ライフサイエンスコーパス: GLI1

1 letions that fuse the promoter of INHBE with GLI1.

2 , SOX9, AMH, CYP17A1, LIN28, WNT2B, ETV5 and GLI1.

3 erived Hedgehog signals, become positive for GLI1.

4 inhibits ciliary PKA activity, and increases Gli1.

5 sed K48-linked ubiquitination/degradation of GLI1.

6 this HHIP putative enhancer requires intact GLI1.

7 isms, all triggering the downstream effector Gli1.

8 moothened (Smo) and the transcription factor Gli1.

9 by genetic or pharmacological inhibition of Gli1.

10 known to underlie the oncogenic function of GLI1.

11 cells relative to that of CLL cells without GLI1.

12 on and enhanced sensitivity to inhibition of GLI1.

13 Treatment with GANT61, a GLI1/2 inhibitor, but not with IPI 926, a Smoothened inh

14 re not able to give rise to eRMS upon Smo or Gli1/2 overactivation in vivo, suggesting that Hh-induce

15 We also identified that GLI1, a candidate stem cell-associated gene, is signific

16 roteins bind to and suppress the promoter of GLI1, a critical mediator of progesterone action in the

17 dent editing and transcriptional activity of GLI1, a Hedgehog (Hh) pathway transcriptional activator

18 ow that the zinc-finger transcription factor GLI1, a terminal effector of the Hedgehog (Hh) pathway,

19 tem cells, identified by their expression of Gli1, a transcriptional effector of the sonic hedgehog p

20 of MDS we demonstrated that constitutive Hh/Gli1 activation accelerated leukemic transformation and

21 Our data suggest that GLI1 activation is frequent in MDS during disease progre

22 Hh/Gli1 activation resulted in clonal expansion of phenotyp

23 self-renewal pathways, operating via direct Gli1 activation.

24 -committed REST(TG) cells also had decreased GLI1 activity and increased histone H3K9 methylation at

25 le binding to Gli1 zinc finger and impairing Gli1 activity by interfering with its interaction with D

26 sistance pathway that amplifies noncanonical Gli1 activity, but characteristics and drivers of the nM

27 nsequence of its robust inhibitory effect on Gli1 activity, Glabrescione B inhibited the growth of He

28 cal Hedgehog signaling, a known regulator of Gli1 activity, is required for pancreas recovery.

29 ibroblast-specific deletion of Gli2, but not Gli1, also limited kidney fibrosis, and induction of myo

30 in the downstream transcriptional activator GLI1 and a decrease in the GLI3 transcriptional represso

31 l effect of IKBKE involves the activation of GLI1 and AKT signaling and is independent of the levels

32 Here we show that GLI1 and an active mutant of GLI2 (DeltaNGLI2) promote a

33 analysis confirmed significant inhibition of GLI1 and c-MYC protein expression in DAOY and HD-MB03 ce

34 lies having biallelic truncating variants in GLI1 and developmental defects overlapping with Ellis-va

35 ate that SMARCA2 endogenously interacts with GLI1 and enhances its transcriptional activity.

36 gehog (Hh) pathway transcriptional effectors GLI1 and GLI2 are expressed in myofibroblast progenitors

37 Gli1 and Gli2 bound to the promoter and repressed ANO1 t

38 Finally, we identified that Gli1 and Gli2 exhibited different functions in the regul

39 We conclude that Gli1 and Gli2 repress ANO1 by a novel mechanism that is

40 Knockdown of GLI1 and GLI2 restored sensitivity to vemurafenib-resist

41 Finally, GLI1 and GLI2 were upregulated in the kidneys of patient

42 f the activators of this family of proteins (Gli1 and Gli2) inhibited the proliferation of p63(+) and

43 g the abundance of the transcription factors GLI1 and GLI3.

44 AA-induced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activ

45 IVD of IFT80(fl/fl) ; Col2-creERT mice, and Gli1 and Patch1 expression in the OAF of IFT80(fl/fl) ;

46 edgehog (Hh) signaling components, including Gli1 and Patch1 in the IVD of IFT80(fl/fl) ; Col2-creERT

47 The expression of the direct Hh targets, Gli1 and Patched 1, is inhibited, while the expression o

48 terozygosity of Ptc1, despite high levels of Gli1 and phosphorylated Stat3.

49 Furthermore, co-inhibition of GLI1 and PI3K induced apoptosis of hematopoietic stem/pr

50 K gene PIK3CA was attenuated by antagonizing GLI1 and PI3K.

51 dgehog signaling, using the pathway readouts Gli1 and Ptch1 as a model system.

52 ular chondrocytes such that the induction of GLI1 and PTCH1 expression is reduced by 71 and 55%, resp

53 uccessfully predicting expression changes of Gli1 and Ptch1 in mutants at different developmental sta

54 ing protein) as a model, we demonstrate that GLI1 and SMARCA2 co-occupy a distal chromatin peak and t

55 erminal transcriptional activation domain of GLI1 and SMARCA2's central domains, including its ATPase

56 moted a GLI1-STAT3 interaction and increased GLI1 and STAT3 enrichment at the promoters of their targ

57 arly regulated by SULF2, dependent on intact GLI1 and STAT3 functions in HCC cells.

58 r GLI1 knockdown reduced promoter binding of GLI1 and STAT3, respectively.

59 fied a new transcriptional complex including GLI1 and the TGFbeta-regulated transcription factor, SMA

60 Furthermore, co-localization of GLI1(+) and MKX(+) cells is also found in human tendinop

61 f Hedgehog signaling pathway components Shh, Gli1, and Patched1 was greatly decreased in Wls(Shh-Cre)

62 ing single-cell RNA sequencing, we show that Gli1- and Ascl1-targeted cells have highly similar yet d

63 fy the Hedgehog pathway transcription factor GLI1 as a critical driver of lung SCC.

64 We identified the HH effector GLI1 as a target for dual PI3Kalpha and mTOR inhibition

65 aPKC functions to promote GLI1 association with LAP2alpha, promoting egress off th

66 scriptional repressor REST and the activator GLI1 at Ptch1 Expression of Arrb1, which encodes beta-ar

67 tes with key transcription factors including Gli1, Atoh1 and REST to regulate the expression of both

68 Moreover, in-activation of SHH/GLI1 axis also significantly restricted cell migration a

69 These findings suggest that targeting SHH/GLI1 axis alters expression of EMT markers and abrogates

70 as conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invas

71 showed that SHH signaling activated the SHH/GLI1/BCL-2 axis, leading to the inhibition of myeloma ce

72 We found that both GLI3 and GLI1 bind to the pluripotency factor NANOG.

73 is of the Bid promoter identified a putative Gli1 binding site, and further studies using luciferase

74 Falpha) mediated IKKbeta activation-impaired GLI1 binding with the E3 ubiquitin ligase-ITCH, leading

75 ation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecu

76 was ineffective, indicating that the role of Gli1 both in augmenting hedgehog signalling and in retar

77 mouse Gli1 gene, repressing the induction of Gli1 by SHH by binding to both GATA and Gli binding site

78 RNA oligonucleotide significantly decreased GLI1, c-myc, and CD44 mRNA levels, in a panel of colon a

79 geting of Gli proteins with GANT61 inhibited Gli1(+) cell expansion and myofibroblast differentiation

80 In addition, BMP signaling in the Gli1+ cell lineage is also required for the maintenance

81 e incisor after loss of BMP signaling in the Gli1+ cell lineage, indicating that BMP signaling is req

82 acing studies demonstrated that the original Gli1+ cell population had the capacity to heal immature

83 Genetic ablation of Gli1(+) cells abolished BMF and rescued bone marrow fail

84 Our data indicate that Gli1(+) cells are a major source of osteoblast-like cell

85 These findings implicate Gli1(+) cells as critical adventitial progenitors in vas

86 Genetic ablation of Gli1(+) cells before induction of kidney injury dramatic

87 Finally, postnatal Gli1(+) cells contribute to both chondrocytes and osteob

88 In vitro, Gli1(+) cells express typical MSC markers, exhibit trili

89 Here, we show that Gli1(+) cells located in the arterial adventitia are pro

90 in fetal or postnatal mice, we discover that Gli1(+) cells progressively produce osteoblasts in all s

91 s that tissue-resident, but not circulating, Gli1(+) cells proliferate after kidney, lung, liver, or

92 Most notably, in postnatal growing mice, the Gli1(+) cells residing immediately beneath the growth pl

93 Likewise, incisor Gli1(+) cells, but not NG2(+) cells, exhibit typical MSC

94 lation supporting mouse molar root growth as Gli1(+) cells.

95 To further examine the involvement of Gli1+ cells and hedgehog signaling in enthesis healing,

96 In summary, Gli1+ cells are the multipotential PDLSCs in vivo.

97 In contrast, injured mature entheses had few Gli1+ cells early in the healing process, with limited r

98 Here, we identified Gli1+ cells in adult mouse molar PDL as multi-potential

99 nce of these mutations and the expression of GLI1 (chi(2) test, P < .0001), reflecting activation of

100 ed mutations also were GLI1(+) Patients with GLI1(+) CLL cells had a shorter median treatment-free su

101 t can inhibit GLI1, was highly cytotoxic for GLI1(+) CLL cells relative to that of CLL cells without

102 Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulato

103 These findings provide insights into how GLI1 controls gene expression in cancer cells and may in

104 We performed studies with Gli1:Cre(ERT2);Rosa26:lox-STOP-lox-tdTomato mice.

105 Using bigenic Gli1-CreER(t2); R26tdTomato reporter mice, we observed i

106 Glioma-associated oncogene (Gli1)-CreERT2 and Patched (Ptch)-lacZ reporter mice were

107 We show that Gli1:CreERT2 marks both AMFs as well as ALFs, and lineag

108 IKKbeta-GLI1 crosstalk is significant because combined inhibitio

109 reviously shown that resistant BCCs increase GLI1 deacetylation through atypical protein kinase Ciota

110 SLFN4+ MDSCs were not observed in infected GLI1-deficient mice.

111 nts with homozygous C-terminal truncation of GLI1 demonstrated that the corresponding mutant GLI1 pro

112 r, these results indicate that SLFN4 marks a GLI1-dependent population of MDSCs that predict a shift

113 s using luciferase reporter assays confirmed Gli1-dependent promoter activity.

114 tification of the structural requirements of Gli1/DNA interaction highlights their relevance for phar

115 Using a Gli1-driven Cre-mediated recombination system, our resul

116 Here, we demonstrated that GLI2, but not GLI1, drives myofibroblast cell-cycle progression in cul

117 l knockdown in Hh-receiving cells (marked by Gli1+) during E8 to E10.5, a previously established mode

118 l knockdown in Hh-receiving cells (marked by Gli1+) during E8 to E10.5, a previously established mode

119 ith upregulation of the transcription factor GLI1 Ectopic expression of SHH or IHH in mouse T cells i

120 tingly, the SULF2 overexpression resulted in GLI1 enrichment at select STAT3 consensus sites, and vic

121 Notably, we observed that innervated Gli1-expressing progenitors within mechanosensory touch

122 t-induced and CRD-BP-dependent regulation of GLI1 expression and activities is important for the deve

123 er characterization showed that AA represses GLI1 expression by stimulating nuclear translocation of

124 In breast tumor tissues, GLI1 expression enhanced tissue identification and discr

125 erent Stat3 inhibitors reduced viability and Gli1 expression in ASZ001 cells but not in HaCaT cells.

126 ame pathway is also active in human BMF, and Gli1 expression in BMF significantly correlates with the

127 her Hedgehog pathway agonists did not affect GLI1 expression in lung SCC cells.

128 In eutopic endometrium, GLI1 expression is reduced in women with endometriosis.

129 and hedgehog signaling in enthesis healing, Gli1 expression was examined via lineage tracing approac

130 Moreover, Shh and Gli1 expression was increased in Tmem107(-/-) animals as

131 Furthermore, radiotherapy-induced GLI1 expression was mediated in part by the mTOR/S6K1 pa

132 However, GLI1 expression was modulated by either inhibition or ac

133 ure injured entheses retained high levels of Gli1 expression, a marker of hedgehog activation, consis

134 y bind to the GLI1 promoter, thus inhibiting GLI1 expression, and loss of ARP-T1 led to activation of

135 vels, but not those with low or undetectable GLI1 expression, were sensitive to hedgehog pathway inhi

136 of Stat3 in ASZ001 cells with IL-6 increased Gli1 expression.

137 e paralleled the domain of reduced Foxf2 and Gli1 expression.

138 erses the ability of GATA factors to repress Gli1 expression.

139 on of phosphorylated Stat3 and regulation of Gli1 expression.

140 he transcriptional activity of the truncated GLI1 factor was found to be severely impaired by cell cu

141 uctural requirements of the pathway effector Gli1 for binding to DNA and identify Glabrescione B as t

142 g to CSC renewal, and TGLI1 outcompetes with GLI1 for binding to target promoters.

143 tron regions of ROS1 target genes, CXCL1 and GLI1, for upregulating their expressions.

144 u, mediated by Fbxl17, allows the release of Gli1 from Sufu for proper Hh signal transduction.

145 anonical Gli-dependent Hedgehog signaling by Gli1 gene transfer is sufficient to recover salivary fun

146 ZFPM1) to the regulatory region of the mouse Gli1 gene, repressing the induction of Gli1 by SHH by bi

147 RNA levels of the GLI family zinc finger 1 (GLI1) gene (HH-pathway target gene) in biopsy specimens

148 HCA characterized by fusion of the INHBE and GLI1 genes and activation of sonic hedgehog pathway.

149 The transcription factor GLI1 (GLI family zinc finger 1) plays a key role in the

150 GLI1, GLI2 and GLI3 form a family of transcription facto

151 r of several important genes, including SHH, GLI1, GLI2, and PDGFA, previously linked to the maintena

152 ned agonist (SAG) increased levels of Ptch1, Gli1, Gli2, Gli3, Hes1 and Hes5, and stimulated the form

153 (controls), and searched for mutation(s) in GLI1, GLI2, GLI3, SUFU, and SOX10.

154 (CD24 and CD133), components of Shh pathway (Gli1, Gli2, Patched1/2, and Smoothened), Gli targets (Bc

155 ment of vemurafenib-resistant cells with the GLI1/GLI2 inhibitor Gant61 led to decreased invasion of

156 ased expression of the transcription factors GLI1/GLI2 was independent of canonical Hh signaling and

157 glioma-associated oncogene homolog 1 and 2 (GLI1/GLI2) compared with naive cells.

158 In contrast, loss-of-function mutations in GLI1 have remained elusive, maintaining enigmatic the ro

159 We saw increased Gli1 (hedgehog readout) in postnatal Six2creFrs2alphaKO

160 repair of demyelinated lesions by inhibiting Gli1, identifying a new therapeutic avenue for the treat

161 Indeed, inhibition of Gli1 improves the functional outcome in a relapsing/remi

162 tic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells.

163 Overexpression of GLI1 in AML cells led to increased AKT phosphorylation a

164 , we demonstrate that IKKbeta phosphorylates GLI1 in DLBCL.

165 Inhibition of GLI1 in human lung SCC cell lines suppressed tumor cell

166 By genetically demarcating cells expressing Gli1 in response to Hedgehog (Hh) signaling, we discover

167 ese progenitors acquire theca lineage marker Gli1 in response to paracrine signals Desert hedgehog (D

168 cription factor glioma-associated protein 1 (GLI1) in AA-treated cells is the underlying mechanism co

169 essing with Gli1-knockout mice revealed that Gli1 inactivation impairs SULF2-induced HCC.

170 We conclude that GLI1 inactivation is associated with a phenotypic spectr

171 However, mechanisms underlying GLI1-increased activity in DLBCL are poorly characterize

172 atients with CLL cells lacking expression of GLI1 independent of IGHV mutation status.

173 These results indicated that GLI1 inhibition alone, but not combined inhibition, is s

174 ed drug sensitivity, which was attenuated by GLI1 inhibition.

175 Interestingly, GANT61 (GLI1 inhibitor) exposure significantly reduced cell viab

176 on of Arrb1, which encodes beta-arrestin1 (a GLI1 inhibitor), was substantially reduced in proliferat

177 Inhibiting GLI1 interferes with rDNA DSB repair and impacts RNA pol

178 The GLI1(+) interstitial cells eventually develop into two c

179 GLI1 intranuclear trafficking by LAP2 isoforms represent

180 tion of the Hh effector transcription factor Gli1 is a poor prognostic factor in this disease setting

181 that in addition to canonical Hh signaling, GLI1 is activated in a Smoothened-independent manner.

182 We found that GLI1 is activated in triple-negative breast cancer cells

183 during disease progression and inhibition of GLI1 is an attractive therapeutic target for a subset of

184 Furthermore, Gli1 is upregulated, suggesting an ectopic activation of

185 ating or deleting these residues facilitated GLI1-ITCH interaction and decreased the protective effec

186 Here, we directly tested the role of Gli1(+) kidney pericytes in the maintenance of peritubul

187 GLI1 knockdown or inhibition with GANT61 resulted in dec

188 siRNA-mediated STAT3 or GLI1 knockdown reduced promoter binding of GLI1 and STAT

189 e chromatin with sequencing (ATAC-seq) after GLI1 knockdown supported these findings, revealing that

190 Interestingly, the Gli1 knockout abrogated SULF2-mediated induction of seve

191 A cross of the Sulf2-overexpressing with Gli1-knockout mice revealed that Gli1 inactivation impai

192 darinaparsin ameliorated fibrosis in WT and Gli1-KO mice, it was not effective in conditional Gli2-K

193 former response was verified by increases in Gli1-LacZ activity and Gli1 mRNA expression.

194 interfering RNA-mediated knockdown of SMO or GLI1 led to decreased cell proliferation.

195 ctivity, whereas IKKbeta silencing decreased GLI1 levels and transcriptional activity.

196 Stat3 phosphorylation and further increased Gli1 levels, in both an autocrine and paracrine manner.

197 ineage-tracing experiments revealed that the Gli1 lineage cells that originate in utero eventually po

198 Brd4 binding to the Gli1 locus is controlled by Casein Kinase 1delta (CK1 de

199 Thus Gli1 marks mesenchymal progenitors responsible for both

200 Here, we demonstrate that Gli1 marks perivascular MSC-like cells that substantiall

201 ategy that targets the PI3K-mTOR pathway and GLI1 may lead to effective outcomes for PI3K pathway-dep

202 rstanding the poorly elucidated mechanism of Gli1-mediated transcription allows to identify novel mol

203 The ectopic expression of NANOG inhibits GLI1-mediated transcriptional responses in a dose-depend

204 anscription factor GLI family zinc finger 1 (GLI1) mediates Sulf2 expression during HCC development.

205 es: Wt1(+) cells indigenous to the ovary and Gli1(+) mesenchymal cells that migrate from the mesoneph

206 ate tracing in two murine models of BMF that Gli1(+) mesenchymal stromal cells (MSCs) are recruited f

207 Here, we show that Gli1(+) mesenchymal stromal cells (MSCs), previously sho

208 that bone marrow myofibroblasts derive from Gli1(+) mesenchymal stromal cells and that a Gli inhibit

209 identified its downstream target as stromal GLI1+ mesenchymal stem cell-like cells.

210 l, arsenic trioxide and itraconazole reduced GLI1 messenger RNA levels by 75% from baseline (P < .001

211 Moreover, primary T-ALL cases with high GLI1 messenger RNA levels, but not those with low or und

212 Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor gr

213 nt nuclear chaperoning system that regulates GLI1 movement between the nuclear lamina and nucleoplasm

214 ified by increases in Gli1-LacZ activity and Gli1 mRNA expression.

215 ibitors that act by destabilizing the CRD-BP-GLI1 mRNA interaction.

216 the physical interaction between CRD-BP and GLI1 mRNA so as to find inhibitors for such interaction.

217 is of human lung cancer datasets showed that GLI1 mRNA was highly expressed in human lung SCC and por

218 abilization of glioma-associated oncogene 1 (GLI1) mRNA by coding region determinant binding protein

219 These findings implicate perivascular Gli1(+) MSC-like cells as a major cellular origin of org

220 etic fate tracing indicates that adventitial Gli1(+) MSC-like cells migrate into the media and neoint

221 During fibrotic repair, Gli1(+) MSCs integrate hedgehog activation signalling to

222 These findings show that Gli1(+) MSCs integrate hedgehog signalling as a rheostat

223 ssion by expression of the GLI3 repressor in GLI1+ myofibroblast progenitors limited kidney fibrosis.

224 By contrast, neither the expression of GLI1 nor apoptosis in response to Ara-C treatment of AML

225 urther analysis reveals that IKBKE regulates GLI1 nuclear translocation and promotes the reactivation

226 e developing molars showed changes in Runx2, Gli1, Numb, and Notch expression in the dental pulp cell

227 filing reveals transcriptional expression of GLI1, of Hedgehog (Hh) signaling, in poor-risk MDS/AML.

228 GLI1 oncogene has been implicated in the pathobiology of

229 expression is associated with an increase in GLI1 or GLI2 expression.

230 n-regulation of GLI transcriptional factors (GLI1 or GLI2), but not SMO signaling inhibition, reduces

231 ll-expressed genes GLI family zinc finger 1 (Gli1) or achaete-scute homolog 1 (Ascl1).

232 Interestingly, similar to SMARCA2, GLI1 overexpression increased chromatin accessibility, a

233 The previously unreported Msi2-Shh-Gli1 pathway adds to the growing understanding of the co

234 cases without identified mutations also were GLI1(+) Patients with GLI1(+) CLL cells had a shorter me

235 Alveolar bone osteocytes negatively regulate Gli1+ PDLSCs activity through sclerostin, a Wnt inhibito

236 Gli1+ PDLSCs are surrounding the neurovascular bundle an

237 mice, we observed increased distance between Gli1(+) pericytes and endothelial cells after AKI (mean+

238 l Stem Cell, Kramann et al. (2016) show that Gli1+ perivascular cells in the outermost vessel layer a

239 Interestingly, in this model, GLI1 played a tumor-protective function, where survival

240 neage-tracing studies of mice, we found that Gli1(+) PMCs are a subset of stromal cells characterized

241 Compared with stellate cells, Gli1(+) PMCs expressed a different subset of genes, incl

242 Lineage-traced Gli1(+) PMCs proliferated and acquired a myofibroblast p

243 broblast phenotype after cholestatic injury; Gli1(+) PMCs were found only surrounding the main duct o

244 Overexpression of Vimentin and Snail in SHH/GLI1 positive patients was also associated with poor ove

245 SHH/GLI1 positive samples demonstrated high expression of Sn

246 ates from a specific pool of hedgehog-active Gli1+ progenitor cells that differentiate and produce mi

247 ed that ectopic expression of TGLI1, but not GLI1, promoted preferential metastasis to the brain.

248 ranslocation of NFATc1, which then binds the GLI1 promoter and represses its transcription.

249 ARP-T1 was found to directly bind to the GLI1 promoter, thus inhibiting GLI1 expression, and loss

250 ibitor of Hh signal transduction by inducing GLI1 protein degradation in vitro and in vivo.

251 a novel Hh pathway component stabilizing the GLI1 protein in a demethylase-independent manner.

252 1 demonstrated that the corresponding mutant GLI1 protein is fabricated by patient cells and becomes

253 IKKbeta activation increased GLI1 protein levels and transcriptional activity, wherea

254 enesis (VEGFR2, p-ERK, p-PLCr1/2), hedgehog (Gli1, Ptch1, SMO), and mTOR (pS6K1) signaling pathways t

255 Finally, using the GLI1-regulated gene HHIP (Hedgehog-interacting protein)

256 lls revealed an unexpected mechanism whereby Gli1 regulates ATR-mediated Chk1 phosphorylation by tran

257 own supported these findings, revealing that GLI1 regulates chromatin accessibility at several region

258 light a key role for PI3K/mTOR signalling in GLI1 regulation in HH-driven cancers and suggest that co

259 ng root development in the AP and HERS using Gli1 reporter mice.

260 ation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxyge

261 Deletion of a single allele of Gli1 results in improper stromal remodeling and perduran

262 by genetic or pharmacological inhibition of GLI1, revealing a potential strategy to overcome drug re

263 The smallest region of GLI1 RNA binding to CRD-BP was mapped to nucleotides (nt

264 the two stem-loops are important for CRD-BP-GLI1 RNA binding.

265 rget region for the inhibition of the CRD-BP-GLI1 RNA interaction and Hedgehog signaling pathway.

266 was found to be effective in blocking CRD-BP-GLI1 RNA interaction.

267 istinct stem-loops present in nts 320-380 of GLI1 RNA, was found to be effective in blocking CRD-BP-G

268 d KH2 domain are critical for the binding of GLI1 RNA.

269 In this study, we found that a BMP-Smad4-SHH-Gli1 signaling network may provide a niche supporting tr

270 tive regulator of both FGFR and canonical Hh-GLI1 signaling, and additionally in the non-canonical re

271 new player in Epo induction and perivascular Gli1(+)SMA(+)PDGFRbeta(+) cells as a previously unrecogn

272 kidney, liver, and spleen in a population of Gli1(+)SMA(+)PDGFRbeta(+) cells, a signature shared with

273 dependent phosphorylation sites that mediate GLI1 stability.

274 creased the protective effect of TNFalpha on GLI1 stability.

275 SULF2 overexpression promoted a GLI1-STAT3 interaction and increased GLI1 and STAT3 enri

276 LF2 drives HCC by stimulating formation of a GLI1-STAT3 transcriptional complex.

277 2 promoter and are required for TGFbeta- and GLI1-stimulated gene expression.

278 r shrinkage, which may be owing to transient GLI1 suppression with sequential dosing.

279 ously, we identified schlafen 4 (Slfn4) as a GLI1 target gene and myeloid differentiation factor that

280 d their progeny, we identify a population of Gli1-targeted NSCs showing long-term self-renewal in the

281 her novel combinations of JAK2-STAT3 and SMO-GLI1/tGLI1 inhibitors synergistically target TNBC and HE

282 ns expressed higher levels of TGLI1, but not GLI1, than radiosensitive counterparts.

283 Our results demonstrate that Gli1 that is upregulated at the tumor-stroma intersectio

284 ses Sox2 expression through the mediation of Gli1, the Hedgehog pathway transcription factor.

285 itionally in the non-canonical regulation of GLI1 through pERK1/2.

286 guingly, loss of EPHA2 induces activation of GLI1 transcription factor and hedgehog signaling that fu

287 The GLI1 transcription factor must maintain maximal Hedgehog

288 ement binding protein that in turn represses gli1 transcription.

289 a mechanism regulated by the oncogenic SOX2-GLI1 transcriptional complex driving melanoma invasion t

290 Gli2, but not Gli1, transcriptionally regulated the expression levels

291 Gli1 was a marker of mesenchymal cells that surround the

292 Importantly, reduced expression of Shh and Gli1 was also observed in these mice, demonstrating dimi

293 significantly higher than in testis, whereas GLI1 was significantly higher in testis than ovaries.

294 at GANT61, a small molecule that can inhibit GLI1, was highly cytotoxic for GLI1(+) CLL cells relativ

295 chemical staining showed that TGLI1, but not GLI1, was increased in lymph node metastases compared to

296 mediated nuclear factor-kappaB activity with GLI1, we identified a crosstalk between these 2 pathways

297 Expression of PTCH1 and GLI1 were less, and ARRB1 was somewhat greater, in patie

298 plasmic LAP2alpha competes with LAP2beta for GLI1 while scaffolding HDAC1 to deacetylate the secondar

299 tc1) and its associated transcription factor Gli1 with genesis of specific neuronal progeny.

300 one B as the first small molecule binding to Gli1 zinc finger and impairing Gli1 activity by interfer

301 P2beta forms a two-site interaction with the GLI1 zinc-finger domain and acetylation site, stabilizin