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1 , SM22alpha, calponin, phospho-vimentin, and Slug.
2 or-promoting transcription factors, Sox9 and Slug.
3 e expression of the EMT transcription factor slug.
4 how that SOX2 is a transcriptional target of SLUG.
5 sed by joint knockdown of BMPR2 and HMGA1 or Slug.
6 ll as expression of the transcription factor Slug.
7 mesenchymal transition regulators: snail and slug.
8 E-cadherin subsequent to decreased levels of SLUG.
9 ent upregulation of the transcription factor SLUG.
10 on of the proapoptotic gene, Puma (Bbc3), by Slug.
11 brogating the expression of the EMT mediator SLUG.
12 ition by regulating the transcription factor SLUG.
13 ligands for the NmU/PRXamide receptor in the slug.
14 functionality of the chloroplasts inside the slugs.
15 euopisthobranch and panpulmonate snails and slugs.
16 tic activity in kleptoplasts retained by sea slugs.
17 relative lengths of the sender and receiver slugs.
18 osal glands using mucus vesicles from banana slugs.
19 to the rise and burst of conduit-filling gas slugs.
25 he up-regulation of the EMT master regulator Slug, a process that is dependent on both MEK/ERK signal
26 alphavbeta3 was necessary and sufficient for Slug activation, tumorsphere formation, and tumor initia
36 EMT and mesenchymal differentiation through Slug and functions in tumor-suppressive programs by regu
37 We found that PBT-1 reduced the level of Slug and inhibits the migration, invasion, and filopodia
38 ctin-bundling protein fascin is regulated by slug and involved in late-stage PanIN and PDAC formation
40 tly greater expression of Ki67, p53, VEGFR1, SLUG and SNAIL in the metastases compared with the prima
41 cadherin, N-cadherin, fibronectin, vimentin, slug and snail) and stem cell markers (CD44 and CD87) in
42 luminal layer exploit the paralogous EMT-TFs Slug and Snail, respectively, which induce distinct EMT
44 inding with ten endogenous peptides from the slug and some insect PRXamide and vertebrate NmU peptide
53 s include migration vectors (such as snails, slugs and isopods) and pathogens (such as microsporidia,
54 chatinoid clades of the Stylommatophora (and slugs and shelled slugs), which diverged 90-130 MYA.
55 ct and systemic molluscicide for controlling slugs and snails in a wide range of agricultural and hor
56 ft-bodied aquatic invertebrates, such as sea slugs and snails, are capable of diverse locomotion mode
58 cterial isolates acquired from a sponge, sea slug, and coral to examine the functional landscape of t
59 ibiting N-cadherin and transcription factors Slug, and pluripotency maintaining factors Nanog, c-Myc,
65 echanically isolated from the CNS of the sea slug Aplysia californica, a well characterized neurobiol
66 5-500 mum in diameter) isolated from the sea slug (Aplysia californica) central and rat (Rattus norve
72 uman geriatric SCs, these findings highlight Slug as a potential therapeutic target for aging-associa
74 n (EMT) markers as N-cadherin, vimentin, and Slug, as well as metastasis-related integrins (integrin-
79 Interestingly, depletion of Snail, but not Slug, attenuated TGF-beta1-induced down-regulation of VE
80 t cancer through the estrogen receptor alpha/Slug axis and that it is a potential noninvasive biomark
81 a is obtained by cycling a discrete reaction slug back and forth between two residence coils, with an
82 nducible factor 1alpha (Hif-1alpha), Snail1, Slug, basic fibroblast growth factor (bFgf), and retinal
84 -encoding genes were highly expressed in the slug brain, while the receptor gene was expressed at low
89 lated E-cadherin, beta-catenin, vimentin and Slug, but it partially rescued Twist1-silenced ERalpha a
91 MAR1-dependent transcriptional repression of Slug by direct recruitment of SMAR1/HDAC1 complex to the
94 lgae, we show that the plastoquinone pool of slug chloroplasts remains oxidized, which can suppress r
99 pment stages of D. discoideum when migrating slugs differentiate into fruiting bodies that contain pe
100 ntactless" mass transfer between two aqueous slugs (droplets) separated by an oil slug in Taylor flow
103 nthophyll cycle were investigated in the sea slugs Elysia viridis and E. chlorotica using chlorophyll
106 e and others previously established that the Slug epithelial-to-mesenchymal transition-inducing trans
109 In addition, blocking ROCK1/2 activity in Slug-expressing Kras mice reversed the inhibitory effect
115 1 integrin efficiently inhibited RCP-induced Slug expression and subsequent cancer cell invasion.
116 31 cells impaired the induction of Snail and Slug expression by EGF, and this effect was associated w
118 we provide evidence that hTERT links Src to Slug expression in NE-induced ovarian cancer EMT and met
125 s where its expression level correlates with Slug expression, enhanced invasiveness, and poor clinica
126 ockdown reduced the ability of Akt to induce Slug expression, indicating an essential role that HSF-1
136 he development of a single-step method using slug-flow microextraction and nano-electrospray ionizati
138 gas-driven oscillatory motion of a biphasic slug for high-throughput in situ measurement and screeni
139 nce 1 (GFI1) is comprised of conserved Snail/Slug/Gfi1 (SNAG) and zinc finger motifs separated by a l
140 ge continuous laboratory culture of both the slugs (>500 individuals) and their prey algae, we show t
142 directly binds to the DNA-binding domain of Slug, impeding histone deacetylase 1 (HDAC1) recruitment
143 ranscription factor -2 ( SNAI2) (also called SLUG), implicating LGR4 in regulation of epithelial-mese
144 ts increase our understanding of the role of Slug in ADM, an early event that can eventually lead to
145 This study demonstrates a pivotal role for Slug in carcinoma cell survival, implying that disruptio
147 ry stem cells, and that forced expression of Slug in collaboration with Sox9 in breast cancer cells c
148 gether, our data support a critical role for Slug in determining the angiogenic response during devel
152 These results delineate a novel role for Slug in the nutrient stress response and provide insight
153 ntified the zinc-finger transcription factor Slug in WNK1-mediated control of endothelial functions.
154 t on radio-tracking of individual grey field slugs in an arable field and associated data modelling d
158 dherin transcriptional repressors, snail and slug, induced by transforming growth factor-beta1 or ext
159 vation of a signaling cascade culminating in Slug induction, epithelial-to-mesenchymal transition and
165 rt that the zinc-finger transcription factor Slug is highly expressed in quiescent SCs of mice and fu
166 ictyostelium discoideum into a multicellular slug is known to result from single-cell chemotaxis towa
171 onfirmed in human breast cancer cells, where Slug knockdown increased Puma expression and inhibited l
172 s, inhibition of Puma by RNA interference in Slug-knockdown cells rescued lung colonization, whereas
176 exhibited nuclear localization of Twist and Slug, markers of epithelial-mesenchymal transition (EMT)
178 nd its transcriptional regulators; Snail and Slug may serve as indicators for assessing the stage of
179 a repressor in controlling HIF-1alpha/HDAC1/Slug-mediated cancer cell invasion and is a potential th
180 rast, SOX9 bound the SLUG promoter to induce SLUG-mediated cell invasion with a spindle-like phenotyp
181 downregulated during tumorigenesis via Snail/Slug-mediated E-cadherin transcriptional reduction.
182 herin and occludin expression and suppresses Slug-mediated epithelial-mesenchymal transition (EMT) an
184 er cells results in a coordinative action of Slug-mediated repression of E-cadherin transcription, as
185 methylation-specific PCR further revealed a SLUG-mediated temporal regulation of epigenetic modifica
186 ive (GABA-ir) neurons in four species of sea slugs (Mollusca, Gastropoda, Opisthobranchia, Nudibranch
187 The analysis revealed that all components of slug movement (mean speed, turning angles and movement/r
189 discovered that IMP3 binds avidly to SNAI2 (SLUG) mRNA and regulates its expression by binding to th
192 y regulated the expression of EndMT markers (Slug, N-cadherin, alpha-SMA) in EC exposed to low shear
193 expression of the mesenchymal markers Snail, Slug, N-cadherin, and vimentin in the recipient cells, w
196 Kras mice reversed the inhibitory effects of Slug on ADM, ERK1/2 phosphorylation, proliferation and f
197 lated by the usual increase in expression of Slug or Snail, the transcriptional regulators for E-cadh
199 hand, genetic deletion or acute depletion of Slug, or Lsd1 inhibition, reduced lipogenesis and protec
201 ic expression of hTERT induced expression of Slug, ovarian cancer cell epithelial-mesenchymal transit
205 provide evidence of a de novo GSK3beta-CHIP-Slug pathway that may be involved in the progression of
206 ciated MaSCs require a TGF-beta2/alphavbeta3/Slug pathway, which may contribute to breast cancer prog
208 ome-team offensive performance, for example, slugging percentage, but did not similarly affect away-t
209 gregation of amoeboid cells into a migratory slug phase in cellular slime molds at times of starvatio
213 herin is post-transcriptionally regulated by Slug-promoted miR-221, which serves as an additional blo
215 matrix attachment region site present in the Slug promoter restores E-cadherin expression, SMAR1 also
219 T1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes.
222 ncer cells up-regulate classic EMT regulator Slug, providing a link between nutrient stress and metas
223 arian cancer aggressiveness through inducing Slug, providing novel biomarkers and potential therapeut
225 ll survival, implying that disruption of the Slug-Puma axis may impinge on the survival of metastatic
228 xpression of mesenchymal proteins (VIMENTIN, SLUG), reduced migration and tumor sphere formation, and
231 eleased as a group disperse more slowly than slugs released individually and their turning angle has
232 finger-containing transcriptional repressor, Slug, represses E-cadherin transcription and enhances ep
234 trolling fibroblast proliferation, TGF-beta1-Slug signaling, collagen accumulation, and EMT processin
235 uppression of MARCKS phosphorylation and AKT/Slug signalling pathway but not the expression of total
237 del that N-cadherin (Cdh2) expression causes Slug (Snai2) upregulation, which in turn promotes carcin
239 EMT master regulator Snail (SNAI1), but not Slug (SNAI2), shows evidence of Pol II pausing before ac
241 expression in sh-AhR cells reduced Snail and Slug/Snai2 levels and cell migration and restored E-cadh
242 on of the EMT-promoting transcription factor SLUG/SNAI2, repressing its transcription by recruiting H
243 sed expression of mesenchymal markers Snail, Slug/Snai2, vimentin, fibronectin, and alpha-smooth musc
244 rkers and transcription factors (N-cadherin, Slug, Snail and Zeb1), and upregulation of E-cadherin.
245 richment in mesenchymal markers (N-cadherin, slug, snail, fibronectin) and cell invasiveness, relativ
246 E-cadherin, and decreased those of vimentin, Slug, Snail, matrix metalloproteinase (MMP)-2, -9, and a
247 TS subpopulation expresses higher levels of SLUG, SNAIL, VIMENTIN and N-CADHERIN while show a lack o
249 stic insight into the regulation of CSCs via SLUG-SOX9 regulatory axis, which represents a potential
250 ir) neurons in the buccal ganglia of six sea slug species (Mollusca, Gastropoda, Euthyneura, Nudipleu
251 that Sentinel (S) cells of the multicellular slug stage of the social amoeba Dictyostelium discoideum
252 a3, Src kinase, and the transcription factor Slug suppresses PUMA in these cells, promoting tumor ste
253 peptide corresponding to the SNAG domain of Slug, suppresses the motility and invasiveness of cancer
254 helial mesenchymal transition, expression of Slug, TGF-beta3, phospho-AKT and phospho-PRAS40, but inc
256 consumption (reactions performed in 300 muL slugs), this represents an improvement in efficiency for
257 -mesenchymal transition transcription factor SLUG to directly repress pro-apoptotic BMF, limiting dru
258 ent, vimentin acted as a scaffold to recruit Slug to ERK and promote Slug phosphorylation at serine-8
259 perates with the transcription factor Snail2/Slug to modulate neural crest development in Xenopus.
263 eness by inhibiting expression of the SNAI2 (Slug) transcriptional repressor, which leads to expressi
264 Injection of the bioactive peptides into slugs triggered defensive behavior such as copious mucus
266 our results provide the first evidence that Slug-upregulated miR-221 promotes breast cancer progress
267 novel Akt-HSF-1 signaling axis that leads to Slug upregulation and EMT, and potentially contributes t
270 genitor like properties, involving Snail and Slug upregulation, mammosphere formation and aldehyde de
271 ll expansion, together with miR-452 loss and Slug upregulation, providing a novel mechanism whereby c
274 mesenchymal transition (EMT) markers (Snail, Slug, vimentin and N-cadherin) were induced in human pro
275 The positive association between HSF-1 and Slug was confirmed by immunohistochemical staining of a
278 of slug and fascin correlated in PDAC cells; slug was found to regulate transcription of Fascin along
279 high expression of the transcription factor SLUG was indispensable for the establishment of EMT memo
283 ned that transcriptional induction of SNAI2 (Slug) was essential for cyclin D1b-mediated proliferativ
288 cesses (pPI3K, pAKT, pERK, Bcl2, Zeb, Snail, Slug) were significantly changed in response to alterati
294 ility and expression of beta-catenin, Snail, Slug, Zeb1 and N-cadherin, and upregulated E-cadherin.
295 ression of key transcription factors (Snail, Slug, Zeb1) or by acquiring drug resistance produces a s
296 n of metastasis-associated markers VIMENTIN, SLUG, ZEB1, and MMP9, with a concurrent decrease in mRNA
300 asis of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic