TRIM16 Monoclonal Antibody (M02A), Clone 5G11

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TRIM16 monoclonal antibody (M02A), clone 5G11 Catalog # : H00010626-M02A 規格 : [ 200 uL ] List All Specification Application Image Product Mouse monoclonal antibody raised against a partial recombinant Western Blot (Cell lysate) Description: TRIM16. Immunogen: TRIM16 (NP_006461, 165 a.a. ~ 273 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: LDAARRDKEAELQCTQLDLERKLKLNENAISRLQANQKSVLVSVSEVKAV AEMQFGELLAAVRKAQANVMLFLEEKEQAALSQANGIKAHLEYRSAEME enlarge KSKQELERMA Western Blot (Recombinant protein) Host: Mouse ELISA Reactivity: Human Isotype: IgG2a Kappa Quality Control Antibody Reactive Against Recombinant Protein. Testing: Western Blot detection against Immunogen (37.73 KDa) . Storage Buffer: In ascites fluid Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Datasheet: Download Applications Western Blot (Cell lysate) Page 1 of 2 2020/6/25 TRIM16 monoclonal antibody (M02A), clone 5G11 Western Blot analysis of TRIM16 expression in Jurkat ( Cat # L017V1 ). Protocol Download Western Blot (Recombinant protein) Protocol Download ELISA Gene Information Entrez GeneID: 10626 GeneBank NM_006470 Accession#: Protein NP_006461 Accession#: Gene Name: TRIM16 Gene Alias: EBBP Gene tripartite motif-containing 16 Description: Omim ID: 609505 Gene Ontology: Hyperlink Gene Summary: This gene was identified as an estrogen and anti-estrogen regulated gene in epithelial cells stably expressing estrogen receptor. The protein encoded by this gene contains two B box domains and a coiled-coiled region that are characteristic of the B box zinc finger protein family. The proteins of this family have been reported to be involved in a variety of biological processes including cell growth, differentiation and pathogenesis. Expression of this gene was detected in most tissues. Its function, however, has not yet been determined. [provided by RefSeq Other estrogen-responsive B box protein Designations: 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2020 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 2 of 2 2020/6/25.

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TRIM16 Antibody Cat
TRIM16 Antibody Cat. No.: 59-182 TRIM16 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This TRIM16 antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 38-67 amino acids from the N-terminal region of human TRIM16. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 64 kDa WEIGHT: Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated October 2, 2021 1 https://www.prosci-inc.com/trim16-antibody-59-182.html PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: TRIM16 ALTERNATE NAMES: Tripartite motif-containing protein 16, Estrogen-responsive B box protein, TRIM16, EBBP ACCESSION NO.: O95361 GENE ID: 10626 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References This gene was identified as an estrogen and anti-estrogen regulated gene in epithelial cells stably expressing estrogen receptor. The protein encoded by this gene contains two B box domains and a coiled-coiled region that are characteristic of the B box zinc finger BACKGROUND: protein family. The proteins of this family have been reported to be involved in a variety of biological processes including cell growth, differentiation and pathogenesis.
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Developmental Timing of Mutations Revealed by Whole-Genome Sequencing of Twins with Acute Lymphoblastic Leukemia
Developmental timing of mutations revealed by whole-genome sequencing of twins with acute lymphoblastic leukemia Yussanne Maa,1, Sara E. Dobbinsa,1, Amy L. Sherbornea,1, Daniel Chubba, Marta Galbiatib, Giovanni Cazzanigab, Concetta Micalizzic, Rick Tearled, Amy L. Lloyda, Richard Haine, Mel Greavesf,2,3, and Richard S. Houlstona,2,3 aMolecular and Population Genetics, Division of Genetics and Epidemiology, Institute of Cancer Research, Sutton, Surrey SM2 5NG, United Kingdom; bCentro Ricerca Tettamanti, Clinica Pediatrica, Università di Milano-Bicocca, Ospedale San Gerardo, 20900 Monza (Mi), Italy; cExperimental Clinical Hematology Unit, Istituto di Ricovero e Cura a Carattere Scientiﬁco (IRCCS) G. Gaslini, 16148 Genova, Italy; dComplete Genomics, Inc., Mountain View, CA 94043; ePaediatric Palliative Medicine, Children’s Hospital for Wales, University Hospital of Wales, Cardiff CF14 4XW, United Kingdom; and fHaemato-Oncology Research Unit, Division of Molecular Pathology, Institute of Cancer Research, Surrey SM2 5NG, United Kingdom Edited* by Max D. Cooper, Emory University, Atlanta, GA, and approved March 5, 2013 (received for review December 10, 2012) Acute lymphoblastic leukemia (ALL) is the major pediatric cancer. ETV6-RUNX1 fusion-negative ALL. Sequencing of matched tu- At diagnosis, the developmental timing of mutations contributing mor-normal (remission) samples from each patient was carried critically to clonal diversiﬁcation and selection can be buried in the out using unchained combinatorial probe anchor ligation chem- leukemia’s covert natural history. Concordance of ALL in monozy- istry on arrays of self-assembling DNA nanoballs (11). Paired-end gotic, monochorionic twins is a consequence of intraplacental reads were aligned to the Human Genome [National Center for spread of an initiated preleukemic clone.
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Androgen-Dependent Alternative Mrna Isoform Expression in Prostate Cancer Cells[Version 1; Peer Review: 3 Approved]
F1000Research 2018, 7:1189 Last updated: 21 AUG 2021 RESEARCH ARTICLE Androgen-dependent alternative mRNA isoform expression in prostate cancer cells [version 1; peer review: 3 approved] Jennifer Munkley 1, Teresa M. Maia2,3, Nekane Ibarluzea1,4,5, Karen E. Livermore1, Daniel Vodak6, Ingrid Ehrmann1, Katherine James7,8, Prabhakar Rajan9, Nuno L. Barbosa-Morais2, David J. Elliott1 1Institute of Genetic Medicine, University of Newcastle, Newcastle upon Tyne, Newcastle, NE1 3BZ, UK 2Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, 1649-028, Portugal 3VIB Proteomics Core, Albert Baertsoenkaai 3, Ghent, 9000, Belgium 4Biocruces Bizkaia Health Research Institute, Cruces University Hospital, Barakaldo, 48903, Spain 5Centre for Biomedical Research on Rare Diseases (CIBERER), ISCIII, Valencia, 46010, Spain 6Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway 7Interdisciplinary Computing and Complex BioSystems Research Group, Newcastle University, Newcastle upon Tyne, NE4 5TG, UK 8Life and Earth Sciences, Natural History Museum, Cromwell Road, London, SW7 5BD, UK 9Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, EC1M 6BQ, UK v1 First published: 03 Aug 2018, 7:1189 Open Peer Review https://doi.org/10.12688/f1000research.15604.1 Latest published: 03 Aug 2018, 7:1189 https://doi.org/10.12688/f1000research.15604.1 Reviewer Status Invited Reviewers Abstract Background: Androgen steroid hormones are key drivers of prostate 1 2 3 cancer. Previous work has shown that androgens can drive the expression of alternative mRNA isoforms as well as transcriptional version 1 changes in prostate cancer cells. Yet to what extent androgens control 03 Aug 2018 report report report alternative mRNA isoforms and how these are expressed and differentially regulated in prostate tumours is unknown.
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A Large New Subset of TRIM Genes Highly Diversified by Duplication and Positive Selection in Teleost Fish
A large new subset of TRIM genes highly diversified by duplication and positive selection in teleost fish. Lieke M van der Aa, Jean-Pierre Levraud, Malika Yahmi, Emilie Lauret, Valérie Briolat, Philippe Herbomel, Abdenour Benmansour, Pierre Boudinot To cite this version: Lieke M van der Aa, Jean-Pierre Levraud, Malika Yahmi, Emilie Lauret, Valérie Briolat, et al.. A large new subset of TRIM genes highly diversified by duplication and positive selection in teleost fish.. BMC Biology, BioMed Central, 2009, 7 (7), pp.7. 10.1186/1741-7007-7-7. pasteur-00400402 HAL Id: pasteur-00400402 https://hal-pasteur.archives-ouvertes.fr/pasteur-00400402 Submitted on 30 Jun 2009 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. BMC Biology BioMed Central Research article Open Access A large new subset of TRIM genes highly diversified by duplication and positive selection in teleost fish Lieke M van der Aa1,2, Jean-Pierre Levraud3, Malika Yahmi1, Emilie Lauret1, Valérie Briolat3, Philippe Herbomel3, Abdenour Benmansour1 and Pierre Boudinot*1 Address: 1Virologie et Immunologie
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UC San Diego Electronic Theses and Dissertations
UC San Diego UC San Diego Electronic Theses and Dissertations Title Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent Permalink https://escholarship.org/uc/item/7m04f0b0 Author Buchholz, Kyle Stephen Publication Date 2016 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Bioengineering by Kyle Stephen Buchholz Committee in Charge: Professor Jeffrey Omens, Chair Professor Andrew McCulloch, Co-Chair Professor Ju Chen Professor Karen Christman Professor Robert Ross Professor Alexander Zambon 2016 Copyright Kyle Stephen Buchholz, 2016 All rights reserved Signature Page The Dissertation of Kyle Stephen Buchholz is approved and it is acceptable in quality and form for publication on microfilm and electronically: Co-Chair Chair University of California, San Diego 2016 iii Dedication To my beautiful wife, Rhia. iv Table of Contents Signature Page ................................................................................................................... iii Dedication .......................................................................................................................... iv Table of Contents ................................................................................................................ v List of Figures ...................................................................................................................
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TRIM Proteins and CXC Chemokines Evolutionary Dynamics and Functional Characterization
TRIM proteins and CXC chemokines Evolutionary dynamics and functional characterization of two large protein families in teleost fish Lieke M. van der Aa TRIM proteins and CXC chemokines Evolutionary dynamics and functional characterization of two large protein families in teleost fish Lieke M. van der Aa Thesis committee Thesis supervisor Prof. dr. ir. H.F.J. Savelkoul Professor of Cell Biology and Immunology Wageningen University, the Netherlands Thesis co-supervisors Dr. B.M.L. van Kemenade Assistant professor, Cell Biology and Immunology group Wageningen University, the Netherlands Dr. P. Boudinot Directeur de Recherches, Virologie et Immunologie Moléculaires Institut National de la Recherche Agronomique, Jouy-en-Josas, France Other members Prof. Dr. Just Vlak Wageningen University, the Netherlands Prof Dr. Chris J. Secombes University of Aberdeen, Scotland Dr. Annemarie H. Meijer Leiden University, the Netherlands Dr. Sebastian Nisole Pasteur Institute, Paris, France This research was conducted under the auspices of the Graduate School of the Wageningen Institute of Animal Sciences, WIAS TRIM proteins and CXC chemokines Evolutionary dynamics and functional characterization of two large protein families in teleost fish Lieke M. van der Aa Thesis at Wageningen University submitted in fulfillment of the requirements for the degree of doctor Prof. Dr. M.J. Kropff, by the authorityin the presence of the Rector of the Magnificus Thesis Committee appointed by the Academic Board to be defended in public on Friday 20 January 2012 at 4 p.m.
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TRIM16 Antibody Cat
TRIM16 Antibody Cat. No.: 28-947 TRIM16 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Antibody produced in rabbits immunized with a synthetic peptide corresponding a region IMMUNOGEN: of human TRIM16. TESTED APPLICATIONS: ELISA, WB TRIM16 antibody can be used for detection of TRIM16 by ELISA at 1:62500. TRIM16 APPLICATIONS: antibody can be used for detection of TRIM16 by western blot at 1.25 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50,000 - 100,000. POSITIVE CONTROL: 1) Cat. No. 1211 - HepG2 Cell Lysate PREDICTED MOLECULAR 64 kDa, 31 kDa WEIGHT: Properties PURIFICATION: Antibody is purified by protein A chromatography method. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid September 30, 2021 1 https://www.prosci-inc.com/trim16-antibody-28-947.html Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% BUFFER: sucrose. CONCENTRATION: batch dependent For short periods of storage (days) store at 4˚C. For longer periods of storage, store STORAGE CONDITIONS: TRIM16 antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles. Additional Info OFFICIAL SYMBOL: TRIM16 ALTERNATE NAMES: TRIM16, EBBP ACCESSION NO.: NP_006461 PROTEIN GI NO.: 48255913 GENE ID: 10626 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References This gene was identified as an estrogen and anti-estrogen regulated gene in epithelial cells stably expressing estrogen receptor. TRIM16 contains two B box domains and a coiled-coiled region that are characteristic of the B box zinc finger protein family. The proteins of this family have been reported to be involved in a variety of biological processes including cell growth, differentiation and pathogenesis.
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A Genomic View of Estrogen Actions in Human Breast Cancer Cells by Expression Profiling of the Hormone-Responsive Transcriptome
719 A genomic view of estrogen actions in human breast cancer cells by expression profiling of the hormone-responsive transcriptome Luigi Cicatiello1, Claudio Scafoglio1, Lucia Altucci1, Massimo Cancemi1, Guido Natoli1, Angelo Facchiano2, Giovanni Iazzetti3, Raffaele Calogero4, Nicoletta Biglia6, Michele De Bortoli5,7, Christian Sfiligoi7, Piero Sismondi6,7, Francesco Bresciani1 and Alessandro Weisz1 1Dipartimento di Patologia generale, Seconda Università degli Studi di Napoli, Vico L. De Crecchio 7, 80138 Napoli, Italy 2Istituto di Scienze dell’Alimentazione del Consiglio Nazionale delle Ricerche, Avellino, Italy 3Dipartimento di Genetica, Biologia generale e molecolare, Università di Napoli ‘Federico II’, Napoli, Italy 4Dipartimento di Scienze cliniche e biologiche, Università degli Studi di Torino, Torino, Italy 5Dipartimento di Scienze oncologiche, Università degli Studi di Torino, Torino, Italy 6Dipartimento di Discipline ostetriche e ginecologiche, Università degli Studi di Torino, Torino, Italy 7Laboratorio di Ginecologia oncologica, Istituto per la Ricerca e la Cura del Cancro, Candiolo, Italy (Requests for offprints should be addressed to A Weisz; Email: [email protected]) Abstract Estrogen controls key cellular functions of responsive cells including the ability to survive, replicate, communicate and adapt to the extracellular milieu. Changes in the expression of 8400 genes were monitored here by cDNA microarray analysis during the first 32 h of human breast cancer (BC) ZR-75·1 cell stimulation with a mitogenic dose of 17-estradiol, a timing which corresponds to completion of a full mitotic cycle in hormone-stimulated cells. Hierarchical clustering of 344 genes whose expression either increases or decreases significantly in response to estrogen reveals that the gene expression program activated by the hormone in these cells shows 8 main patterns of gene activation/inhibition.
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Inbred Mouse Strains Expression in Primary Immunocytes Across
Downloaded from http://www.jimmunol.org/ by guest on September 28, 2021 Daphne is online at: average * The Journal of Immunology published online 29 September 2014 from submission to initial decision 4 weeks from acceptance to publication Sara Mostafavi, Adriana Ortiz-Lopez, Molly A. Bogue, Kimie Hattori, Cristina Pop, Daphne Koller, Diane Mathis, Christophe Benoist, The Immunological Genome Consortium, David A. Blair, Michael L. Dustin, Susan A. Shinton, Richard R. Hardy, Tal Shay, Aviv Regev, Nadia Cohen, Patrick Brennan, Michael Brenner, Francis Kim, Tata Nageswara Rao, Amy Wagers, Tracy Heng, Jeffrey Ericson, Katherine Rothamel, Adriana Ortiz-Lopez, Diane Mathis, Christophe Benoist, Taras Kreslavsky, Anne Fletcher, Kutlu Elpek, Angelique Bellemare-Pelletier, Deepali Malhotra, Shannon Turley, Jennifer Miller, Brian Brown, Miriam Merad, Emmanuel L. Gautier, Claudia Jakubzick, Gwendalyn J. Randolph, Paul Monach, Adam J. Best, Jamie Knell, Ananda Goldrath, Vladimir Jojic, J Immunol http://www.jimmunol.org/content/early/2014/09/28/jimmun ol.1401280 Koller, David Laidlaw, Jim Collins, Roi Gazit, Derrick J. Rossi, Nidhi Malhotra, Katelyn Sylvia, Joonsoo Kang, Natalie A. Bezman, Joseph C. Sun, Gundula Min-Oo, Charlie C. Kim and Lewis L. Lanier Variation and Genetic Control of Gene Expression in Primary Immunocytes across Inbred Mouse Strains Submit online. Every submission reviewed by practicing scientists ? is published twice each month by http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2014/09/28/jimmunol.140128 0.DCSupplemental Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2014 by The American Association of Immunologists, Inc.
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New Insights from the Complete TRIM Repertoire of Zebrafish and Pufferfish
Origin and evolution of TRIM proteins: new insights from the complete TRIM repertoire of zebrafish and pufferfish Pierre Boudinot, Lieke M van der Aa, Luc Jouneau, Louis Du Pasquier, Pierre Pontarotti, Valérie Briolat, Abdenour Benmansour, Jean-Pierre Levraud To cite this version: Pierre Boudinot, Lieke M van der Aa, Luc Jouneau, Louis Du Pasquier, Pierre Pontarotti, et al.. Origin and evolution of TRIM proteins: new insights from the complete TRIM repertoire of ze- brafish and pufferfish. PLoS ONE, Public Library of Science, 2011, 6 (7), pp.e22022. 10.1371/jour- nal.pone.0022022. hal-00831143 HAL Id: hal-00831143 https://hal.archives-ouvertes.fr/hal-00831143 Submitted on 1 Oct 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution| 4.0 International License Origin and Evolution of TRIM Proteins: New Insights from the Complete TRIM Repertoire of Zebrafish and Pufferfish Pierre Boudinot1*, Lieke M. van der Aa1,2, Luc Jouneau1, Louis Du Pasquier3, Pierre Pontarotti4, Vale´rie Briolat5,6, Abdenour Benmansour1,
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How Far Can Regulating TRIM16 Help Reduce Malignant Transformation of OPMD S to OSCC? T
Oral Oncology 90 (2019) 123 Contents lists available at ScienceDirect Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology Letter to the editor ’ How far can regulating TRIM16 help reduce malignant transformation of OPMD s to OSCC? T Wirth quoted in his paper about chemopreventive agents for squa- showed that TRIM16 inhibits cancer cell viability by a novel me- mous cell carcinoma (SCC) in head and neck ‘Getting the drug right is, chanism involving interaction and stabilisation of TDP43 with of course, the holy grail of chemoprevention” [1]. Regrettably, he too consequent effects on E2F1 and pRb proteins [8]. accepted, a clear winner has not yet emerged irrespective of several themes over decades. As stated in the paper by Jena et al., TRIM16 streamlines the process For that matter, Vitamin A and its biologically active derivatives, of stress-induced aggregate clearance and protects cells against oxida- retinal and retinoic acid (RA), collectively with a gamut of synthetic tive/proteotoxic stress-induced toxicity both in vitro and in vivo. analogues referred to as retinoids [2] are well-known to induce growth Literature search reveals, along with quantification of allelic imbalance, arrest, cell death, and differentiation in cancer cells [3]. A complete including loss of heterozygosity (LOH) or allelic amplification, TP53 network of nuclear receptors have now been acknowledged to mediate mutation, non-genomic activation of pro-proliferative signaling by the the action of retinoids and can impede cell proliferation signals by in- epidermal growth factor receptor (EGFR) and cyclooxygenase-2 (COX- teracting with transcription factors [3]. Retinoids are also known to 2), field cancerization, etc., oxidative stress too can propagate the exert an impact on the role immune cells including macrophages, T evolution from normal to premalignant to frankly malignant cell po- cells and dendritic cells (DCs) in tumour tissue to execute anti-tumour pulations [9].
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AKT-Induced Lncrna VAL Promotes EMT-Independent Metastasis Through Diminishing Trim16-Dependent Vimentin Degradation
ARTICLE https://doi.org/10.1038/s41467-020-18929-0 OPEN AKT-induced lncRNA VAL promotes EMT-independent metastasis through diminishing Trim16-dependent Vimentin degradation Han Tian 1,9, Rong Lian1,9, Yun Li2,9, Chenying Liu1, Shujun Liang1, Wei Li1, Tianyu Tao1, Xingui Wu3, ✉ Yaokai Ye4, Xia Yang1, Jian Han5, Xuwei Chen1, Jun Li3, Yukai He6, Mengfeng Li 1,5, Jueheng Wu 1 & ✉ Junchao Cai 7,8 1234567890():,; Despite the importance of AKT overactivation in tumor progression, results from clinical trials of various AKT inhibitors remain suboptimal, suggesting that AKT-driven tumor metastasis needs to be further understood. Herein, based on long non-coding RNA (lncRNA) proﬁling induced by active AKT, we identify that VAL (Vimentin associated lncRNA, LINC01546), which is directly induced by AKT/STAT3 signaling, functions as a potent pro-metastatic molecule and is essential for active AKT-induced tumor invasion, metastasis and anoikis resistance in lung adenocarcinoma (LAD). Impressively, chemosynthetic siRNAs against VAL shows great therapeutic potential in AKT overactivation-driven metastasis. Interestingly, similar to activated AKT in LAD cells, although unable to induce epithelial-mesenchymal transition (EMT), VAL exerts potent pro-invasive and pro-metastatic effects through directly binding to Vimentin and competitively abrogating Trim16-depedent Vimentin poly- ubiquitination and degradation. Taken together, our study provides an interesting demon- stration of a lncRNA-mediated mechanism for active AKT-driven EMT-independent LAD metastasis and indicates the great potential of targeting VAL or Vimentin stability as a therapeutic approach. 1 Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080 Guangdong, China. 2 Institute of Tissue Transplantation and Immunology, Department of Immunobiology, Jinan University, Guangzhou 510632 Guangdong, China.
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