ライフサイエンスコーパス: MITF

1 MITF and SOX10 actively recruit BRG1 to a set of MITF-as

2 MITF and TFE3, homologues of TFEB belonging to the same

3 MITF exerts its regulatory functions through its associa

4 MITF expression in the tetracycline-inducible C32 melano

5 MITF is regulated by multiple intracellular signaling pa

6 MITF itself binds to the c-Jun regulatory genomic region

7 MITF overexpression resulted in direct transcriptional a

8 MITF positively correlated with PEDF expression in invas

9 MITF protein levels vary between and within clinical spe

10 MITF stabilization caused an increase in multivesicular

11 MITF transcriptional activity is inhibited by the histid

12 MITF-BRG1 interplay thus plays an essential role in tran

13 MITF-low activity coupled with a p53 mutation was suffic

14 MITF-low zebrafish melanomas resembled human MITF-low me

15 MITF.KO cells showed markedly reduced growth and invasio

16 Using the angiomyolipoma cell line 621-101, MITF knockout (MITF.KO) and MITF-A overexpressing (MITF.

17 fast-growing melanomas were detected among 2 MITF p.E318K carriers during dermatologic digital follow

18 , establishing the PEDF gene (SERPINF1) as a MITF target in melanocytes and melanoma cells.

19 favoured by microenvironments that induce a MITF(HI)/differentiated/proliferative state.

20 Remarkably, abrogating MITF activity in BRAF(V600E)mitf melanoma leads to drama

21 h melanomas, whereas BRAF(V600E) accelerated MITF-low melanoma onset and further promoted the develop

22 Accordingly MITF reconstitution enhances KIT expression levels in 3B

23 sly unreported gene fusions, including ACTG1-MITF fusion.

24 Ectopic expression of the ACTG1-MITF fusion led to cellular transformation and induced t

25 yrosine activity inhibition reduced 3BP2 and MITF expression, demonstrating again a tight and recipro

26 e inhibitor bortezomib also reduced 3BP2 and MITF expression.

27 ), the chromatin remodeling ATPase BRG1, and MITF form a trimeric complex that is regulated by phosph

28 the transcription factors, IRF8, GATA2, and MITF as well as of the cell-cycle inhibitor p27, which a

29 ll line 621-101, MITF knockout (MITF.KO) and MITF-A overexpressing (MITF.OE) cell lines were generate

30 f proliferative progeny by fueling LEF1- and MITF-dependent differentiation.

31 o a shift in open reading frames of MLPH and MITF.

32 as other factors, such as HIF1alpha, Myc and MITF, are among those that control the balance between n

33 nelfinavir as potent suppressor of PAX3 and MITF expression.

34 ning region Y-box 10, vimentin proteins, and MITF-regulated melan A.

35 Also, KITLG-KIT signaling and MITF are suggested to mutually interact in melanocyte de

36 d Tyr, genes that are regulated by SOX10 and MITF and for chromatin remodeling at distal and proximal

37 associated syndrome (Waardenburg (SOX10 and MITF), Kallmann (CHD7 and SOX10), Noonan/LEOPARD (PTPN11

38 analyzing mRNA expression of TYR, SOX10, and MITF, melanosome structure, and immunofluorescence with

39 e to BRAF(V600E)-induced transformation, and MITF potentiates the oncogenic effect of BRAF(V600E) in

40 s dependent on transcription factors such as MITF and Sox9.

41 sed by melanocyte lineage signal(s), such as MITF.

42 mpted us to examine the relationship between MITF, endolysosomal biogenesis, and Wnt signaling.

43 An inverse relationship between MITF, vemurafenib resistance, and EGFR was then observed

44 COMMAD is associated with biallelic MITF mutant alleles and hence suggests a role for MITF i

45 transduces key prosurvival signals driven by MITF, further supporting its important role in promoting

46 The suppression of cell growth mediated by MITF silencing was rescued by overexpression of BPTF cDN

47 genes ATG1 and ATG17, which are regulated by MITF, had similar effect.

48 ion, CDK7 is dependent on transactivation by MITF or c-MYC to maintain a steady state.

49 hat the TSC/mTORC1/AKT/GSK3beta/beta-catenin/MITF axis plays a central role in regulating melanogenes

50 ) induced elevated expression of CDK2, CDK4, MITF and EST1/2 protein in hNCPCs, and also induced mela

51 mass spectrometry to define a comprehensive MITF interactome identifying novel cofactors involved in

52 Concomitantly, MITF-depleted cells display larger number of invadopodia

53 Consistently, MITF knockdown increased PTX3 expression in MITF(high) p

54 By contrast MITF(Low) cells are insensitive to SCD inhibition.

55 In contrast, MITF.OE cells grew faster in vitro and as xenografted tu

56 although the exact mechanisms that determine MITF expression and activity remain incompletely underst

57 e monophosphate reductase (GMPR) is a direct MITF target, and that the partial repression of GMPR acc

58 programmed the melanocytes and downregulated MITF in a HMGA1-dependent manner.

59 h mutant to conditionally control endogenous MITF activity.

60 We show that low levels of endogenous MITF activity are oncogenic with BRAF(V600E) to promote

61 g in attenuated mTORC1 activity and enhanced MITF-dependent Gpnmb induction.

62 the melanocyte lineage transcription factor MITF and c-Jun, which interconnects inflammation-induced

63 o overexpression of the transcription factor MITF and of the melanogenic enzymes tyrosinase and dopac

64 t overexpression of the transcription factor MITF was sufficient to rescue the small eye and adult le

65 rophthalmia-associated transcription factor (MITF) acts via pigment epithelium-derived factor (PEDF),

66 rophthalmia-associated transcription factor (MITF) and IFNgamma) to construct the evolving trajectori

67 rophthalmia-associated transcription factor (MITF) and paired-box 3 (PAX3) are at the top of the casc

68 rophthalmia-associated transcription factor (MITF) as a critical downstream target of p300 driving hu

69 rophthalmia-associated transcription factor (MITF) contributes to melanoma progression and resistance

70 rophthalmia-associated transcription factor (MITF) correlates with invasion, senescence, and drug res

71 rophthalmia-associated transcription factor (MITF) directly controls general transcription and UVR-in

72 rophthalmia-associated transcription factor (MITF) expression, a transcription factor involved in KIT

73 Microphthalmia transcription factor (MITF) is a basic helix-loop-helix leucine zipper (bHLH-Z

74 rophthalmia-associated transcription factor (MITF) is a hallmark of the proliferative-to-invasive phe

75 rophthalmia-associated transcription factor (MITF) is a key regulator of melanocyte development and a

76 rophthalmia-associated transcription factor (MITF) is a master regulator of melanocyte development an

77 rophthalmia-associated transcription factor (MITF) is required for terminal osteoclast differentiatio

78 rophthalmia-associated transcription factor (MITF) is the master regulator of the melanocyte lineage.

79 e impact of melanocyte transcription factor (MITF) on melanoma development.

80 rophthalmia-associated transcription factor (MITF) plays a critical and complex role in melanocyte tr

81 Microphthalmia transcription factor (MITF) regulates the development, number, and function of

82 rophthalmia-associated transcription factor (MITF) target genes were found to be up-regulated.

83 rophthalmia-associated transcription factor (MITF) that regulate melanosome transport and neural-cres

84 rovoked microphthalmia transcription factor (MITF) translocation to the nucleus, and knockdown of MIT

85 rophthalmia-associated transcription factor (MITF) was first isolated, MITF has emerged as a key coor

86 rophthalmia-associated transcription factor (MITF) were higher in the P-MSCs compared to the PDL-MSCs

87 rophthalmia-associated transcription factor (MITF), along with its melanocyte lineage program, and wi

88 rophthalmia-associated transcription factor (MITF), and subsequent reductions in tyrosinase and other

89 rophthalmia-associated transcription factor (MITF), and ultimately the loss of a key redox effector,

90 rophthalmia-associated transcription factor (MITF), confirmed the functionality of the delivered mRNA

91 rophthalmia-associated transcription factor (MITF), sex-determining region Y-box 10, vimentin protein

92 he melanocyte-inducing transcription factor (MITF)-low melanoma transcriptional signature is predicti

93 on by RNAPII at master transcription factor (MITF)-regulated endolysosomal vesicle genes.

94 rophthalmia-associated transcription factor (MITF).

95 ify that a combination of the three factors, MITF, SOX10 and PAX3, directly converts mouse and human

96 Like all transcription factors, MITF binds to specific DNA sequences and up-regulates or

97 eterogeneity contribute to poor outcomes for MITF-low melanoma patients and that MITF-independent sub

98 esaturase (SCD) and that SCD is required for MITF(High) melanoma cell proliferation.

99 lly, transactivation of GMPR is required for MITF-dependent suppression of melanoma cell invasion, tu

100 esponses and point toward a crucial role for MITF in driving part of the ATM phenotype.

101 mutant alleles and hence suggests a role for MITF in regulating processes such as optic-fissure closu

102 Testing for MITF p.E318K should not exclude patients with known muta

103 mors for ETV6 and 45 basal breast tumors for MITF and confirm that the corresponding protein expressi

104 id cell-directed therapies may be useful for MITF(low)/c-Jun(high) melanomas to counteract their grow

105 h the Ap4A-triggered HINT1 dissociation from MITF.

106 -stimulated cytokine expression with further MITF suppression.

107 epressed the melanocyte differentiation gene MITF and the proapoptotic factor SOX9, thereby preventin

108 The gene MITF variant p.E318K also predisposes to melanoma and re

109 cells showed a dedifferentiated c-Jun(high)/MITF(low) phenotype, possibly associated with immunosupp

110 thout translation reprogramming an ATF4-high/MITF-low state is insufficient to drive invasion.

111 le that manipulation of the LysRS-Ap4A-HINT1-MITF signalling pathway in melanoma through post-transla

112 e-to-invasive phenotype switch, although how MITF promotes proliferation and suppresses invasion is p

113 ever, how MITF is suppressed in vivo and how MITF-low cells in tumors escape senescence are poorly un

114 ubset of individuals with colobomas, but how MITF functions during CF closure is unknown.

115 However, how MITF is suppressed in vivo and how MITF-low cells in tum

116 To understand how MITF regulates transcription, we used tandem affinity pu

117 Human MITF is, by convention, called the "microphthalmia-assoc

118 MITF-low zebrafish melanomas resembled human MITF-low melanomas and were enriched for stem and invasi

119 In cell lines with a hypermethylated MITF-pathway, overexpression of MITF did not alter the e

120 beta-catenin and Akt-NF-kappaB converging in MITF-M, the master regulator of melanomagenesis, were in

121 MITF knockdown increased PTX3 expression in MITF(high) proliferative and poorly invasive cells.

122 Because mutations in MITF are causative of Waardenburg syndrome type 2 (WS2),

123 mouse genetic studies; however, mutations in MITF have never been associated with microphthalmia in h

124 accounts mostly for the above phenotypes in MITF-depleted cells.

125 in vemurafenib-resistant biopsies, including MITF-high and -low clones in a relapsed patient.

126 the miRNA-539-3p/USP13 signaling to increase MITF protein degradation through a reduction of de-ubiqu

127 lation treatment of these cell lines induced MITF-pathway activity, confirming that gene regulation w

128 Consistently, inflammatory MITF(low)/c-Jun(high) syngeneic mouse melanomas recruit

129 ate MITF transcriptional activity, inhibited MITF interactions with FUS and BRG1 in a p38 MAPK phosph

130 h (CDKN2A, CDK4, and BAP1) and intermediate (MITF) susceptibility genes; statistical effect of histol

131 noma cells displaying a mesenchymal invasive MITF(low) phenotype.

132 nvironment induces switches between invasive/MITF(LO) versus proliferative/MITF(HI) states.

133 RNA-seq analyses showed that MITF A isoform (MITF-A) was consistently highly expressed in angiomyolip

134 nscription factor (MITF) was first isolated, MITF has emerged as a key coordinator of many aspects of

135 omyolipoma cell line 621-101, MITF knockout (MITF.KO) and MITF-A overexpressing (MITF.OE) cell lines

136 n metastatic melanoma tumors and cell lines, MITF positively correlates with the expression of lysoso

137 Our data uncover novel mechanisms linking MITF-dependent inhibition of invasion to suppression of

138 Four other loci (MITF, CCND1, MX2, and PLA2G6) were also significantly as

139 Our results demonstrate that a low MITF/AXL ratio predicts early resistance to multiple tar

140 ription factor also contained cells with low MITF and elevated levels of the AXL kinase.

141 pression, which contrasted with a c-Jun(low)/MITF(high) phenotype of T cell-edited tumor cells derive

142 nd innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differen

143 We then manipulated MITF RNA and protein levels at early developmental stage

144 he activity of the melanocyte lineage marker MITF in melanoma, thereby reducing the expression of pig

145 What marks MITF as being remarkable among its peers is the sheer ra

146 low-DNA-binding-affinity acetylation-mimetic MITF mutation supports melanocyte development and drives

147 h genetic models with low activity of Mitfa (MITF-low) and established that the MITF-low state is cau

148 Furthermore, mitochondrial MITF regulates PDH activity.

149 The association of mitochondrial MITF with PDH emerges as an important regulator of mast

150 lly seen in individuals carrying monoallelic MITF mutations.

151 Moreover, MITF controls c-MYC implicated in general transcription

152 to combat resistance of BRAF and NRAS mutant MITF-low melanomas.

153 MITF-independent cells) with very low-to-no MITF activity or protein.

154 mice, which coincided with increased nuclear MITF localization and Gpnmb transcription.

155 d by DW-F5, leading to complete abolition of MITF-M.

156 expression, and transcriptional activity of MITF.

157 well as decreased expression and activity of MITF.

158 Transcriptomic analysis of MITF-independent residual disease showed enrichment of m

159 The dichotomous behaviour of MITF in drug response is corroborated in vemurafenib-res

160 Binding of MITF to the BPTF promoter was demonstrated using ChIP an

161 xome sequence(WES)-based characterization of MITF(E318K) risk for various cancers in sporadic samples

162 Combinations of MITF, SOX10, TFAP2A, and YY1 bind between two BRG1-occup

163 Direct transcriptional control of MITF by p300-dependent histone acetylation within proxim

164 lts demonstrate that FUS is a coregulator of MITF activity and provide new insights into how the RANK

165 Depletion of MITF in melanoma cells and melanocytes attenuates the re

166 through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CA

167 report for the first time that depletion of MITF results in elevation of intracellular GTP levels an

168 nset and further promoted the development of MITF-high nodular growth melanomas.

169 , loss of GMPR accompanies downregulation of MITF in vemurafenib-resistant BRAF(V600E)-melanoma cells

170 Accordingly, downregulation of MITF induces invasion in melanoma cells; however, little

171 BRG1 also regulates the dynamics of MITF genomic occupancy.

172 We found minimal evidence of MITF(E318K)'s contribution to non-melanoma cancer risk a

173 In contrast, forced expression of MITF in melanoma and colon cancer cells inhibited EGFR a

174 that melanoma cells favor the expression of MITF mRNA with a shorter 3'-UTR.

175 wed that the activation of the expression of MITF target genes was higher following transfection with

176 sion data, we found that hypermethylation of MITF and its co-regulated differentiation pathway genes

177 Induction of MITF and depletion of COX2 and PGE2 were also observed i

178 nstrated direct transcriptional influence of MITF on PEDF, establishing the PEDF gene (SERPINF1) as a

179 Genetic inhibition of MITF activity led to rapid regression; recurrence occurr

180 anslocation to the nucleus, and knockdown of MITF by short hairpin RNA indicated its absolute require

181 d highlight key areas where our knowledge of MITF regulation and function is limited.

182 Here we show that the lack of MITF is associated with more severe resistance to a rang

183 to the expression of roughly equal levels of MITF, primarily localized in the nucleus.

184 in melanoma cells expressing high levels of MITF.

185 Furthermore, mitochondrial localization of MITF and its effect on PDH activity were determined.

186 Localization of MITF to the mitochondria and its interaction with mitoch

187 bition triggered cytoplasmic localization of MITF, decreasing PGC1alpha expression and inhibiting OxP

188 sidual disease that was resistant to loss of MITF activity (termed MITF-independent cells) with very

189 l crest and depends on mitfa, an ortholog of MITF, a key regulator of melanocyte development that is

190 nous GPNMB expression upon overexpression of MITF and HINT1 as well as promoter reporter assays using

191 ermethylated MITF-pathway, overexpression of MITF did not alter the expression level or methylation s

192 Furthermore, overexpression of MITF in hNCPCs(V600E) dramatically increased their tumor

193 ced autophagy, whereas the overexpression of MITF in melanoma cells increases the number of autophago

194 Overexpression of MITF resulted in up-regulation of BPTF in a panel of mel

195 plex that is regulated by phosphorylation of MITF at Ser-307 by p38 MAPK during osteoclast differenti

196 invasive cells but not in the population of MITF(high) differentiated melanoma cells.

197 production was observed in the population of MITF(low) invasive cells but not in the population of MI

198 To date, the prevalence of MITF p.E318K and its clinical and phenotypical implicati

199 ecurrence occurred following reactivation of MITF.

200 an important mechanism for the regulation of MITF in melanocytes and malignant melanomas.

201 shRNA-mediated down-regulation of MITF in melanoma cells was accompanied by down-regulatio

202 kinase 5 (Cdk5) is an essential regulator of MITF and PAX3.

203 g the normal and pathophysiological roles of MITF and related transcription factors may provide impor

204 NRPCs), to investigate the earliest roles of MITF.

205 and SOX10 actively recruit BRG1 to a set of MITF-associated regulatory elements (MAREs) at active en

206 get sites, resulting in the stabilization of MITF transcripts, elevated expression, and transcription

207 The crystal structure of MITF bound to the CLEAR-box reveals how the palindromic

208 and therapeutic target in a subpopulation of MITF(low) invasive and/or refractory melanoma.

209 iation toward a retinal lineage, a subset of MITF isoforms was expressed in a sequence and tissue dis

210 Furthermore, sumoylation of MITF at Lys-316, known to negatively regulate MITF trans

211 s TNF-alpha instigate gradual suppression of MITF expression through c-Jun.

212 gh activation of BCL2, a canonical target of MITF signaling.

213 Although several downstream targets of MITF action have been identified, the precise mechanisms

214 Directly comparing the transcriptomes of MITF versus TEN1-ICD-overexpressing BS149 cells revealed

215 icle we present our current understanding of MITF's role and regulation in development and disease, a

216 is induced by PAX3-mediated upregulation of MITF.

217 in melanoma, directly binds to the 3'-UTR of MITF mRNA, and prevents the binding of miR-340 to its ta

218 eneurin-1 ICD binds HINT1, thus switching on MITF-dependent transcription of GPNMB.

219 actors, which includes the melanoma oncogene MITF (micropthalmia-associated transcription factor) and

220 affect the activity of the melanoma oncogene MITF.

221 nd discovered the melanoma survival oncogene MITF as a driver of an early non-mutational and reversib

222 using the melanoma lineage survival oncogene MITF as a model, we show that low-affinity binding sites

223 of the melanocyte-lineage survival oncogene MITF, highlighting a new role for PARP1 in melanomagenes

224 rosinase, dopachrome tautomerase, Pmel17, or MITF mRNA levels.

225 nockout (MITF.KO) and MITF-A overexpressing (MITF.OE) cell lines were generated.

226 box M1 (FOXM1) as a key effector of the p300-MITF axis driving cell growth that is selectively activa

227 e data confirm the critical role of the p300-MITF-FOXM1 axis in melanoma and support p300 as a promis

228 ity of the master regulator of pigmentation, MITF, and its downstream targets may be regulated by hyp

229 tween invasive/MITF(LO) versus proliferative/MITF(HI) states.

230 s confirmed that these modifications promote MITF transcriptional and oncogenic activity in melanoma

231 In human PDA cells, the MiT/TFE proteins--MITF, TFE3 and TFEB--are decoupled from regulatory mecha

232 s of the BPTF promoter identified a putative MITF-binding site, suggesting that MITF may regulate BPT

233 Recently, MITF was shown to be mutated in a subset of individuals

234 ITF at Lys-316, known to negatively regulate MITF transcriptional activity, inhibited MITF interactio

235 d by the melanocyte lineage master regulator MITF.

236 ell immunotherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation i

237 Importantly, CYR61 overexpression rescued MITF.KO cell growth in vitro and tumor growth in vivo.

238 Both in primary and acquired resistance, MITF levels inversely correlate with the expression of s

239 Restoring MITF can reverse AR-enhanced melanoma cell invasion.

240 Single-cell RNA sequencing revealed MITF-independent residual disease was heterogeneous depe

241 In addition to melanoma risk, MITF p.E318K is associated with a high nevi count and co

242 Since MITF also induces pigmentation, we hypothesize that macr

243 tive variants in different SHL genes (SOX10, MITF, PTPN11, CHD7, and KMT2D) in five (4.9%) probands.

244 dependence of TFIIH-CAK on sequence-specific MITF and c-MYC constitutes a previously unrecognized mec

245 al. (2016) report that nelfinavir suppresses MITF expression induced by MAPK pathway inhibition in me

246 romic nature of this motif induces symmetric MITF homodimer binding.

247 significant because they show that targeting MITF activity is a potent antitumor mechanism, but also

248 s resistant to loss of MITF activity (termed MITF-independent cells) with very low-to-no MITF activit

249 he methyltransferase G9a repress a TFEB/TFE3/MITF-independent transcriptional program that promotes a

250 ced short palindromic repeats-generated TFEB/MITF/TFE3/TFEC single, double, and triple knockout cell

251 mental or polygenic risk factors rather than MITF(E318K).

252 omes for MITF-low melanoma patients and that MITF-independent subpopulations are an important therape

253 Here we report that MITF expression levels correlated with the expression of

254 Our results reveal that MITF is a lineage-specific regulator of metabolic reprog

255 Functional studies revealed that MITF depletion activated EGFR signaling and consequently

256 Here we show that MITF binds the CLEAR-box element in the promoters of lys

257 We show that MITF interacts with a PBAF chromatin remodelling complex

258 Here, we show that MITF is a lineage-restricted activator of the key lipoge

259 These results show that MITF is a major downstream target of p300 in human melan

260 n addition, for the first time, we show that MITF is partially located in the mitochondria and intera

261 RNA-seq analyses showed that MITF A isoform (MITF-A) was consistently highly expresse

262 Our results suggest that MITF and the related factors TFEB and TFE3 have separate

263 These findings suggest that MITF-A is a transcriptional oncogenic driver of angiomyo

264 putative MITF-binding site, suggesting that MITF may regulate BPTF expression.

265 The MITF transcription factor is a master regulator of melan

266 The MITF(E318K) variant confers moderate risk for cutaneous

267 The MITF-low/AXL-high/drug-resistance phenotype is common am

268 results reported as odds ratio (95% CI), the MITF p.E318K was associated with an increased melanoma r

269 In addition, we found that promoters for the MITF-A, -D and -H isoforms were directly targeted by Vis

270 AXL and suppresses senescence to impose the MITF-low/AXL-high drug-resistant phenotype observed in h

271 ased in the MITF.OE cells and reduced in the MITF.KO cells, and luciferase assays showed this was due

272 R61) expression levels were increased in the MITF.OE cells and reduced in the MITF.KO cells, and luci

273 L was upregulated, leading to a shift in the MITF/AXL balance.

274 es melanoma cell invasion via modulating the MITF-AXL signals via altering the miRNA-539-3p/USP13 sig

275 Targeted genomic deletion (<7 bp) of the MITF motif within the MET enhancer suppressed inducible

276 mong the 531 patients, the prevalence of the MITF p.E318K variant was calculated among the different

277 The genetic results of the MITF p.E318K variant were correlated with clinical and p

278 xpression level or methylation status of the MITF pathway genes.

279 t tumors characterized by high levels of the MITF transcription factor also contained cells with low

280 f miRNA biogenesis through alteration of the MITF-DICER pathway.

281 lopment and disease, as well as those of the MITF-related factors TFEB and TFE3, and highlight key ar

282 nteracts with two of its target sites on the MITF 3'-UTR, causing mRNA degradation as well as decreas

283 Significantly, the MITF-SCD axis suppresses metastasis, inflammatory signal

284 We also show that the MITF protein was stabilized by Wnt signaling, through th

285 pitation Sequencing analysis showed that the MITF-A transcriptional start site was highly enriched wi

286 of Mitfa (MITF-low) and established that the MITF-low state is causal of melanoma progression and a p

287 eening recommendations for patients with the MITF(E318K) variant.

288 Thus, MITF ensures the rapid resumption of transcription after

289 FUS was recruited to MITF target gene promoters Acp5 and Ctsk during osteocla

290 is required because low levels of wild-type MITF activity are oncogenic.

291 tastasis via altering the miRNA-539-3p/USP13/MITF/AXL signal and targeting this newly identified sign

292 levels of beta-catenin-regulated genes VIM, MITF-M, melan A, and TYRP1 (a tyrosinase family member c

293 ast cell exocytosis and to determine whether MITF is localized in the mitochondria and involved in re

294 identified, the precise mechanisms by which MITF promotes melanocytic tumor progression are incomple

295 ene of which is frequently co-amplified with MITF, highlights a new cell-type-specific therapeutic vu

296 a Unit of Hospital Clinic of Barcelona, with MITF p.E318K genotyped in all patients using TaqMan prob

297 Our data show that SOX10 cooperates with MITF to facilitate BRG1 binding to distal enhancers of m

298 sms underlying colobomas in individuals with MITF mutations and identify a novel role for Mitf functi

299 PDH interaction with MITF was measured before and after immunologic activatio

300 nduced by Mitf by physical interference with MITF transcriptional activity.