs, the MCM2-MCM7 proteins assemble as multimeric complexes at chromo

187 M8 co-immunoprecipitates with MCM4, MCM6 and MCM7, proteins reportedly forming a helicase complex inv

188 The phosphorylation of MCM7 reduced MCM7 chromatin association and inhibited ce

189 The addition of Mcm6 to Mcm4/Mcm7 results in the formation of an active Mcm4/Mcm6/Mcm

190 emonstrated markedly increased expression of MCM7 RNA and protein in MYCN-amplified neuroblastoma tum

191 aspergilli based on the sequence analysis of Mcm7, RPB2, and Tsr1 indicated that the new species, whi

192 Indeed, Mcm7 stimulates Mcm1 binding to the early cell cycle box

193 CMG unloading involves ubiquitylation of its Mcm7 subunit and the action of the p97 ATPase.

194 The Mcm7 subunit is the only component of the active helicas

195 ases the efficiency of ubiquitylation of the Mcm7 subunit of CMG, both in vitro and in vivo.

196 iform staining pattern and strong signal for MCM7 suggest that MCM7 may be a highly informative bioma

197 In an mcm7-td (temperature-inducible degron) mutant, MAT switc

198 it of the MCM2-7 complex (also known as MCM2-MCM7), the replication licensing factor and presumptive

199 on with Mcm5 and the recruitment of Mcm3 and Mcm7 to a replication origin.

200 ipts from the four genes encoding cyclin D1, MCM7, TRIM29, and UBE2C have previously been included in

201 We found the expression of cyclin D1, MCM7, TRIM29, and UBE2C to be significantly associated w

202 Oral tumors expressed p16 and MCM7, two biomarkers associated with HPV-positive tumors

203 We show that Mcm7 ubiquitylation and CRL2(Lrr1) binding to chromatin

204 ressor protein BRCA1, which acts upstream of MCM7 ubiquitylation and p97 recruitment.

205 gest interaction between endogenous Plk1 and Mcm7 was detected in a soluble chromatin fraction.

206 gammaH2AX was significantly upregulated when MCM7 was knocked down in TamR cells.

207 disease, strong, full thickness staining for MCM7 was seen selectively in the epithelium of high-grad

208 Amplification or overexpression of MCM7 was significantly associated with relapse, local in

209 MCM7 was the most upregulated gene in the gene set we an

210 Protein complexes between Rb and MCM7 were also detected in anti-Rb immunoprecipitates pr

211 Similarly, the signals from Orc1, Mcm3, and Mcm7 were at background levels in cells arrested in M ph

212 One of the identified genes, MCM7, which is a component of the DNA replication licens

213 fferent and essential subunits (Mcm2 through Mcm7), with the corresponding dimer interfaces forming A

214 Both p56(Lyn) Y32 and MCM7 Y600 phosphorylation are enhanced in proliferating