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1دورية أكاديمية
المؤلفون: Martins, Manuella, Galfrè, Silvia, Terrigno, Marco, Pandolfini, Luca, Appolloni, Irene, Dunville, Keagan, Marranci, Andrea, Rizzo, Milena, Mercatanti, Alberto, Poliseno, Laura, Morandin, Francesco, Pietrosanto, Marco, Helmer-Citterich, Manuela, Malatesta, Paolo, Vignali, Robert, Cremisi, Federico
المساهمون: Martins, Manuella, Galfrè, Silvia, Terrigno, Marco, Pandolfini, Luca, Appolloni, Irene, Dunville, Keagan, Marranci, Andrea, Rizzo, Milena, Mercatanti, Alberto, Poliseno, Laura, Morandin, Francesco, Pietrosanto, Marco, Helmer-Citterich, Manuela, Malatesta, Paolo, Vignali, Robert, Cremisi, Federico
مصطلحات موضوعية: Cell fate, cell identity, corpus callosum, cortex, cortical layering, developmental timing, in vitro corticogenesi, mammalian evolution, microRNA, miR-catch, neural stem cell, post-transcriptional control, SATB2, 3' Untranslated Region, Animal, Cell Differentiation, Cell Line, Cerebral Cortex, Eutheria, Gene Expression Regulation, Developmental, Human, Matrix Attachment Region Binding Protein, Mice, Neurogenesi, Repressor Protein, Transcription Factor, Tumor Suppressor Proteins, Settore BIO/06 - Anatomia Comparata e Citologia
الوصف: Cerebral cortical development is controlled by key transcription factors that specify the neuronal identities in the different cortical layers. These transcription factors are crucial for the identity of the different neurons, but the mechanisms controlling their expression in distinct cells are only partially known. Here we investigate the expression and stability of the mRNAs of Tbr1, Bcl11b, Fezf2, Satb2 and Cux1 in single developing mouse cortical cells. We focus on Satb2 and find that its mRNA expression occurs much earlier than its protein synthesis and in a set of cells broader than expected, suggesting an initially tight control of its translation, which is subsequently de-repressed at late developmental stages. Mechanistically, Satb2 3’UTR modulates protein translation of GFP reporters during mouse corticogenesis. By in vitro pull-down of Satb2 3’UTR-associated miRNAs, we select putative miRNAs responsible for SATB2 inhibition, focusing on those strongly expressed in early progenitor cells and reduced in late cells. miR-541, an Eutherian-specific miRNA, and miR-92a/b are the best candidates and their inactivation triggers robust and premature SATB2 translation in both mouse and human cortical cells. Our findings indicate that RNA interference plays a major role in the timing of cortical cell identity and may be part of the toolkit involved in specifying supra-granular projection neurons.
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/34019815; info:eu-repo/semantics/altIdentifier/wos/WOS:000659201500012; volume:16; issue:6; firstpage:1496; lastpage:1509; numberofpages:14; journal:STEM CELL REPORTS; info:eu-repo/grantAgreement/EC/H2020/732678; http://hdl.handle.net/11384/94206Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85107153422
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2دورية أكاديمية
المؤلفون: Küçüksayan, Hakan, Akça, Hakan
مصطلحات موضوعية: epithelial–mesenchymal transition, Akt, non-small-cell lung cancer, p38, SATB2, mitogen activated protein kinase p38, phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, protein kinase B, transcription factor, transcription factor SATB2, unclassified drug, matrix attachment region binding protein, PTEN protein, human, SATB2 protein, Akt signaling, Article, AT rich sequence, controlled study, enzyme activation, epigenetics, epithelial mesenchymal transition, gene silencing, lung metastasis, lung non-small cell carcinoma cell line, molecular dynamics, molecular interaction, non small cell lung cancer, priority journal, protein expression
الوصف: Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators. Special AT-rich sequence-binding protein 2 is an epigenetic regulator involved in epithelial–mesenchymal transition and osteoblastic differentiation. It has been reported that the crosstalk between several pathways is responsible for the regulation of epithelial–mesenchymal transition in cancer cells. However, crosstalks between p38 and Akt pathways involved in epithelial–mesenchymal transition are still unknown. We recently reported that there is a crosstalk between p38 and Akt pathways in non-small-cell lung carcinoma cells, and this crosstalk is associated with E-cadherin and special AT-rich sequence-binding protein 2 expressions. Therefore, we aimed to determine whether this crosstalk has a mediator role in the regulation of epithelial–mesenchymal transition in non-small-cell lung carcinoma. Our results showed that inhibition of p38 leads to the disruption of this crosstalk via decreased expression of phosphatase and tensin homolog (PTEN) and subsequently increased activation of Akt in non-small-cell lung carcinoma cells. Then, we found that p38 inhibition upregulated special AT-rich sequence-binding protein 2 expression and reversed epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. Furthermore, special AT-rich sequence-binding protein 2 knockdown abolished the effect of p38 inhibition on epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. In conclusion, our results strongly indicate that the crosstalk between p38 and Akt pathways can determine special AT-rich sequence-binding protein 2 expression and epithelial character of non-small-cell lung carcinoma cells, and special AT-rich sequence-binding protein 2 is a critical epigenetic regulator for epithelial–mesenchymal transition mediated by p38 pathway in non-small-cell lung ...
العلاقة: Tumor Biology; Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı; https://hdl.handle.net/11499/8928Test; https://doi.org/10.1177/1010428317706212Test; 39; 2-s2.0-85031408155; WOS:000383616901419
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3دورية أكاديمية
المؤلفون: Taze C., Drakouli S., Samiotaki M., Panayotou G., Simos G., Georgatsou E., Mylonis I.
المصدر: Redox Biology ; https://www.scopus.com/inward/record.uri?eid=2-s2.0-85142441085&doi=10.1016%2fj.redox.2022.102545&partnerID=40&md5=8667d3a3b201713a4ae724e5432dba37Test
مصطلحات موضوعية: estrogen receptor, hypoxia inducible factor 1alpha, matrix attachment region binding protein, messenger RNA, nuclear matrix protein, reactive oxygen metabolite, SAFB protein, human, SRPK1 protein, vasculotropin A, cell hypoxia, cell nucleus matrix, genetics, hypoxia, metabolism, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Matrix Attachment Region Binding Proteins, Nuclear Matrix, Nuclear Matrix-Associated Proteins, Protein Serine-Threonine Kinases, Reactive Oxygen Species, Receptors, Estrogen, RNA, Messenger, Vascular Endothelial Growth Factor A, Elsevier B.V
الوصف: The cellular response to hypoxia, in addition to HIF-dependent transcriptional reprogramming, also involves less characterized transcription-independent processes, such as alternative splicing of the VEGFA transcript leading to the production of the proangiogenic VEGF form. We now show that this event depends on reorganization of the splicing machinery, triggered after short-term hypoxia by ROS production and intranuclear redistribution of the nucleoskeletal proteins SAFB1/2. Exposure to low oxygen causes fast dissociation of SAFB1/2 from the nuclear matrix, which is reversible, inhibited by antioxidant treatment, and also observed under normoxia when the mitochondrial electron transport chain is blocked. This is accompanied by altered interactions between SAFB1/2 and the splicing machinery, translocation of kinase SRPK1 to the cytoplasm, and dephosphorylation of RS-splicing factors. Depletion of SAFB1/2 under normoxia phenocopies the hypoxic and ROS-mediated switch in VEGF mRNA splicing. These data suggest that ROS-dependent remodeling of the nuclear architecture can promote production of splicing variants that facilitate adaptation to hypoxia. © 2022
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4دورية أكاديمية
المؤلفون: Inzani F., Angelico G., Santoro A., Travaglino A., Insabato L., Raffone A., Arciuolo D., Scaglione G., D'Alessandris N., Valente M., Carlino A., Rindi G., Zannoni G. F.
المساهمون: Inzani, F., Angelico, G., Santoro, A., Travaglino, A., Insabato, L., Raffone, A., Arciuolo, D., Scaglione, G., D'Alessandris, N., Valente, M., Carlino, A., Rindi, G., Zannoni, G. F.
مصطلحات موضوعية: Cervical cancer, Gynecological neuroendocrine neoplasm, Immunohistochemistry, NET, Neuroendocrine tumor, SATB2, Biomarkers, Tumor, Female, Human, Infant, Newborn, Transcription Factor, Carcinoma, Neuroendocrine, Matrix Attachment Region Binding Protein, Skin Neoplasm, Uterine Cervical Neoplasms
الوصف: Neuroendocrine carcinoma (NEC) of the uterine cervix is less characterized than neuroendocrine neoplasms of other sites such as of the digestive system and the lung. Special AT-rich sequence-binding protein 2 (SATB2) recently emerged as a marker of well-differentiated neuroendocrine tumors of the lower gastrointestinal (GI) tract. Among NECs, SATB2 is more frequently expressed in cutaneous Merkel cell carcinoma than in NEC of other anatomical sites. In our study, we performed an immunohistochemical study of SATB2 in 16 NECs of the uterine cervix, where the expression of these markers is still undefined. SATB2 was expressed in 12/16 cervical NECs (75%), with 7/16 cases (44%) showing SATB2 positivity in ≥ 50% of cells. In 7 cervical NECs associated with a non-neuroendocrine component, the expression of SATB2 was restricted to the neuroendocrine component. SATB2 was positive in all cases that expressed CDX2 (n = 7) and TTF1 (n = 5), with no evident association with p16 and p53. Our study demonstrated that SATB2 is often expressed in NECs of the uterine cervix. This information should be taken into account when assessing the origin of a NEC.
العلاقة: info:eu-repo/semantics/altIdentifier/wos/WOS:000749110700001; volume:480; issue:4; firstpage:873; lastpage:877; numberofpages:5; journal:VIRCHOWS ARCHIV; http://hdl.handle.net/11588/884227Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85123760474
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5دورية أكاديمية
المؤلفون: Girolami, Ilaria, Mancini, Irene, Simoni, Antonella, Baldi, Giacomo Giulio, Simi, Lisa, Campanacci, Domenico, Beltrami, Giovanni, Scoccianti, Guido, D'Arienzo, Antonio, CAPANNA, RODOLFO, FRANCHI, ALESSANDRO
المساهمون: Girolami, Ilaria, Mancini, Irene, Simoni, Antonella, Baldi, Giacomo Giulio, Simi, Lisa, Campanacci, Domenico, Beltrami, Giovanni, Scoccianti, Guido, D'Arienzo, Antonio, Capanna, Rodolfo, Franchi, Alessandro
مصطلحات موضوعية: BONE TUMOURS, CANCER GENETICS, IMMUNOCYTOCHEMISTRY, Adolescent, Adult, Aged, Angiogenesis Inhibitor, Bone Density Conservation Agent, Bone Neoplasm, Cell Proliferation, Core Binding Factor Alpha 1 Subunit, Denosumab, Female, Giant Cell Tumor of Bone, Histone, Human, Male, Matrix Attachment Region Binding Protein, Middle Aged, Mutation, Neovascularization, Pathologic, Predictive Value of Test, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B, Transcription Factor, Treatment Outcome, Young Adult, Biomarkers, Tumor
الوقت: 2734
الوصف: Aims: Denosumab, a fully human monoclonal antibody directed against RANKL, has recently been introduced in the treatment strategy of giant cell tumour of bone (GCTB). Aim of this study was to investigate the phenotypical modifications induced by denosumab treatment in a series of 15 GCTB. Methods: The tumours were characterised for histone 3.3 mutations, and studied immunohistochemically for the modifications of RANKL, RANK, SATB2 and RUNX2 expression, as well as of tumour proliferative activity and angiogenesis. Results: Nine of 11 tumours investigated presented a histone 3.3 mutation in H3F3A, and 2 of these for which the analysis was carried out in pretreatment and post-treatment specimens showed the same mutation in both. Denosumab induced the disappearance of osteoclast-like giant cells, leaving residual spindle neoplastic cells arranged in a storiform pattern, with deposition of trabecular collagen matrix and osteoid, which tended to maturation in the peripheral portions of the lesion. RANK and RANKL expression was variable, with no significant variation after treatment. Moreover, we did not observe any significant modification of the expression of the osteoblastic markers SATB2 and RUNX2. Denosumab treatment determined a significant reduction of the proliferative index and of tumour angiogenesis (p=0.001, Wilcoxon rank-sum test). Conclusions: These results indicate that denosumab induces a partial maturation towards the osteoblastic phenotype of the neoplastic cells of GCTB, with production of fibrous and osteoid matrix, but with minor immunophenotypical changes. Finally, we first report an antiangiogenic activity of denosumab in GCTB, possibly mediated by a RANKL-dependent pathway.
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/26338802; info:eu-repo/semantics/altIdentifier/wos/WOS:000370829100008; volume:69; issue:3; firstpage:240; lastpage:247; numberofpages:8; journal:JOURNAL OF CLINICAL PATHOLOGY; http://hdl.handle.net/11568/804508Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84959345838; https://jcp.bmj.com/content/69/3/240lTest
الإتاحة: https://doi.org/10.1136/jclinpath-2015-203248Test
http://hdl.handle.net/11568/804508Test
https://jcp.bmj.com/content/69/3/240lTest -
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المؤلفون: Frediano Inzani, Giuseppe Angelico, Angela Santoro, Antonio Travaglino, Luigi Insabato, Antonio Raffone, Damiano Arciuolo, Giulia Scaglione, Nicoletta D’Alessandris, Michele Valente, Angela Carlino, Guido Rindi, Gian Franco Zannoni
المساهمون: Inzani, F., Angelico, G., Santoro, A., Travaglino, A., Insabato, L., Raffone, A., Arciuolo, D., Scaglione, G., D'Alessandris, N., Valente, M., Carlino, A., Rindi, G., Zannoni, G. F.
المصدر: Virchows Archiv : an international journal of pathology. 480(4)
مصطلحات موضوعية: Skin Neoplasms, Transcription Factor, Uterine Cervical Neoplasms, Gynecological neuroendocrine neoplasm, Pathology and Forensic Medicine, Neuroendocrine tumor, SATB2, Biomarkers, Tumor, Humans, Skin Neoplasm, Molecular Biology, Settore MED/08 - ANATOMIA PATOLOGICA, Matrix Attachment Region Binding Protein, Infant, Newborn, Cell Biology, General Medicine, Matrix Attachment Region Binding Proteins, Immunohistochemistry, Carcinoma, Neuroendocrine, Gynecological neuroendocrine neoplasms, NET, Cervical cancer, Female, Neuroendocrine tumors, Human, Transcription Factors
الوصف: Neuroendocrine carcinoma (NEC) of the uterine cervix is less characterized than neuroendocrine neoplasms of other sites such as of the digestive system and the lung. Special AT-rich sequence-binding protein 2 (SATB2) recently emerged as a marker of well-differentiated neuroendocrine tumors of the lower gastrointestinal (GI) tract. Among NECs, SATB2 is more frequently expressed in cutaneous Merkel cell carcinoma than in NEC of other anatomical sites. In our study, we performed an immunohistochemical study of SATB2 in 16 NECs of the uterine cervix, where the expression of these markers is still undefined. SATB2 was expressed in 12/16 cervical NECs (75%), with 7/16 cases (44%) showing SATB2 positivity in ≥ 50% of cells. In 7 cervical NECs associated with a non-neuroendocrine component, the expression of SATB2 was restricted to the neuroendocrine component. SATB2 was positive in all cases that expressed CDX2 (n = 7) and TTF1 (n = 5), with no evident association with p16 and p53. Our study demonstrated that SATB2 is often expressed in NECs of the uterine cervix. This information should be taken into account when assessing the origin of a NEC.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5609f2b7e8c2eb18ea4ebfe00042764aTest
https://pubmed.ncbi.nlm.nih.gov/35091815Test -
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المؤلفون: Silvia Giulia Galfrè, Manuela Helmer-Citterich, Milena Rizzo, Robert Vignali, Laura Poliseno, Irene Appolloni, Keagan Dunville, Francesco Morandin, Paolo Malatesta, Manuella Martins, Andrea Marranci, Marco Pietrosanto, Luca Pandolfini, Marco Terrigno, Federico Cremisi, Alberto Mercatanti
المساهمون: Martins, Manuella, Galfrè, Silvia, Terrigno, Marco, Pandolfini, Luca, Appolloni, Irene, Dunville, Keagan, Marranci, Andrea, Rizzo, Milena, Mercatanti, Alberto, Poliseno, Laura, Morandin, Francesco, Pietrosanto, Marco, Helmer-Citterich, Manuela, Malatesta, Paolo, Vignali, Robert, Cremisi, Federico
المصدر: Stem Cell Reports
مصطلحات موضوعية: 0301 basic medicine, Transcription Factor, Biochemistry, corpus callosum, neural stem cell, Mice, Settore BIO/06 - Anatomia Comparata e Citologia, 0302 clinical medicine, RNA interference, developmental timing, 3' Untranslated Regions, neural stem cells, Cerebral Cortex, cell fate, biology, microRNA, Settore BIO/11, Eutheria, Matrix Attachment Region Binding Protein, Gene Expression Regulation, Developmental, Translation (biology), Cell Differentiation, Neural stem cell, Cell biology, mammalian evolution, Corticogenesis, cortex, Human, in vitro corticogenesi, Neurogenesis, 3' Untranslated Region, Cell fate determination, post-transcriptional control, Article, Cell Line, 03 medical and health sciences, SATB2, cell identity, cortical layering, in vitro corticogenesis, miR-catch, Genetics, Animals, Humans, Progenitor cell, Post-transcriptional regulation, Animal, Tumor Suppressor Proteins, Matrix Attachment Region Binding Proteins, Cell Biology, Repressor Protein, Repressor Proteins, MicroRNAs, 030104 developmental biology, Cell fate, biology.protein, Neurogenesi, in vitro corticogenesis, TBR1, 030217 neurology & neurosurgery, Transcription Factors, Developmental Biology
الوصف: Summary Cerebral cortical development is controlled by key transcription factors that specify the neuronal identities in the different layers. The mechanisms controlling their expression in distinct cells are only partially known. We investigated the expression and stability of Tbr1, Bcl11b, Fezf2, Satb2, and Cux1 mRNAs in single developing mouse cortical cells. We observe that Satb2 mRNA appears much earlier than its protein and in a set of cells broader than expected, suggesting an initial inhibition of its translation, subsequently released during development. Mechanistically, Satb2 3′UTR modulates protein translation of GFP reporters during mouse corticogenesis. We select miR-541, a eutherian-specific miRNA, and miR-92a/b as the best candidates responsible for SATB2 inhibition, being strongly expressed in early and reduced in late progenitor cells. Their inactivation triggers robust and premature SATB2 translation in both mouse and human cortical cells. Our findings indicate RNA interference as a major mechanism in timing cortical cell identities.
Graphical abstract
Highlights • mRNAs for key transcription factors are differentially stable during corticogenesis • miRNAs show a dynamic profile of expression in a model of mouse corticogenesis • miR-541 and miR-92a/b bind Satb2 3′UTR and prevent SATB2 translation • Antagonizing mir-541 and miR-92a/b anticipates SATB2 protein production
In this article, Cremisi and colleagues show that post-transcriptional mechanisms are involved in controlling key functional aspects of SATB2-expressing cortical neurons. They show that mir-541, a eutherian-specific miRNA, delays SATB2 protein production in an in vitro model of cortical cell differentiation. These results may explain the heterochronic shift of SATB2 appearance in the eutherian compared with the metatherian cortex.الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ff37e0b84ee1a85682af8cc2e372669fTest
https://hdl.handle.net/11384/94206Test -
8دورية أكاديمية
المؤلفون: Agostini F., Cirillo D., Bolognesi B., Tartaglia G. G.
المساهمون: Agostini, F., Cirillo, D., Bolognesi, B., Tartaglia, G. G.
مصطلحات موضوعية: Animal, binding, enhancer of Zeste homolog 2 protein, female, heterogeneous-nuclear ribonucleoprotein U, matrix attachment region binding protein, mice, nuclear protein, polycomb repressive complex 2, RNA, long noncoding, RNA-binding protein, repetitive sequences, nucleic acid, serine-arginine splicing factor, YY1 transcription factor, algorithm, X chromosome inactivation
الوصف: The transcriptional silencing of one of the female X-chromosomes is a finely regulated process that requires accumulation in cis of the long non-coding RNA X-inactive-specific transcript (Xist) followed by a series of epigenetic modifications. Little is known about the molecular machinery regulating initiation and maintenance of chromosomal silencing. Here, we introduce a new version of our algorithm catRAPID to investigate Xist associations with a number of proteins involved in epigenetic regulation, nuclear scaffolding, transcription and splicing processes. Our method correctly identifies binding regions and affinities of protein interactions, providing a powerful theoretical framework for the study of X-chromosome inactivation and other events mediated by ribonucleoprotein associations. © 2012 The Author(s). Published by Oxford University Press.
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/23093590; info:eu-repo/semantics/altIdentifier/wos/WOS:000312889900031; volume:41; issue:1; firstpage:e31; numberofpages:9; journal:NUCLEIC ACIDS RESEARCH; http://hdl.handle.net/11573/1451739Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84871806618
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المؤلفون: Bergman, Annika, Abel, Frida, Behboudi, Afrouz, Yhr, Maria, Mattsson, Jan, Svensson, Jan H., Karlsson, Per, Nordling, Margareta
المصدر: BMC Medical Genetics. 9
مصطلحات موضوعية: estrogen receptor, matrix attachment region binding protein, nuclear matrix protein, SAFB protein, human, SAFB2 protein, article, breast tumor, chromosome 19, DNA sequence, female, genetic linkage, genetics, mutation, nucleic acid amplification, polymerase chain reaction, Sweden, tumor suppressor gene, Breast Neoplasms, Chromosomes, Human, Pair 19, Genes, BRCA1, BRCA2, Germ-Line Mutation, Humans, Linkage (Genetics), Matrix Attachment Region Binding Proteins, Nuclear Matrix-Associated Proteins, Nucleic Acid Amplification Techniques, Receptors, Estrogen, Sequence Analysis, DNA
الوصف: BACKGROUND: The scaffold attachment factor B1 and B2 genes, SAFB1/SAFB2 (both located on chromosome 19p13.3) have recently been suggested as tumour suppressor genes involved in breast cancer development. The assumption was based on functional properties of the two genes and loss of heterozygosity of intragenic markers in breast tumours further strengthened the postulated hypothesis. In addition, linkage studies in Swedish breast cancer families also indicate the presence of a susceptibility gene for breast cancer at the 19p locus. Somatic mutations in SAFB1/SAFB2 have been detected in breast tumours, but to our knowledge no studies on germline mutations have been reported. In this study we investigated the possible involvement of SAFB1/SAFB2 on familiar breast cancer by inherited mutations in either of the two genes.RESULTS: Mutation analysis in families showing linkage to the SAFB1/2 locus was performed by DNA sequencing. The complete coding sequence of the two genes SAFB1 and SAFB2 was analyzed in germline DNA from 31 affected women. No missense or frameshift mutations were detected. One polymorphism was found in SAFB1 and eight polymorphisms were detected in SAFB2. MLPA-anlysis showed that both alleles of the two genes were preserved which excludes gene inactivation by large deletions.CONCLUSION: SAFB1 and SAFB2 are not likely to be causative of the hereditary breast cancer syndrome in west Swedish breast cancer families.
وصف الملف: print
الوصول الحر: https://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-39621Test
https://doi.org/10.1186/1471-2350-9-108Test -
10دورية أكاديمية
المؤلفون: Drakouli S., Lyberopoulou A., Papathanassiou M., Mylonis I., Georgatsou E.
المصدر: FEBS Journal ; https://www.scopus.com/inward/record.uri?eid=2-s2.0-85021884636&doi=10.1111%2ffebs.14141&partnerID=40&md5=4f771c2559845b409aba6b723bd4fa3fTest
مصطلحات موضوعية: estrogen receptor alpha, serine arginine rich protein, cell cycle protein, ERH protein, human, estrogen receptor, green fluorescent protein, hybrid protein, matrix attachment region binding protein, nuclear matrix protein, peptide fragment, protein serine threonine kinase, SAFB protein, SAFB2 protein, serine arginine rich splicing factor, SRPK1 protein, transcription factor, Article, carboxy terminal sequence, cell nucleus matrix, controlled study, ERH gene, gene function, gene interaction, gene location, gene silencing, genetic transcription, human cell, in vitro study, priority journal
الوصف: Scaffold attachment factor B1 (SAFB1) is an integral component of the nuclear matrix of vertebrate cells. It binds to DNA on scaffold/matrix attachment region elements, as well as to RNA and a multitude of different proteins, affecting basic cellular activities such as transcription, splicing and DNA damage repair. In the present study, we show that enhancer of rudimentary homologue (ERH) is a new molecular partner of SAFB1 and its 70% homologous paralogue, scaffold attachment factor B2 (SAFB2). ERH interacts directly in the nucleus with the C-terminal Arg-Gly-rich region of SAFB1/2 and co-localizes with it in the insoluble nuclear fraction. ERH, a small ubiquitous protein with striking homology among species and a unique structure, has also been implicated in fundamental cellular mechanisms. Our functional analyses suggest that the SAFB/ERH interaction does not affect SAFB1/2 function in transcription (e.g. as oestrogen receptor α co-repressors), although it reverses the inhibition exerted by SAFB1/2 on the splicing kinase SR protein kinase 1 (SRPK1), which also binds on the C-terminus of SAFB1/2. Accordingly, ERH silencing decreases lamin B receptor and SR protein phosphorylation, which are major SRPK1 substrates, further substantiating the role of SAFB1 and SAFB2 in the co-ordination of nuclear function. © 2017 Federation of European Biochemical Societies