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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Snail homolog 2

Slug, SNAI2, Snail2
This gene encodes a member of the Snail family of C2H2-type zinc finger transcription factors. The encoded protein acts as a transcriptional repressor that binds to E-box motifs and is also likely to repress E-cadherin transcription in breast carcinoma. This protein is involved in epithelial-mesenchymal transitions and has antiapoptotic activity. Mutations in this gene may be associated with sporatic cases of neural tube defects. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: SNAIL, E-cadherin, vimentin, V1a, CAN
Papers using Slug antibodies
The hypoxia-inducible factor 2alpha N-terminal and C-terminal transactivation domains cooperate to promote renal tumorigenesis in vivo
Griffin J D et al., In British Journal of Cancer, 2006
... antibody (C-20-R), Notch3 antibody (M-134), Notch4 antibody (H-225), Jagged1 antibody (C-20), Maml1 antibody N-20) and Slug antibody (D-19) were from Santa Cruz Biotechnology Inc ...
Reduction in connective tissue growth factor by antisense treatment ameliorates renal tubulointerstitial fibrosis
Chauhan Ashok, In PLoS ONE, 2003
... NS4A, TGF-β1 (Chemicon, Temecula, CA), Phospho-Smad2, Phospho-Smad3, Smad2, Smad3, Phospho-P38, P-38, Phospho-JNK, JNK, vimentin and Slug (Cell Signaling, Danvers, MA), TGF-β receptor ...
Technical considerations for studying cancer metastasis in vivo
Šmarda Jan et al., In Molecular Cancer, 1996
... Protein extracts were resolved by SDS-PAGE and analyzed by immunoblotting with anti-Slug (9585, Cell Signaling), anti-vimentin (13.2, Sigma) and ...
Slug is a direct Notch target required for initiation of cardiac cushion cellularization
Karsan Aly et al., In The Journal of Cell Biology, 1995
... Goat anti–VE-cadherin (C-19), goat anti-CD31 (C-20), and goat anti-Slug (G-18) were obtained from Santa Cruz Biotechnology Inc ...
Papers on Slug
Sprouty4 mediates amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.
Leung et al., Vancouver, Canada. In Tumour Biol, Feb 2016
In addition, we showed that small interfering RNA (siRNA)-mediated knockdown of SPRY4 attenuated the AREG-induced down-regulation of E-cadherin by inhibiting the expression of SNAIL but not SLUG.
TGFβ1-Smad3-Jagged1-Notch1-Slug signaling pathway takes part in tumorigenesis and progress of tongue squamous cell carcinoma.
Liao et al., Shiqi, China. In J Oral Pathol Med, Feb 2016
The aims of this study are to examine deregulation of TGFβ1-Smad3-Jagged1-Notch1-Slug signaling in TSCC and to investigate its roles in TSCC progression.
Proteomic analysis of epithelial to mesenchymal transition reveals crosstalk between SNAIL and HDAC1 in breast cancer cells.
Faca et al., São Paulo, Brazil. In Mol Cell Proteomics, Feb 2016
Overexpression of transcription factors such as SNAIL, SLUG, ZEB1/2, and TWIST1, also induce EMT and are correlated to cancer aggressiveness.
Clinical and genetic investigation of families with type II Waardenburg syndrome.
Wu et al., Changsha, China. In Mol Med Report, Feb 2016
The coding sequences of paired box 3 (PAX3), microphthalmia‑associated transcription factor (MITF), sex‑determining region Y‑box 10 (SOX10) and snail family zinc finger 2 (SNAI2) were analyzed by polymerase chain reaction and DNA sequencing.
The transcription factors Slug (SNAI2) and Snail (SNAI1) regulate phospholipase D (PLD) promoter in opposite ways towards cancer cell invasion.
Gomez-Cambronero et al., Dayton, United States. In Mol Oncol, Jan 2016
UNASSIGNED: Slug (SNAI2) and Snail (SNAI1) are master regulatory transcription factors for organogenesis and wound healing, and they are involved in the epithelial to mesenchymal transition (EMT) of cancer cells.
F-box proteins: Keeping the epithelial-to-mesenchymal transition (EMT) in check.
de Herreros et al., Barcelona, Spain. In Semin Cancer Biol, Dec 2015
Specific EMT transcription factors (EMT-TFs), such as Snail, Slug, Twist and Zeb, control EMT induction both during development and in cancer.
Distinct EMT programs control normal mammary stem cells and tumour-initiating cells.
Weinberg et al., Cambridge, United States. In Nature, Oct 2015
Supporting this notion, we and others previously established that the Slug epithelial-to-mesenchymal transition-inducing transcription factor (EMT-TF), a member of the Snail family, serves as a master regulator of the gland-reconstituting activity of normal mammary stem cells, and that forced expression of Slug in collaboration with Sox9 in breast cancer cells can efficiently induce entrance into the TIC state.
Multifaceted roles of HSF1 in cancer.
Zhao et al., Chengdu, China. In Tumour Biol, Jul 2015
Third, HSF1 serves as a regulator of different signaling pathways, such as HuR-HIF-1, Slug, protein kinase C (PKC), nuclear factor-kappaB (NF-κB), PI3K-AKT-mTOR, and mitogen-activated protein kinase (MAPK) pathways.
[SNAI1 and SNAI2 - transcriptional master-regulators of epithelial-mesenchimal transition].
Sverdlov et al., In Patol Fiziol Eksp Ter, Apr 2015
In this review we analyze molecular structure and mechanisms of regulation of two closely-related transcription factors SNAI1 and SNAI2, which play an important role in induction and progression of epithelial-mesenchymal transition during both normal development and carcinogenesis.
The functions of F-box proteins in regulating the epithelial to mesenchymal transition.
Wang et al., Boston, United States. In Curr Pharm Des, 2014
Specifically, we discuss how these F-box proteins directly control the stability of EMT regulators such as E-cadherin, β-catenin, Twist, Slug, Snail and ZEB.
SLUG: Critical regulator of epithelial cell identity in breast development and cancer.
Kuperwasser et al., Boston, United States. In Cell Adh Migr, 2013
SLUG, a member of the SNAIL family of transcriptional repressors, is known to play a diverse number of roles in the cell, and its deregulation has been observed in a variety of cancers including breast.
A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
Tulchinsky et al., Lyon, France. In Cancer Cell, 2013
SNAIL2 and ZEB2 transcription factors are expressed in normal melanocytes and behave as tumor-suppressor proteins by activating an MITF-dependent melanocyte differentiation program.
DNp73 exerts function in metastasis initiation by disconnecting the inhibitory role of EPLIN on IGF1R-AKT/STAT3 signaling.
Pützer et al., Rostock, Germany. In Cancer Cell, 2013
DNp73 facilitates an EMT-like phenotype with loss of E-cadherin and Slug upregulation.
Sequential introduction of reprogramming factors reveals a time-sensitive requirement for individual factors and a sequential EMT-MET mechanism for optimal reprogramming.
Zheng et al., Guangzhou, China. In Nat Cell Biol, 2013
Surprisingly, the sequential protocol activates an early epithelial-to-mesenchymal transition (EMT) as indicated by the upregulation of Slug and N-cadherin followed by a delayed mesenchymal-to-epithelial transition (MET).
Integrated analyses identify a master microRNA regulatory network for the mesenchymal subtype in serous ovarian cancer.
Zhang et al., Houston, United States. In Cancer Cell, 2013
Follow-up functional experiments illustrate that miR-506 augmented E-cadherin expression, inhibited cell migration and invasion, and prevented TGFβ-induced epithelial-mesenchymal transition by targeting SNAI2, a transcriptional repressor of E-cadherin.
Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis.
Rudnicki et al., Ottawa, Canada. In Mol Cell, 2012
In primary myoblasts, snai1-HDAC1/2 repressive complex binds and excludes MyoD from its targets.
Functional regulation of Slug/Snail2 is dependent on GSK-3β-mediated phosphorylation.
Cho et al., Cheju, South Korea. In Febs J, 2012
GSK-3beta-mediated phosphorylation of Slug/Snail2 controls its turnover and localization during EMT.
High motility of triple-negative breast cancer cells is due to repression of plakoglobin gene by metastasis modulator protein SLUG.
Chaudhuri et al., Nashville, United States. In J Biol Chem, 2012
This study thus implicates SLUG-induced repression of plakoglobin as a motility determinant in highly disseminating breast cancer.
Slug expression during melanoma progression.
Kusewitt et al., United States. In Am J Pathol, 2012
The studies suggest a role for Slug early in the transformation of melanocytes to melanoma cells.
A multi-cancer mesenchymal transition gene expression signature is associated with prolonged time to recurrence in glioblastoma.
Anastassiou et al., New York City, United States. In Plos One, 2011
Gene expression signature of the transcription factor SNAI2 and the putative stem cell marker CD44 are strongly correlated and highly expressed in glioblastomas versus lower grade gliomas.
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