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  1. Article: Characterization of

    Farkas, Carlos / Quiroz, Aracelly / Alvarez, Claudia / Hermosilla, Viviana / Aylwin, Carlos F / Lomniczi, Alejandro / Castro, Ariel F / Hepp, Matias I / Pincheira, Roxana

    Frontiers in genetics

    2021  Volume 12, Page(s) 613808

    Abstract: The SALL2 transcription factor, an evolutionarily conserved gene through vertebrates, is involved in normal development and neuronal differentiation. In disease, SALL2 is associated with eye, kidney, and brain disorders, but mainly is related to cancer. ... ...

    Abstract The SALL2 transcription factor, an evolutionarily conserved gene through vertebrates, is involved in normal development and neuronal differentiation. In disease, SALL2 is associated with eye, kidney, and brain disorders, but mainly is related to cancer. Some studies support a tumor suppressor role and others an oncogenic role for SALL2, which seems to depend on the cancer type. An additional consideration is tissue-dependent expression of different SALL2 isoforms. Human and mouse
    Language English
    Publishing date 2021-02-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2021.613808
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Functional studies of MP62 during male chromatin decondensation in sea urchins.

    Iribarren, Claudio / Hermosilla, Viviana / Morin, Violeta / Puchi, Marcia

    Journal of cellular biochemistry

    2013  Volume 114, Issue 8, Page(s) 1779–1788

    Abstract: In amphibians, sperm histone transition post-fertilization during male pronucleus formation is commanded by histone chaperone Nucleoplasmin (NPM). Here, we report the first studies to analyze the participation of a Nucleoplasmin-like protein on male ... ...

    Abstract In amphibians, sperm histone transition post-fertilization during male pronucleus formation is commanded by histone chaperone Nucleoplasmin (NPM). Here, we report the first studies to analyze the participation of a Nucleoplasmin-like protein on male chromatin remodeling in sea urchins. In this report, we present the molecular characterization of a nucleoplasmin-like protein that is present in non fertilized eggs and early zygotes in sea urchin specie Tetrapygus niger. This protein, named MP62 can interact with sperm histones in vitro. By male chromatin decondensation assays and immunodepletion experiments in vitro, we have demonstrated that this protein is responsible for sperm nucleosome disorganization. Furthermore, as amphibian nucleoplasmin MP62 is phosphorylated in vivo immediately post-fertilization and this phosphorylation is dependent on CDK-cyclin activities found after fertilization. As we shown, olomoucine and roscovitine inhibits male nucleosome decondensation, sperm histone replacement in vitro and MP62 phosphorylation in vivo. This is the first report of a nucleoplasmin-like activity in sea urchins participating during male pronucleus formation post-fecundation.
    MeSH term(s) Animals ; Chromatin Assembly and Disassembly/drug effects ; Chromatin Assembly and Disassembly/physiology ; Histones/metabolism ; Kinetin/pharmacology ; Male ; Nucleoplasmins/metabolism ; Protein Kinase Inhibitors/pharmacology ; Purines/pharmacology ; Sea Urchins/cytology ; Sea Urchins/metabolism ; Spermatozoa/cytology ; Spermatozoa/metabolism
    Chemical Substances Histones ; Nucleoplasmins ; Protein Kinase Inhibitors ; Purines ; roscovitine (0ES1C2KQ94) ; olomoucine (6A839B2HYS) ; Kinetin (P39Y9652YJ)
    Language English
    Publishing date 2013-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.24520
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1114: Show issues Location:
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  3. Article: A Trichostatin A (TSA)/Sp1-mediated mechanism for the regulation of SALL2 tumor suppressor in Jurkat T cells.

    Hepp, Matías I / Escobar, David / Farkas, Carlos / Hermosilla, Viviana E / Álvarez, Claudia / Amigo, Roberto / Gutiérrez, José L / Castro, Ariel F / Pincheira, Roxana

    Biochimica et biophysica acta. Gene regulatory mechanisms

    2018  

    Abstract: SALL2 is a transcription factor involved in development and disease. Deregulation of SALL2 has been associated with cancer, suggesting that it plays a role in the disease. However, how SALL2 is regulated and why is deregulated in cancer remain poorly ... ...

    Abstract SALL2 is a transcription factor involved in development and disease. Deregulation of SALL2 has been associated with cancer, suggesting that it plays a role in the disease. However, how SALL2 is regulated and why is deregulated in cancer remain poorly understood. We previously showed that the p53 tumor suppressor represses SALL2 under acute genotoxic stress. Here, we investigated the effect of Histone Deacetylase Inhibitor (HDACi) Trichostatin A (TSA), and involvement of Sp1 on expression and function of SALL2 in Jurkat T cells. We show that SALL2 mRNA and protein levels were enhanced under TSA treatment. Both, TSA and ectopic expression of Sp1 transactivated the SALL2 P2 promoter. This transactivation effect was blocked by the Sp1-binding inhibitor mithramycin A. Sp1 bound in vitro and in vivo to the proximal region of the P2 promoter. TSA induced Sp1 binding to the P2 promoter, which correlated with dynamic changes on H4 acetylation and concomitant recruitment of p300 or HDAC1 in a mutually exclusive manner. Our results suggest that TSA-induced Sp1-Lys703 acetylation contributes to the transcriptional activation of the P2 promoter. Finally, using a CRISPR/Cas9 SALL2-KO Jurkat-T cell model and gain of function experiments, we demonstrated that SALL2 upregulation is required for TSA-mediated cell death. Thus, our study identified Sp1 as a novel transcriptional regulator of SALL2, and proposes a novel epigenetic mechanism for SALL2 regulation in Jurkat-T cells. Altogether, our data support SALL2 function as a tumor suppressor, and SALL2 involvement in cell death response to HDACi.
    Language English
    Publishing date 2018-05-18
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 1874-9399 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 1874-9399 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439
    DOI 10.1016/j.bbagrm.2018.05.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.247: Show issues Location:
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  4. Article ; Online: Developmental SALL2 transcription factor: a new player in cancer.

    Hermosilla, Viviana E / Hepp, Matias I / Escobar, David / Farkas, Carlos / Riffo, Elizabeth N / Castro, Ariel F / Pincheira, Roxana

    Carcinogenesis

    2017  Volume 38, Issue 7, Page(s) 680–690

    Abstract: SALL2, also known as Spalt-like transcription factor 2, is a member of the SALL family of transcription factors involved in development and conserved through evolution. Since its identification in 1996, findings indicate that SALL2 plays a role in ... ...

    Abstract SALL2, also known as Spalt-like transcription factor 2, is a member of the SALL family of transcription factors involved in development and conserved through evolution. Since its identification in 1996, findings indicate that SALL2 plays a role in neurogenesis, neuronal differentiation and eye development. Consistently, SALL2 deficiency associates with neural tube defects and coloboma, a congenital eye disease. Relevant to cancer, clinical studies indicate that SALL2 is deregulated in various cancers and is a specific biomarker for Synovial Sarcoma. However, the significance of SALL2 deregulation in this disease is controversial. Here, we present and discuss all available information about SALL2 since its discovery, including isoforms, regulation, targets and functions. We specifically discuss the role of SALL2 in the regulation of cell proliferation and survival within the context of the identified target genes, its interaction with viral oncogenes, and its association with the TP53 tumor suppressor and MYC oncogene. Special attention is given to p53-independent SALL2 regulation of pro-apoptotic genes BAX and PMAIP1, and the implication of these findings on the apoptotic response of cancer cells to therapy. Understanding SALL2 function and the molecular mechanisms governing its expression and activity is critical to comprehend why and how SALL2 could contribute to disease. This knowledge will open new perspectives for the development of molecular targeted approaches in disease.
    MeSH term(s) Apoptosis/genetics ; Biomarkers, Tumor/biosynthesis ; Biomarkers, Tumor/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Transcription Factors/biosynthesis ; Transcription Factors/genetics ; Tumor Suppressor Protein p53/genetics ; bcl-2-Associated X Protein/genetics
    Chemical Substances Biomarkers, Tumor ; PMAIP1 protein, human ; Proto-Oncogene Proteins c-bcl-2 ; SALL2 protein, human ; Transcription Factors ; Tumor Suppressor Protein p53 ; bcl-2-Associated X Protein
    Language English
    Publishing date 2017-07-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgx036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1558: Show issues Location:
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  5. Article ; Online: SALL2 represses cyclins D1 and E1 expression and restrains G1/S cell cycle transition and cancer-related phenotypes.

    E Hermosilla, Viviana / Salgado, Ginessa / Riffo, Elizabeth / Escobar, David / Hepp, Matías I / Farkas, Carlos / Galindo, Mario / Morín, Violeta / García-Robles, María A / Castro, Ariel F / Pincheira, Roxana

    Molecular oncology

    2018  Volume 12, Issue 7, Page(s) 1026–1046

    Abstract: SALL2 is a poorly characterized transcription factor that belongs to the Spalt-like family involved in development. Mutations on SALL2 have been associated with ocular coloboma and cancer. In cancers, SALL2 is deregulated and is proposed as a tumor ... ...

    Abstract SALL2 is a poorly characterized transcription factor that belongs to the Spalt-like family involved in development. Mutations on SALL2 have been associated with ocular coloboma and cancer. In cancers, SALL2 is deregulated and is proposed as a tumor suppressor in ovarian cancer. SALL2 has been implicated in stemness, cell death, proliferation, and quiescence. However, mechanisms underlying roles of SALL2 related to cancer remain largely unknown. Here, we investigated the role of SALL2 in cell proliferation using mouse embryo fibroblasts (MEFs) derived from Sall2
    MeSH term(s) Animals ; Cell Cycle/genetics ; Cell Proliferation ; Cell Transformation, Neoplastic/pathology ; Cyclin D1/genetics ; Cyclin D1/metabolism ; Cyclin E/genetics ; Cyclin E/metabolism ; Fibroblasts/metabolism ; G1 Phase ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Intracellular Signaling Peptides and Proteins/deficiency ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice, Knockout ; Models, Biological ; Neoplasms/genetics ; Neoplasms/pathology ; Phenotype ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Repressor Proteins/metabolism ; S Phase ; Transcription, Genetic
    Chemical Substances Ccnd1 protein, mouse ; Cyclin E ; Intracellular Signaling Peptides and Proteins ; RNA, Messenger ; Repressor Proteins ; Sall2 protein, mouse ; Cyclin D1 (136601-57-5)
    Language English
    Publishing date 2018-05-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.12308
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6637: Show issues Location:
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