ライフサイエンスコーパス: BRM

1 BRM (SMARCA2) and BRG1 (SMARCA4) are mutually exclusive

2 BRM binds decondensed chromatin but is excluded from con

3 BRM cells were established in the lung early after infec

4 BRM differentiation temporally coincided with transient

5 BRM encodes the catalytic ATPase required for chromatin

6 BRM has the capability to perform cross-species identifi

7 BRM interacts with two ankyrin repeat proteins that are

8 BRM is developed using Java and other open-source techno

9 BRM provides the ability to mine complex data for identi

10 BRM v2.3 has the capability to query predicted miRNA tar

11 BRM was identified as a transcriptional activator of Hox

12 BRM, a key SWI/SNF complex subunit and a putative tumor

13 BRM-chromatin interactions are highly dynamic, whereas h

14 BRM-specific complexes are present only on the repressed

15 7%), SAIDs in 29 (7.4%), IMT in 149 (38.0%), BRMs in 56 (14.3%), and none (N = 14).

16 ddress this question, we sequenced BRM in 10 BRM/BRG1-deficient cancer cell lines and found that BRM

17 E2F binding-deficient basic region mutant 2 (BRM-2) carrying the Ile294Ala and Arg297Ala substitution

18 we report the characterization of BAP111, a BRM-associated protein that contains a high mobility gro

19 modifying antirheumatic drug before use of a BRM).

20 ility of biologic response modifying agents (BRMs) by mandating that health plans that provide covera

21 e pathway regulates both BRM acetylation and BRM silencing as MAP kinase pathway inhibitors both indu

22 Furthermore, we show that AN3 and BRM genetically interact.

23 Lastly, we demonstrate that both BAF57 and BRM are required for the proliferation of AR-dependent p

24 t the SWI/SNF ATPase subunits cell, BRG1 and BRM (BRG1/BRM), are lost in approximately 30% of human n

25 t provides supportive evidence that BRG1 and BRM act as tumor suppressor proteins and implicates a ro

26 long terminal repeat), we show that BRG1 and BRM are recruited to the MMTV promoter in a hormone-depe

27 Thus, BRG1 and BRM are silenced by different mechanisms, and it may be

28 ng either of the mutually exclusive BRG1 and BRM ATPases, promoted NIPBL recruitment at active enhanc

29 netic and mechanistic basis for the BRG1 and BRM chromatin-remodeling complexes in regulating gene ex

30 Thus, BRG1 and BRM complexes may direct distinct cellular processes by

31 f tumors show a concomitant loss of BRG1 and BRM expression.

32 Because BRG1 and BRM function as mutually exclusive catalytic subunits of

33 show concomitant down-regulation of BRG1 and BRM in six human tumor cell lines.

34 The recruitment of BRG1 and BRM resulted in chromatin remodeling and decondensation

35 , at active promoters, depletion of BRG1 and BRM showed minimal effect on NIPBL occupancy.

36 BRG1 and BRM were required for the viability of VECs but not othe

37 BRG1 and BRM, central components of the BAF (mSWI/SNF) chromatin

38 e of two highly homologous ATPases, BRG1 and BRM, yet little is known about their specialized functio

39 chromatin-remodeling complex called BRG1 and BRM.

40 subunits including the two ATPases BRG1 and BRM.

41 nges in the relative importance of BRG1- and BRM-catalyzed SWI/SNF complexes during the development o

42 ction was required for a subset of BRG1- and BRM-dependent gene expression.

43 Furthermore, CHD9 and BRM were required for GR occupancy and chromatin remodel

44 tively inhibits GR interaction with CHD9 and BRM, thereby blocking chromatin remodeling and robust GR

45 AMPK2 phoshorylation site impaired KU70 and BRM recruitment to DSB sites.

46 ded direct evidence that BRG1, BRG1-K-R, and BRM chromatin-remodeling complexes have distinct kinetic

47 y, the core ATPase subunits, BRG/SMARCA4 and BRM/SMARCA2, are functionally distinct and may contribut

48 BRG1 (SMARCA4) and BRM (SMARCA2) are the mutually exclusive core ATPases of

49 ved Brm complex core subunits, SNR1/SNF5 and BRM/SNF2-SWI2, on target gene regulation.

50 A widespread distribution of SNR1 and BRM on the salivary gland polytene chromosomes showed th

51 5, GRF3, COL5, and ARR4, and both SWP73B and BRM occupy the HEC1 promoter.

52 SYD and BRM act as trithorax proteins, and the requirement for S

53 ax proteins, and the requirement for SYD and BRM in flower patterning can be overcome by partial loss

54 We show that UTX and BRM are physically associated with CBP in vivo and that

55 UTX and BRM bind directly to conserved zinc fingers of CBP, sugg

56 We propose that direct binding of UTX and BRM to CBP and their modulation of H3K27ac play an impor

57 We show that H2A.Z and BRM co-localize at thousands of sites, where they intera

58 RS9 binding sites are dependent on H2A.Z and BRM for accessibility.

59 c and cooperative contributions of H2A.Z and BRM to transcriptional regulation, and illuminated sever

60 how distinct relationships between H2A.Z and BRM with respect to their roles in transcription.

61 ncluded RCTs that compared the safety of any BRMs used in RA patients with placebo and/or any traditi

62 roader biological interest, in areas such as BRM and Polycomb group function and dysfunction, transcr

63 f REF6 results in decreased BRM occupancy at BRM-REF6 co-targets.

64 Downregulation of the single ATPase, BRM, in SK-MEL5 cells inhibited expression of both diffe

65 ing enzymes that contain SNF2 family ATPases BRM (Brahma) or BRG1 (Brahma Related Gene 1) and that co

66 owered by either of two alternative ATPases, BRM or BRG1.

67 an be either of two closely related ATPases, BRM or BRG1, with the potential that the choice of alter

68 BAPID protein-inhibited interaction between BRM and Di19, and suppressed the inhibition of BRM on th

69 Designed in collaboration with biologists, BRM simplifies mundane analysis tasks of merging microar

70 pression, these HDAC inhibitors also blocked BRM function when present.

71 found that, at many genes regulated by both BRM and H2A.Z, both factors overlap with binding sites o

72 that the promoter is a direct target of both BRM- and BRG1-containing complexes.

73 man tumor types and that loss of one or both BRM alleles potentiated tumor development in mice.

74 protein (MAP) kinase pathway regulates both BRM acetylation and BRM silencing as MAP kinase pathway

75 their individual functions implies that both BRM and H2A.Z have more context-dependent roles than pre

76 Brahma (BRM) and Brahma-related gene 1 (BRG1) are the ATP-depend

77 Brahma (BRM) is a novel anticancer gene, which is frequently ina

78 remodeling ATPases SPLAYED (SYD) and BRAHMA (BRM) are redundantly required for flower patterning and

79 F-type chromatin remodelers, such as BRAHMA (BRM), and H3K27 demethylases both have active roles in r

80 WI2/SNF2 chromatin remodeling ATPase BRAHMA (BRM) causes ABA hypersensitivity during postgermination

81 riant H2A.Z and the SWI2/SNF2 ATPase BRAHMA (BRM) have overlapping roles in positively and negatively

82 SWI/SNF chromatin-remodeling ATPase BRAHMA (BRM) modulates response to ABA by preventing premature a

83 and the chromatin-remodeling ATPase Brahma (BRM).

84 complexes formed around the ATPases BRAHMA (BRM) or SPLAYED.

85 rabidopsis thaliana SWI/SNF ATPases, BRAHMA (BRM) and SPLAYED (SYD), are viable, facilitating investi

86 SWI/SNF chromatin remodeling enzyme Brahma (BRM).

87 rahma-related gene-1 (BRG1) or human brahma (BRM), the ATPase subunits of two distinct SWI/SNF enzyme

88 xpress dominant negative versions of Brahma (BRM) and Brahma-related gene 1 (BRG1), the ATPase subuni

89 ATPases as their catalytic subunit: brahma (BRM, also known as SMARCA2) and brahma-related gene 1 (B

90 e of two paralogous ATPase subunits, Brahma (BRM) or BRM-related gene 1 (BRG1), which we previously f

91 bind to itself and it interacts with Brahma (BRM), an SWI2-SNF2 homolog, with which it is associated

92 ID1A is a core member of the polymorphic BRG/BRM-associated factor chromatin remodeling complex.

93 (iii) chromatin remodeling, including BRG1, BRM, hSNF2H, BAF155, mSin3a, and histone deacetylase 2.

94 remodeling multiprotein complexes BAF (BRG1/BRM-associated factor) and PBAF (polybromo-associated BA

95 TPases of the chromatin remodeling BAF (BRG1/BRM-associated factor) complexes.

96 of the 60-kD structural subunit BAF60 (BRG1/BRM-associated factor 60), of which BAF60c is essential

97 SNF ATPase subunits cell, BRG1 and BRM (BRG1/BRM), are lost in approximately 30% of human non-small l

98 eling complexes, specifically canonical BRG1/BRM-associated factor (cBAF) complexes, promote severe a

99 e-stimulated macrophages, the catalytic BRG1/BRM subunits of the SWI/SNF class of ATP-dependent nucle

100 ly bioavailable, selective inhibitor of BRG1/BRM under clinical development in AML.

101 Here, we show that the BRG1/BRM-associated factor (BAF) chromatin remodeling complex

102 Here we show that the BRG1/BRM-associated factor (BAF) chromatin-remodelling comple

103 The BRG1/BRM-associated factor (BAF) complexes are important for

104 estored BRM expression in each of these BRG1/BRM-deficient cancer cell lines, indicating that epigene

105 st that hSNF5 loss is not equivalent to BRG1/BRM loss in human tumor cell lines.

106 Moreover, patients with BRG1/BRM-negative carcinomas, independent of stage, have a st

107 in survival compared with patients with BRG1/BRM.

108 We show that BRG1and BRM associate with different promoters during cellular p

109 e-deficient forms of BRG1 (BRG1-K-R) or BRM (BRM-K-R) inhibited the remodeling of local and higher or

110 Regulation of Antennapedia by BRM and OSA proteins requires sequences 5' to the P2 pro

111 r whole brain radiotherapy for breast cancer BRM.

112 nhibitors both induced BRM as well as caused BRM deacetylation.

113 ction elicited lung-resident memory B cells (BRM cells) that were phenotypically and functionally dis

114 catalytic subunits of the SWI/SNF complexes, BRM, the mammalian ortholog of SWI2/SNF2 in yeast and br

115 apid phosphorylation-based switch to control BRM activity; this property could be potentially harness

116 ing a robust means of identifier conversion, BRM also incorporates a suite of microRNA (miRNA)-target

117 Loss of REF6 results in decreased BRM occupancy at BRM-REF6 co-targets.

118 Since the E2F binding-deficient BRM-2 mutant interacted with E2F-1 but failed to activat

119 Our results offer a rationale to develop BRM-ATPase inhibitors as a strategy to treat BRG1/SMARCA

120 onfidence intervals were calculated for each BRM.

121 transcription factors (TFs) linked to either BRM (GATA3) or HDAC9 (MEF2D) expression.

122 and suggest that vaccines designed to elicit BRM cells must deliver antigen to the lungs.

123 individuals), 1188 (91.1%) had baseline FACT-BRM TOI scores, and 832 were evaluable at cycle 3 (ipili

124 Estimates of FACT-BRM TOI cycle 3 compliance did not differ by arm (ipilim

125 oncurrently, the chromatin-remodeling factor BRM is replaced by BRG1 and histones are hyperacetylated

126 Given that a code for BRM does not exist within ICES, we analyzed the incidenc

127 ate that the BAP111 subunit is important for BRM complex function in vivo.

128 Cumulative incidence of radiotherapy for BRM accounting for the competing risk of death, and time

129 e analyzed the incidence of radiotherapy for BRM.

130 We propose a role for BRM in the balance between growth or stress responses.

131 The results reveal an unexpected role for BRM-specific complexes.

132 The output from BRM can easily and directly be uploaded to freely availa

133 A switch from BRM to BRG1 on the alkaline phosphatase promoter marks t

134 However, assorted tissues from BRM null/BRG1-positive mice lack CD44 expression, sugges

135 Unlike many anticancer genes, BRM is not mutated, but rather epigenetically silenced.

136 teracts with BRG1 and its functional homolog BRM in mammalian cells.

137 nding protein 9 (CHD9) and Brahma homologue (BRM, a product of the SMARCA2 gene) are required for GC-

138 Here, we show that the human BRM (hBRM) bromodomain (BRD) has moderate specificity fo

139 ial sarcoma, is known to interact with human BRM (hBRM), thus providing a link between chromatin remo

140 This screen identified BRM/SMARCA2, a DNA-dependent ATPase of the mammalian SWI

141 To determine if BRM physically interacts with other trithorax group prot

142 and HDAC9 were greatly overexpressed only in BRM-negative cell lines indicating that HDAC9 may be a g

143 que N-terminal domain that is not present in BRM.

144 Here we use workflows provided in BRM to integrate RNA sequencing data across species to i

145 alcin, become constitutively up-regulated in BRM-depleted cells.

146 rentially regulated (p<0.05) gene targets in BRM indicates that nicotine exposure disrupts genes invo

147 The miRNA workflow in BRM allows for efficient processing of multiple miRNA an

148 and found that KAT6A, KAT6B and KAT7 induce BRM expression, whereas KAT2B and KAT8 induce its acetyl

149 and/or MEF2D downregulated HDAC9 and induced BRM.

150 s MAP kinase pathway inhibitors both induced BRM as well as caused BRM deacetylation.

151 ression of BRM-dependent genes and inhibited BRM-dependent growth across a wide range of BRM-deficien

152 MOR thus joins BRM and Snf5-related 1 (SNR1), two known Drosophila SWI-

153 Lung BRM cells, but not systemic memory B cells, contributed

154 re, we investigated the determinants of lung-BRM differentiation upon influenza infection.

155 ion of IFN-gamma in Tfh cells prevented lung-BRM differentiation and impaired protection against hete

156 y B cell differentiation and subsequent lung-BRM responses.

157 The Bioinformatics Resource Manager (BRM) is a software environment that provides the user wi

158 The Bioinformatics Resource Manager (BRM) is a web-based tool developed to facilitate identif

159 The Bioinformatics Resource Manager (BRM) v2.3 is a software environment for data management,

160 xtracted from Botanical Reference Materials (BRMs).

161 ivo but does not affect assembly of the 2-MD BRM complex.

162 l receive radiotherapy for brain metastases (BRM).

163 rapy [IMT]), or biologic response modifiers (BRMs) was assessed.

164 the infusion of biologic response modifiers (BRMs), including antileukocyte antibodies and lipids.

165 o are receiving biologic response modifiers (BRMs).

166 act with BRM and post-translationally modify BRM by phosphorylation/dephosphorylation.

167 Although low-dose MTP, BRM, DOX, or TAM individually had beneficial effects on

168 Although dominant negative BRM and BRG1 inhibited expression of every muscle-specif

169 the presence or absence of dominant negative BRM or BRG1, MyoD was able to activate expression of p21

170 Expression of the dominant-negative BRM protein caused peripheral nervous system defects, ho

171 osphorylation of BRM restores the ability of BRM to repress ABA response.

172 NA repair by suppressing the accumulation of BRM, a catalytic subunit of the SWI/SNF complex, at DSB

173 ion, and PP2CA-mediated dephosphorylation of BRM restores the ability of BRM to repress ABA response.

174 s was seen with BRG1 depletion, depletion of BRM caused accelerated progression to the differentiatio

175 Depletion of BRM in BRG1-deficient cancer cells leads to a cell cycle

176 Dissociation of BRM-containing SWI/SNF depends on p300, and association

177 oth compounds led to robust re-expression of BRM, induced downstream expression of BRM-dependent gene

178 ion of BRM, induced downstream expression of BRM-dependent genes and inhibited BRM-dependent growth a

179 Cumulative incidence of BRM was higher among patients with ERBB2-positive/HR-neg

180 M and Di19, and suppressed the inhibition of BRM on the Di19-PR module by mediating the H3K27me3 depo

181 The strategy relies upon inhibition of BRM/SMARCA2, another catalytic SWI/SNF subunit with a BR

182 ralogous SWI/SNF subunits with low levels of BRM, BAF170, and ARID1B.

183 Moreover, loss of BRM activity led to destabilization of a nucleosome like

184 is a major mechanism underlying the loss of BRM expression.

185 of these genes is not compromised by loss of BRM function.

186 ke other tumor suppressor genes, the loss of BRM has been shown to be a reversible epigenetic change,

187 gest that SnRK2-dependent phosphorylation of BRM leads to its inhibition, and PP2CA-mediated dephosph

188 re induction, but the concurrent presence of BRM-specific complexes overrides their activation functi

189 BRM-dependent growth across a wide range of BRM-deficient cancer cell lines of different origins.

190 ) domains and facilitates the recruitment of BRM.

191 Reduction of BRM function dramatically reduces the association of RNA

192 horylation sites in the C-terminal region of BRM at SnRK2 target sites that are evolutionarily conser

193 which underlie the epigenetic regulation of BRM.

194 NA interference (RNAi)-mediated silencing of BRM suppressed the growth of BRG1-deficient cancer cells

195 We also found that the suppression of BRM occurs in a broad range of human tumor types and tha

196 which underlie the epigenetic suppression of BRM.

197 The bromodomain-containing C terminus of BRM binds to the CBP PHD finger, enhances PHD binding to

198 The use of BRMs among patients with RA included in RCTs of at least

199 complex thus correlates with a dependence on BRM for gene activity.

200 elective dependency of BRG1-mutant tumors on BRM in vivo.

201 ions of SWI/SNF complexes containing BRG1 or BRM are not completely interchangeable.

202 nducibly express mutant forms of the BRG1 or BRM ATPases that are unable to bind and hydrolyze ATP.

203 that expression of dominant negative BRG1 or BRM inhibited the induction of muscle-specific gene expr

204 rmined that expression of the mutant BRG1 or BRM proteins impaired the ability of cells to activate t

205 with data from myoblasts depleted of BRG1 or BRM showed that bromodomain function was required for a

206 SNF complexes composed of either the BRG1 or BRM subunit promote expression of distinct and overlappi

207 posed of one of two related ATPases, BRG1 or BRM, and 9-12-associated factors (BAFs).

208 cells and observed downregulation of BRG1 or BRM, but not concomitant loss of both ATPases.

209 essing dominant negative versions of BRG1 or BRM-based SWI/SNF enzymes.

210 atin remodeling complexes containing BRG1 or BRM.

211 wo highly conserved ATPase subunits: BRG1 or BRM.

212 paralogous ATPase subunits, Brahma (BRM) or BRM-related gene 1 (BRG1), which we previously found are

213 in cell lines that lack functional p300, or BRM and Brg-1.

214 ATPase-deficient forms of BRG1 (BRG1-K-R) or BRM (BRM-K-R) inhibited the remodeling of local and high

215 mall fraction of all genes depends on SYD or BRM for expression, indicating that these SWI/SNF ATPase

216 iated systemic disease may respond to IMT or BRMs.

217 Overall, BRM provides bioinformatics tools to assist biologists h

218 ed for several days, and during this period, BRM activity was detected.

219 Finally, the phosphomimetic BRM(S1760D S1762D) mutant displays ABA hypersensitivity.

220 Our findings position BRM as an attractive therapeutic target for BRG1 mutated

221 human homologue of the SNF2/Brahama protein BRM co-localizes with SYT and SYT-SSX in nuclear speckle

222 Our studies revealed that reduced BRM expression and/or activity drives the malignant beha

223 possible to clinically target and reexpress BRM in a number of tumor types, potentially impacting tu

224 ow which specific proteins, if any, regulate BRM, we sought to identify the proteins, which underlie

225 HDAC, we found that HDAC3 and HDAC9 regulate BRM expression, whereas HDAC2 controls its acetylation.

226 of compounds that could effectively restore BRM expression and function.

227 Despite their ability to restore BRM expression, these HDAC inhibitors also blocked BRM f

228 stone deacetylase (HDAC) inhibitors restored BRM expression in each of these BRG1/BRM-deficient cance

229 are effective at pharmacologically restoring BRM and thereby inhibit cancer cell growth.

230 Consistently, we could show that restoring BRM levels normalized the malignant behavior of transfor

231 s, revealing that SNR1 functions to restrict BRM-dependent nucleosome remodeling activities downstrea

232 rect; chromatin immunoprecipitation revealed BRM binding to the ABI5 locus.

233 mplex (HDAC) inhibitors are known to reverse BRM silencing, but they also inactivate it via acetylati

234 To address this question, we sequenced BRM in 10 BRM/BRG1-deficient cancer cell lines and found

235 ction of a 'core' subunit to block or shield BRM (SWI2/SNF2) activity in specific cells.

236 ive catalytic subunits, SMARCA4 and SMARCA2 (BRM).

237 the bromodomain-containing proteins SMARCA2 (BRM), SMARCA4 (BRG1), and polybromo-1.

238 SMARCA4/BRG1 and SMARCA2/BRM, the two mutually exclusive catalytic subunits of th

239 table components, even though the SWI2/SNF2 (BRM, BRG1, hBRM) ATPase subunit alone is partially suffi

240 lowing secondary infection, antigen-specific BRM cells differentiated in situ, whereas antigen-non-sp

241 tiated in situ, whereas antigen-non-specific BRM cells were maintained as memory cells.

242 WI/SNF chromatic remodeling complex subunit, BRM, is a potentially viable and novel therapeutic appro

243 Drosophila Brahma (SWI/SNF) complex subunits BRM and SNR1 are highly conserved with direct counterpar

244 diabetes-induced reduction in a vision task, BRM or DOX alone totally inhibited the vascular permeabi

245 These data demonstrate that BRM cells are an important component of immunity to resp

246 Genetic approaches demonstrated that BRM acted epistatically to BAPID and Di19 in drought res

247 By transient transfection, we found that BRM can restore RB-mediated cell cycle arrest, induce ex

248 1-deficient cancer cell lines and found that BRM was devoid of abrogating mutations.

249 wever, after their removal, we observed that BRM expression remained elevated for several days, and d

250 l RNAi study conducted in vivo revealed that BRM depletion suppressed the growth of BRG1-deficient tu

251 Prior studies showed that BRM resides at target loci in the ABA pathway in the pre

252 These findings suggest that BRM plays a role in chromatin remodeling that is distinc

253 e mice lack CD44 expression, suggesting that BRM-containing SWI/SNF complexes regulate expression of

254 Genetic evidence suggests that BRM acts downstream of SnRK2.2/2.3 kinases, and biochemi

255 The BRM complex contains at least seven major polypeptides.

256 The BRM complex is associated with nearly all transcriptiona

257 The BRM complex is even more highly related to the human BRG

258 xate group (0.77%; 95% CI, 0.65%-0.92%), the BRM monotherapy group (0.64%; 95% CI, 0.42%-0.95%), and

259 0 and CBP histone acetyltransferases and the BRM and Brg-1 chromatin remodeling complexes are recruit

260 hat it may modulate interactions between the BRM complex and chromatin.

261 mammalian cells, these complexes contain the BRM and BRG1 helicase-like proteins that are thought to

262 steoblasts, SWI/SNF complexes containing the BRM ATPase repress osteoblast-specific genes to maintain

263 Consistent with these findings, the BRM protein is expressed at relatively high levels in nu

264 ibility and show specific enrichment for the BRM remodeler.

265 he first year of therapy was very low in the BRM plus methotrexate group (0.77%; 95% CI, 0.65%-0.92%)

266 our screens: genes encoding subunits of the BRM complex (brm, moira, and osa), other proteins direct

267 isingly, the majority of the subunits of the BRM complex are not encoded by trithorax group genes.

268 Four of the subunits of the BRM complex are related to subunits of the yeast chromat

269 To clarify the role of the BRM complex in the transcription of other genes, we exam

270 hat the chromatin remodeling activity of the BRM complex plays a general role in facilitating transcr

271 The distribution of the BRM complex thus correlates with a dependence on BRM for

272 e targeting, function, and regulation of the BRM complex, we screened for mutations that genetically

273 rget genes by regulating the activity of the BRM complex.

274 equired for the assembly or stability of the BRM complex.

275 eins, the deletion of the bromodomain of the BRM protein has no discernible phenotype.

276 served lysine in the ATP-binding site of the BRM protein with an arginine.

277 te the functions of conserved regions of the BRM protein.

278 Genomic targets of the BRM remodeler overlap significantly with FGT1 targets.

279 ransferases p300, CBP, PCAF, and GCN5 or the BRM and Brg-1 chromatin remodeling complexes did not dim

280 er trithorax group proteins, we purified the BRM complex from Drosophila embryos and analyzed its sub

281 demonstrates its key role in recruiting the BRM chromatin remodeler.

282 propose that the OSA protein may target the BRM complex to Antennapedia and other regulated genes.

283 11 protein in embryos is associated with the BRM complex.

284 heat shock loci, are not associated with the BRM complex; transcription of these genes is not comprom

285 Therefore, BRM may be consistently down-regulated with BRG1 during

286 ing, no mutations were found in any of these BRM-regulating HDACs, HATs or TFs.

287 nown, may be required for optimal binding to BRM.

288 nally, the abi5 null mutant was epistatic to BRM in postgermination growth arrest.

289 In this study, we report recent updates to BRM for miRNA data analysis and cross-species comparison

290 cancer cell lines, the mechanisms underlying BRM silencing are not known.

291 Here we use BRM to show that developmental exposure of zebrafish to

292 We show typical workflows for using BRM to integrate experimental zebrafish miRNA and mRNA m

293 ly associated with CBP in vivo and that UTX, BRM, and CBP colocalize genome-wide on Polycomb response

294 development and embryonic survival, whereas BRM is dispensable.

295 We tested whether BRM could affect aberrant cellular functions attributed

296 ge of different nucleosome properties, while BRM stabilizes nucleosomes where it binds and destabiliz

297 e analyses showed that REF6 colocalizes with BRM at many genomic sites with the CTCTGYTY motif.

298 pathway components physically interact with BRM and post-translationally modify BRM by phosphorylati

299 y through protein-protein interactions, with BRM in the case of SYT, and with Polycomb group represso

300 Successful treatment with BRMs was associated with diffuse or nodular scleritis wi