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 knockdown decreased miR-204/211 expression and caus

8 MITF mRNA levels do not change significantly with KIT si

9 MITF overexpression resulted in direct transcriptional a

10 MITF positively correlated with PEDF expression in invas

11 MITF protein levels vary between and within clinical spe

12 MITF stabilization caused an increase in multivesicular

13 MITF transcriptional activity is inhibited by the histid

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

15 K, and Smad1/5/8 and the expression of PU.1, MITF, c-Fos, and NFATc1, suggesting that Tak1 regulates

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

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

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

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

20 Accordingly MITF reconstitution enhances KIT expression levels in 3B

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

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

23 siRNA against MITF as well as against FoxO3a protected cells from apop

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

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

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

27 C/EBPalpha and MITF silenced each other's transcription in a directly a

28 ing two downstream molecules: C/EBPalpha and MITF.

29 factor for specifying basophil cell fate and MITF as the crucial transcription factor for specifying

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

31 etween 2 critical mast cell factors, KIT and MITF, mediated by miRNAs; dysregulation of this pathway

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

33 esistance, including c-FOS, NR4A1, NR4A2 and MITF.

34 nelfinavir as potent suppressor of PAX3 and MITF expression.

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

36 relationship between expression of Slug and MITF, a transcription factor known to regulate Slug expr

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

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

39 ranslocation kidney cancers (TFE3, TFEB, and MITF), chromophobe kidney cancer (5%), and oncocytoma (5

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

41 melanocyte-related cells (expressing TYR and MITF RNA) may circulate in healthy controls, although th

42 trols had uniformly higher levels of TYR and MITF than melanoma patients (p<0.0001).

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

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

45 f targeting MITF in vivo are unknown because MITF levels have not been directly tested in a genetic a

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

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

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

49 Both MITF and USF1 were activated by glycogen synthase kinase

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

51 Mnt binding and transcriptional induction by MITF and USF1, as well as FoxO.

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

53 Downstream of beta-catenin MITF not only suppresses the Rho-GTPase-regulated cell m

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

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

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

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

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

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

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

61 importance of the recently discovered E318K MITF germline mutation in patients with multiple primary

62 h mutant to conditionally control endogenous MITF activity.

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

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

65 arget of BRAF, the melanocyte lineage factor MITF, directly regulates the expression of PGC1alpha.

66 te eye development, the transcription factor MITF acts to promote the development of the retinal pigm

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

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

69 e lineage-specification transcription factor MITF drives PGC1alpha (PPARGC1A) overexpression in a sub

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

71 rophthalmia-associated transcription factor (MITF) and other genes required for melanocyte differenti

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

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

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

75 rophthalmia-associated transcription factor (MITF) down-regulation.

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

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

78 rophthalmia-associated transcription factor (MITF) is a basic helix-loop-helix leucine zipper protein

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

80 rophthalmia-associated transcription factor (MITF) is a key regulator of RPE differentiation that was

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

82 rophthalmia-associated transcription factor (MITF) is a master regulator of pigmented cell survival a

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

84 rophthalmia-associated transcription factor (MITF) is the "master melanocyte transcription factor" wi

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

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

87 rophthalmia-associated transcription factor (MITF) pathway, clinical efficacy of BRAF-targeted small

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

89 rophthalmia-associated transcription factor (MITF) regulates normal melanocyte development and is als

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

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

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

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

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

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

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

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

98 rophthalmia-associated transcription factor (MITF), is highly expressed in bone marrow biopsies from

99 rophthalmia-associated transcription factor (MITF), known to induce ITGA4 expression.

100 rophthalmia-associated transcription factor (MITF).

101 rophthalmia-associated transcription factor (MITF).

102 rophthalmia associated transcription factor (MITF).

103 rophthalmia-associated transcription factor (MITF).

104 rophthalmia-associated transcription factor (MITF).

105 he melanocyte-specific transcription factor, MITF, mediates this enhancer function.

106 rophthalmia-associated transcription factor, MITF, to drive cells to a more stem cell-like and invasi

107 almia (MiT) family of transcription factors (MITF, TFE3, TFEB, and TFEC) are physiologic regulators o

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

109 a potential survival advantage mechanism for MITF amplification in metastatic melanoma and offers a s

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

111 3 (USP13) that appears to be responsible for MITF deubiquitination, utilizing a short hairpin RNA lib

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

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

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

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

116 h the Ap4A-triggered HINT1 dissociation from MITF.

117 -stimulated cytokine expression with further MITF suppression.

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

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

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

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

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

123 How MITF functions in melanoma development and the effects o

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

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

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

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

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

129 These studies identify MITF-BCL2A1 as a lineage-specific oncogenic pathway in m

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

131 of alanine 73 leads to greater increases in MITF protein levels, melanoblast and melanocyte numbers,

132 ittle is known about the enzymes involved in MITF ubiquitination/deubiquitination.

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

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

135 However, homozygous mutations in MITF have not been identified in humans; therefore, litt

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

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

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

139 ant melanoma cells, MEK inhibition increased MITF expression, which in turn elevated levels of PGC1al

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

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

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

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

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

145 work provides a foundation for investigating MITF and other highly complex, multi-purposed transcript

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

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

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

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

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

151 , exerting antagonistic activities against M-MITF to control melanoma cell invasiveness.

152 s underlying both TGF-beta and GLI2-driven M-MITF gene repression.

153 e melanocyte-specific transcription factor M-MITF is involved in numerous aspects of melanoblast line

154 ently binds and suppresses the promoter of M-MITF (melanocyte-restricted MITF isoform).

155 that was rescued by ectopic expression of M-MITF in vitro.

156 is, however, not needed for inhibition of M-MITF promoter activity by TGF-beta.

157 cule prolyl-hydroxylase inhibitors reduced M-MITF expression, leading to melanoma cell growth arrest

158 ription, allowed maximal inhibition of the M-MITF promoter via two distinct mechanisms.

159 ng site within the -334/-296 region of the M-MITF promoter, critical for GLI2-driven transcriptional

160 ls and CREB-dependent transcription of the M-MITF promoter.

161 poxia response in pigment cells leading to M-MITF suppression, one that suggests a potential survival

162 ansient cell transfection experiments with M-MITF promoter constructs, chromatin immunoprecipitation,

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

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

165 i-67), and partial retention of RPE markers (MITF, cytokeratin, and CRALBP).

166 Furthermore, mitochondrial MITF regulates PDH activity.

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

168 ), and 4 melanocyte target RNAs (TYR, MLANA, MITF, and MIF) were quantified using QPCR.

169 lly seen in individuals carrying monoallelic MITF mutations.

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

171 gression because the human melanoma mutation MITF(4T)(Delta)(2B) promotes increased and serial differ

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

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

174 expression, and transcriptional activity of MITF.

175 well as decreased expression and activity of MITF.

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

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

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

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

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

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

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

183 BRG1 also regulates the dynamics of MITF genomic occupancy.

184 nt synthesis by increasing the expression of MITF (microphthalmia transcription factor) and TYR (tyro

185 USP13 was observed to modulate expression of MITF downstream target genes and, thereby, to be essenti

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

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

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

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

190 RAB7 levels and function were independent of MITF, the best-characterized melanocyte lineage-specific

191 a blocks the alpha-MSH-mediated induction of MITF and melanogenic genes.

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

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

194 olony-forming units with sh-RNA knockdown of MITF.

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

196 BRAF/MAPK pathway have suppressed levels of MITF and PGC1alpha and decreased oxidative metabolism.

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

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

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

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

201 through knockdown) leads to dramatic loss of MITF protein, but not messenger RNA.

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

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

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

205 Importantly, overexpression of MITF in invasive colon cancer cells modifies beta-cateni

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

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

208 summary, the cell-type-specific presence of MITF in melanoma affects beta-catenin's pro-invasive pro

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

210 first, Lister et al. reveal in vivo proof of MITF directly regulating tumor development in BRAF(V600E

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

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

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

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

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

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

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

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

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

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

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

222 expression correlates strongly with that of MITF in human melanoma cell lines and biopsy specimens.

223 as accompanied by increased transcription of MITF (microphthalmia-associated transcription factor) an

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

225 Significantly, co-transfection of MITF siRNA with pre-miR-204/211 rescued RPE phenotype.

226 is induced by PAX3-mediated upregulation of MITF.

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

228 Through its effects on MITF deubiquitination, USP13 was observed to modulate ex

229 ich based on in vitro experiments imparts on MITF an increased transcriptional activity paired with a

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

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

232 scriptional control by the melanoma oncogene MITF.

233 affect the activity of the melanoma oncogene MITF.

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

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

236 ession of BCL2A1 in melanomas with BCL2A1 or MITF amplification.

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

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

239 ctive KIT does not restore growth of primary MITF-deficient mast cells.

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

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

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

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

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

245 how that KIT signaling markedly up-regulates MITF protein.

246 d by the melanocyte lineage master regulator MITF.

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

248 egulated by KIT signaling and they repressed MITF expression through conserved miRNA binding sites in

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

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

251 he promoter of M-MITF (melanocyte-restricted MITF isoform).

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

253 ylation and differentially regulated several MITF targets.

254 Since MITF also induces pigmentation, we hypothesize that macr

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

256 nd histone-deacetylase inhibitors suppressed MITF expression and cAMP-mediated resistance.

257 Forced expression of these miRNAs suppressed MITF protein and inhibited colony-forming capacity of ma

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

259 oma development and the effects of targeting MITF in vivo are unknown because MITF levels have not be

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

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

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

263 We demonstrate that MITF is required for the proliferative phenotype by inhi

264 These data indicate that MITF is a melanoma-predisposition gene and highlight the

265 We have observed that MITF expression is potently reduced under hypoxic condit

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

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

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

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

270 Functional analysis of E318K showed that MITF encoded by the variant allele had impaired sumoylat

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

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

273 The PGC-1s in turn activate the MITF promoter, and their expression correlates strongly

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

275 This study defines the MITF/miR-211 axis that inhibits the invasive program by

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

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

278 through conserved miRNA binding sites in the MITF 3'-untranslated region.

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

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

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

282 all-molecule strategy for suppression of the MITF oncogene in vivo.

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

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

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

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

287 elective activation of TFEB, a member of the MITF/TFE family of transcription factors.

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

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

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

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

292 uitination, USP13 stabilizes and upregulates MITF protein levels.

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

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

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

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

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

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

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

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