Datasheet Unblocked Protein A beads kch-503 DATASHEET Datasheet description | Download |
The unblocked protein A beads are agarose beads that have been extensively validated in chromatin immunoprecipitation assays (ChIP). These beads are intended for isolation of immune complexes (chromatin and specific antibody) in ChIP experiments. The beads are suitable for immunoprecipitation of rabbit polyclonal Abs, mouse IgG2a, IgG2b and IgA, guinea pig IgG, dog IgG, pig IgG. The beads should be washed before use.
Datasheet Unblocked Protein A beads kch-503 DATASHEET Datasheet description | Download |
Unblocked Protein A beads SDS GB en | Download |
Unblocked Protein A beads SDS US en | Download |
Unblocked Protein A beads SDS DE de | Download |
Unblocked Protein A beads SDS JP ja | Download |
Unblocked Protein A beads SDS BE nl | Download |
Unblocked Protein A beads SDS BE fr | Download |
Unblocked Protein A beads SDS FR fr | Download |
Unblocked Protein A beads SDS ES es | Download |
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CTCF is dispensable for immune cell transdifferentiation but facilitates an acute inflammatory response. |
Three-Dimensional Genomic Structure and Cohesin Occupancy Correlate with Transcriptional Activity during Spermatogenesis. |
Lamin B1 mapping reveals the existence of dynamic and functional euchromatin lamin B1 domains. |
The transcriptional factor ZEB1 represses Syndecan 1 expression in prostate cancer. |
ClpX stimulates the mitochondrial unfolded protein response (UPRmt) in mammalian cells |
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In mammals, CTCF and the cohesin complex create submegabase structures with elevated internal chromatin contact frequencies, called topologically associating domains (TADs). Although TADs can contribute to transcriptional regulation, ablation of TAD organization by disrupting CTCF or the cohesin complex causes modest gene expression changes. In contrast, CTCF is required for cell cycle regulation, embryonic development and formation of various adult cell types. To uncouple the role of CTCF in cell-state transitions and cell proliferation, we studied the effect of CTCF depletion during the conversion of human leukemic B cells into macrophages with minimal cell division. CTCF depletion disrupts TAD organization but not cell transdifferentiation. In contrast, CTCF depletion in induced macrophages impairs the full-blown upregulation of inflammatory genes after exposure to endotoxin. Our results demonstrate that CTCF-dependent genome topology is not strictly required for a functional cell-fate conversion but facilitates a rapid and efficient response to an external stimulus.</p>', 'date' => '2020-06-08', 'pmid' => 'http://www.pubmed.gov/32514124', 'doi' => '10.1038/s41588-020-0643-0', 'modified' => '2020-08-12 09:33:45', 'created' => '2020-08-10 12:12:25', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3748', 'name' => 'Three-Dimensional Genomic Structure and Cohesin Occupancy Correlate with Transcriptional Activity during Spermatogenesis.', 'authors' => 'Vara C, Paytuví-Gallart A, Cuartero Y, Le Dily F, Garcia F, Salvà-Castro J, Gómez-H L, Julià E, Moutinho C, Aiese Cigliano R, Sanseverino W, Fornas O, Pendás AM, Heyn H, Waters PD, Marti-Renom MA, Ruiz-Herrera A', 'description' => '<p>Mammalian gametogenesis involves dramatic and tightly regulated chromatin remodeling, whose regulatory pathways remain largely unexplored. Here, we generate a comprehensive high-resolution structural and functional atlas of mouse spermatogenesis by combining in situ chromosome conformation capture sequencing (Hi-C), RNA sequencing (RNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) of CCCTC-binding factor (CTCF) and meiotic cohesins, coupled with confocal and super-resolution microscopy. Spermatogonia presents well-defined compartment patterns and topological domains. However, chromosome occupancy and compartmentalization are highly re-arranged during prophase I, with cohesins bound to active promoters in DNA loops out of the chromosomal axes. Compartment patterns re-emerge in round spermatids, where cohesin occupancy correlates with transcriptional activity of key developmental genes. The compact sperm genome contains compartments with actively transcribed genes but no fine-scale topological domains, concomitant with the presence of protamines. Overall, we demonstrate how genome-wide cohesin occupancy and transcriptional activity is associated with three-dimensional (3D) remodeling during spermatogenesis, ultimately reprogramming the genome for the next generation.</p>', 'date' => '2019-07-09', 'pmid' => 'http://www.pubmed.gov/31291573', 'doi' => '10.1016/j.celrep.2019.06.037', 'modified' => '2019-08-06 16:12:27', 'created' => '2019-07-31 13:35:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '3442', 'name' => 'Lamin B1 mapping reveals the existence of dynamic and functional euchromatin lamin B1 domains.', 'authors' => 'Pascual-Reguant L, Blanco E, Galan S, Le Dily F, Cuartero Y, Serra-Bardenys G, Di Carlo V, Iturbide A, Cebrià-Costa JP, Nonell L, de Herreros AG, Di Croce L, Marti-Renom MA, Peiró S', 'description' => '<p>Lamins (A/C and B) are major constituents of the nuclear lamina (NL). Structurally conserved lamina-associated domains (LADs) are formed by genomic regions that contact the NL. Lamins are also found in the nucleoplasm, with a yet unknown function. Here we map the genome-wide localization of lamin B1 in an euchromatin-enriched fraction of the mouse genome and follow its dynamics during the epithelial-to-mesenchymal transition (EMT). Lamin B1 associates with actively expressed and open euchromatin regions, forming dynamic euchromatin lamin B1-associated domains (eLADs) of about 0.3 Mb. Hi-C data link eLADs to the 3D organization of the mouse genome during EMT and correlate lamin B1 enrichment at topologically associating domain (TAD) borders with increased border strength. Having reduced levels of lamin B1 alters the EMT transcriptional signature and compromises the acquisition of mesenchymal traits. Thus, during EMT, the process of genome reorganization in mouse involves dynamic changes in eLADs.</p>', 'date' => '2018-08-24', 'pmid' => 'http://www.pubmed.gov/30143639', 'doi' => '10.1038/s41467-018-05912-z', 'modified' => '2019-02-28 10:11:55', 'created' => '2019-02-14 15:01:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '3586', 'name' => 'The transcriptional factor ZEB1 represses Syndecan 1 expression in prostate cancer.', 'authors' => 'Farfán N, Ocarez N, Castellón EA, Mejía N, de Herreros AG, Contreras HR', 'description' => '<p>Syndecan 1 (SDC-1) is a cell surface proteoglycan with a significant role in cell adhesion, maintaining epithelial integrity. SDC1 expression is inversely related to aggressiveness in prostate cancer (PCa). During epithelial to mesenchymal transition (EMT), loss of epithelial markers is mediated by transcriptional repressors such as SNAIL, SLUG, or ZEB1/2 that bind to E-box promoter sequences of specific genes. The effect of these repressors on SDC-1 expression remains unknown. Here, we demonstrated that SNAIL, SLUG and ZEB1 expressions are increased in advanced PCa, contrarily to SDC-1. SNAIL, SLUG and ZEB1 also showed an inversion to SDC-1 in prostate cell lines. ZEB1, but not SNAIL or SLUG, represses SDC-1 as demonstrated by experiments of ectopic expression in epithelial prostate cell lines. Inversely, expression of ZEB1 shRNA in PCa cell line increased SDC-1 expression. The effect of ZEB1 is transcriptional since ectopic expression of this gene represses SDC-1 promoter activity and ZEB1 binds to the SDC-1 promoter as detected by ChIP assays. An epigenetic mark associated to transcription repression H3K27me3 was bound to the same sites that ZEB1. In conclusion, this study identifies ZEB1 as a key repressor of SDC-1 during PCa progression and point to ZEB1 as a potentially diagnostic marker for PCa.</p>', 'date' => '2018-07-31', 'pmid' => 'http://www.pubmed.gov/30065348', 'doi' => '10.1038/s41598-018-29829-1', 'modified' => '2019-04-17 15:32:57', 'created' => '2019-04-16 12:25:30', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '2852', 'name' => 'ClpX stimulates the mitochondrial unfolded protein response (UPRmt) in mammalian cells', 'authors' => 'Al-Furoukh N, Ianni A, Nolte H, Hölper S, Krüger M, Wanrooij S, Braun T', 'description' => '<p>Proteostasis is crucial for life and maintained by cellular chaperones and proteases. One major mitochondrial protease is the ClpXP complex, which is comprised of a catalytic ClpX subunit and a proteolytic ClpP subunit. Based on two separate observations, we hypothesized that ClpX may play a leading role in the cellular function of ClpXP. Therefore, we analyzed the effect of ClpX overexpression on a myoblast proteome by quantitative proteomics. ClpX overexpression results in the upregulation of markers of the mitochondrial proteostasis pathway, known as the "mitochondrial unfolded protein response" (UPRmt). Although this pathway is described in detail in Caenorhabditis elegans, it is not clear whether it is conserved in mammals. Therefore, we compared features of the classical nematode UPRmt with our mammalian ClpX-triggered UPRmt dataset. We show that they share the same retrograde mitochondria-to-nucleus signaling pathway that involves the key UPRmt transcription factor CHOP (also known as Ddit3, CEBPZ or GADD153). In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. 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One major mitochondrial protease is the ClpXP complex, which is comprised of a catalytic ClpX subunit and a proteolytic ClpP subunit. Based on two separate observations, we hypothesized that ClpX may play a leading role in the cellular function of ClpXP. Therefore, we analyzed the effect of ClpX overexpression on a myoblast proteome by quantitative proteomics. ClpX overexpression results in the upregulation of markers of the mitochondrial proteostasis pathway, known as the "mitochondrial unfolded protein response" (UPRmt). Although this pathway is described in detail in Caenorhabditis elegans, it is not clear whether it is conserved in mammals. Therefore, we compared features of the classical nematode UPRmt with our mammalian ClpX-triggered UPRmt dataset. We show that they share the same retrograde mitochondria-to-nucleus signaling pathway that involves the key UPRmt transcription factor CHOP (also known as Ddit3, CEBPZ or GADD153). In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. 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In mammals, CTCF and the cohesin complex create submegabase structures with elevated internal chromatin contact frequencies, called topologically associating domains (TADs). Although TADs can contribute to transcriptional regulation, ablation of TAD organization by disrupting CTCF or the cohesin complex causes modest gene expression changes. In contrast, CTCF is required for cell cycle regulation, embryonic development and formation of various adult cell types. To uncouple the role of CTCF in cell-state transitions and cell proliferation, we studied the effect of CTCF depletion during the conversion of human leukemic B cells into macrophages with minimal cell division. CTCF depletion disrupts TAD organization but not cell transdifferentiation. In contrast, CTCF depletion in induced macrophages impairs the full-blown upregulation of inflammatory genes after exposure to endotoxin. Our results demonstrate that CTCF-dependent genome topology is not strictly required for a functional cell-fate conversion but facilitates a rapid and efficient response to an external stimulus.</p>', 'date' => '2020-06-08', 'pmid' => 'http://www.pubmed.gov/32514124', 'doi' => '10.1038/s41588-020-0643-0', 'modified' => '2020-08-12 09:33:45', 'created' => '2020-08-10 12:12:25', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3748', 'name' => 'Three-Dimensional Genomic Structure and Cohesin Occupancy Correlate with Transcriptional Activity during Spermatogenesis.', 'authors' => 'Vara C, Paytuví-Gallart A, Cuartero Y, Le Dily F, Garcia F, Salvà-Castro J, Gómez-H L, Julià E, Moutinho C, Aiese Cigliano R, Sanseverino W, Fornas O, Pendás AM, Heyn H, Waters PD, Marti-Renom MA, Ruiz-Herrera A', 'description' => '<p>Mammalian gametogenesis involves dramatic and tightly regulated chromatin remodeling, whose regulatory pathways remain largely unexplored. Here, we generate a comprehensive high-resolution structural and functional atlas of mouse spermatogenesis by combining in situ chromosome conformation capture sequencing (Hi-C), RNA sequencing (RNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) of CCCTC-binding factor (CTCF) and meiotic cohesins, coupled with confocal and super-resolution microscopy. Spermatogonia presents well-defined compartment patterns and topological domains. However, chromosome occupancy and compartmentalization are highly re-arranged during prophase I, with cohesins bound to active promoters in DNA loops out of the chromosomal axes. Compartment patterns re-emerge in round spermatids, where cohesin occupancy correlates with transcriptional activity of key developmental genes. The compact sperm genome contains compartments with actively transcribed genes but no fine-scale topological domains, concomitant with the presence of protamines. 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Structurally conserved lamina-associated domains (LADs) are formed by genomic regions that contact the NL. Lamins are also found in the nucleoplasm, with a yet unknown function. Here we map the genome-wide localization of lamin B1 in an euchromatin-enriched fraction of the mouse genome and follow its dynamics during the epithelial-to-mesenchymal transition (EMT). Lamin B1 associates with actively expressed and open euchromatin regions, forming dynamic euchromatin lamin B1-associated domains (eLADs) of about 0.3 Mb. Hi-C data link eLADs to the 3D organization of the mouse genome during EMT and correlate lamin B1 enrichment at topologically associating domain (TAD) borders with increased border strength. Having reduced levels of lamin B1 alters the EMT transcriptional signature and compromises the acquisition of mesenchymal traits. 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During epithelial to mesenchymal transition (EMT), loss of epithelial markers is mediated by transcriptional repressors such as SNAIL, SLUG, or ZEB1/2 that bind to E-box promoter sequences of specific genes. The effect of these repressors on SDC-1 expression remains unknown. Here, we demonstrated that SNAIL, SLUG and ZEB1 expressions are increased in advanced PCa, contrarily to SDC-1. SNAIL, SLUG and ZEB1 also showed an inversion to SDC-1 in prostate cell lines. ZEB1, but not SNAIL or SLUG, represses SDC-1 as demonstrated by experiments of ectopic expression in epithelial prostate cell lines. Inversely, expression of ZEB1 shRNA in PCa cell line increased SDC-1 expression. The effect of ZEB1 is transcriptional since ectopic expression of this gene represses SDC-1 promoter activity and ZEB1 binds to the SDC-1 promoter as detected by ChIP assays. An epigenetic mark associated to transcription repression H3K27me3 was bound to the same sites that ZEB1. In conclusion, this study identifies ZEB1 as a key repressor of SDC-1 during PCa progression and point to ZEB1 as a potentially diagnostic marker for PCa.</p>', 'date' => '2018-07-31', 'pmid' => 'http://www.pubmed.gov/30065348', 'doi' => '10.1038/s41598-018-29829-1', 'modified' => '2019-04-17 15:32:57', 'created' => '2019-04-16 12:25:30', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '2852', 'name' => 'ClpX stimulates the mitochondrial unfolded protein response (UPRmt) in mammalian cells', 'authors' => 'Al-Furoukh N, Ianni A, Nolte H, Hölper S, Krüger M, Wanrooij S, Braun T', 'description' => '<p>Proteostasis is crucial for life and maintained by cellular chaperones and proteases. One major mitochondrial protease is the ClpXP complex, which is comprised of a catalytic ClpX subunit and a proteolytic ClpP subunit. Based on two separate observations, we hypothesized that ClpX may play a leading role in the cellular function of ClpXP. Therefore, we analyzed the effect of ClpX overexpression on a myoblast proteome by quantitative proteomics. ClpX overexpression results in the upregulation of markers of the mitochondrial proteostasis pathway, known as the "mitochondrial unfolded protein response" (UPRmt). Although this pathway is described in detail in Caenorhabditis elegans, it is not clear whether it is conserved in mammals. Therefore, we compared features of the classical nematode UPRmt with our mammalian ClpX-triggered UPRmt dataset. We show that they share the same retrograde mitochondria-to-nucleus signaling pathway that involves the key UPRmt transcription factor CHOP (also known as Ddit3, CEBPZ or GADD153). In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. 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In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. 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In mammals, CTCF and the cohesin complex create submegabase structures with elevated internal chromatin contact frequencies, called topologically associating domains (TADs). Although TADs can contribute to transcriptional regulation, ablation of TAD organization by disrupting CTCF or the cohesin complex causes modest gene expression changes. In contrast, CTCF is required for cell cycle regulation, embryonic development and formation of various adult cell types. To uncouple the role of CTCF in cell-state transitions and cell proliferation, we studied the effect of CTCF depletion during the conversion of human leukemic B cells into macrophages with minimal cell division. CTCF depletion disrupts TAD organization but not cell transdifferentiation. In contrast, CTCF depletion in induced macrophages impairs the full-blown upregulation of inflammatory genes after exposure to endotoxin. Our results demonstrate that CTCF-dependent genome topology is not strictly required for a functional cell-fate conversion but facilitates a rapid and efficient response to an external stimulus.</p>', 'date' => '2020-06-08', 'pmid' => 'http://www.pubmed.gov/32514124', 'doi' => '10.1038/s41588-020-0643-0', 'modified' => '2020-08-12 09:33:45', 'created' => '2020-08-10 12:12:25', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3748', 'name' => 'Three-Dimensional Genomic Structure and Cohesin Occupancy Correlate with Transcriptional Activity during Spermatogenesis.', 'authors' => 'Vara C, Paytuví-Gallart A, Cuartero Y, Le Dily F, Garcia F, Salvà-Castro J, Gómez-H L, Julià E, Moutinho C, Aiese Cigliano R, Sanseverino W, Fornas O, Pendás AM, Heyn H, Waters PD, Marti-Renom MA, Ruiz-Herrera A', 'description' => '<p>Mammalian gametogenesis involves dramatic and tightly regulated chromatin remodeling, whose regulatory pathways remain largely unexplored. Here, we generate a comprehensive high-resolution structural and functional atlas of mouse spermatogenesis by combining in situ chromosome conformation capture sequencing (Hi-C), RNA sequencing (RNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) of CCCTC-binding factor (CTCF) and meiotic cohesins, coupled with confocal and super-resolution microscopy. Spermatogonia presents well-defined compartment patterns and topological domains. However, chromosome occupancy and compartmentalization are highly re-arranged during prophase I, with cohesins bound to active promoters in DNA loops out of the chromosomal axes. Compartment patterns re-emerge in round spermatids, where cohesin occupancy correlates with transcriptional activity of key developmental genes. The compact sperm genome contains compartments with actively transcribed genes but no fine-scale topological domains, concomitant with the presence of protamines. Overall, we demonstrate how genome-wide cohesin occupancy and transcriptional activity is associated with three-dimensional (3D) remodeling during spermatogenesis, ultimately reprogramming the genome for the next generation.</p>', 'date' => '2019-07-09', 'pmid' => 'http://www.pubmed.gov/31291573', 'doi' => '10.1016/j.celrep.2019.06.037', 'modified' => '2019-08-06 16:12:27', 'created' => '2019-07-31 13:35:50', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 2 => array( 'id' => '3442', 'name' => 'Lamin B1 mapping reveals the existence of dynamic and functional euchromatin lamin B1 domains.', 'authors' => 'Pascual-Reguant L, Blanco E, Galan S, Le Dily F, Cuartero Y, Serra-Bardenys G, Di Carlo V, Iturbide A, Cebrià-Costa JP, Nonell L, de Herreros AG, Di Croce L, Marti-Renom MA, Peiró S', 'description' => '<p>Lamins (A/C and B) are major constituents of the nuclear lamina (NL). Structurally conserved lamina-associated domains (LADs) are formed by genomic regions that contact the NL. Lamins are also found in the nucleoplasm, with a yet unknown function. Here we map the genome-wide localization of lamin B1 in an euchromatin-enriched fraction of the mouse genome and follow its dynamics during the epithelial-to-mesenchymal transition (EMT). Lamin B1 associates with actively expressed and open euchromatin regions, forming dynamic euchromatin lamin B1-associated domains (eLADs) of about 0.3 Mb. Hi-C data link eLADs to the 3D organization of the mouse genome during EMT and correlate lamin B1 enrichment at topologically associating domain (TAD) borders with increased border strength. Having reduced levels of lamin B1 alters the EMT transcriptional signature and compromises the acquisition of mesenchymal traits. Thus, during EMT, the process of genome reorganization in mouse involves dynamic changes in eLADs.</p>', 'date' => '2018-08-24', 'pmid' => 'http://www.pubmed.gov/30143639', 'doi' => '10.1038/s41467-018-05912-z', 'modified' => '2019-02-28 10:11:55', 'created' => '2019-02-14 15:01:22', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 3 => array( 'id' => '3586', 'name' => 'The transcriptional factor ZEB1 represses Syndecan 1 expression in prostate cancer.', 'authors' => 'Farfán N, Ocarez N, Castellón EA, Mejía N, de Herreros AG, Contreras HR', 'description' => '<p>Syndecan 1 (SDC-1) is a cell surface proteoglycan with a significant role in cell adhesion, maintaining epithelial integrity. SDC1 expression is inversely related to aggressiveness in prostate cancer (PCa). During epithelial to mesenchymal transition (EMT), loss of epithelial markers is mediated by transcriptional repressors such as SNAIL, SLUG, or ZEB1/2 that bind to E-box promoter sequences of specific genes. The effect of these repressors on SDC-1 expression remains unknown. Here, we demonstrated that SNAIL, SLUG and ZEB1 expressions are increased in advanced PCa, contrarily to SDC-1. SNAIL, SLUG and ZEB1 also showed an inversion to SDC-1 in prostate cell lines. ZEB1, but not SNAIL or SLUG, represses SDC-1 as demonstrated by experiments of ectopic expression in epithelial prostate cell lines. Inversely, expression of ZEB1 shRNA in PCa cell line increased SDC-1 expression. The effect of ZEB1 is transcriptional since ectopic expression of this gene represses SDC-1 promoter activity and ZEB1 binds to the SDC-1 promoter as detected by ChIP assays. An epigenetic mark associated to transcription repression H3K27me3 was bound to the same sites that ZEB1. 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In mammals, CTCF and the cohesin complex create submegabase structures with elevated internal chromatin contact frequencies, called topologically associating domains (TADs). Although TADs can contribute to transcriptional regulation, ablation of TAD organization by disrupting CTCF or the cohesin complex causes modest gene expression changes. In contrast, CTCF is required for cell cycle regulation, embryonic development and formation of various adult cell types. To uncouple the role of CTCF in cell-state transitions and cell proliferation, we studied the effect of CTCF depletion during the conversion of human leukemic B cells into macrophages with minimal cell division. CTCF depletion disrupts TAD organization but not cell transdifferentiation. In contrast, CTCF depletion in induced macrophages impairs the full-blown upregulation of inflammatory genes after exposure to endotoxin. Our results demonstrate that CTCF-dependent genome topology is not strictly required for a functional cell-fate conversion but facilitates a rapid and efficient response to an external stimulus.</p>', 'date' => '2020-06-08', 'pmid' => 'http://www.pubmed.gov/32514124', 'doi' => '10.1038/s41588-020-0643-0', 'modified' => '2020-08-12 09:33:45', 'created' => '2020-08-10 12:12:25', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 1 => array( 'id' => '3748', 'name' => 'Three-Dimensional Genomic Structure and Cohesin Occupancy Correlate with Transcriptional Activity during Spermatogenesis.', 'authors' => 'Vara C, Paytuví-Gallart A, Cuartero Y, Le Dily F, Garcia F, Salvà-Castro J, Gómez-H L, Julià E, Moutinho C, Aiese Cigliano R, Sanseverino W, Fornas O, Pendás AM, Heyn H, Waters PD, Marti-Renom MA, Ruiz-Herrera A', 'description' => '<p>Mammalian gametogenesis involves dramatic and tightly regulated chromatin remodeling, whose regulatory pathways remain largely unexplored. Here, we generate a comprehensive high-resolution structural and functional atlas of mouse spermatogenesis by combining in situ chromosome conformation capture sequencing (Hi-C), RNA sequencing (RNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) of CCCTC-binding factor (CTCF) and meiotic cohesins, coupled with confocal and super-resolution microscopy. Spermatogonia presents well-defined compartment patterns and topological domains. However, chromosome occupancy and compartmentalization are highly re-arranged during prophase I, with cohesins bound to active promoters in DNA loops out of the chromosomal axes. Compartment patterns re-emerge in round spermatids, where cohesin occupancy correlates with transcriptional activity of key developmental genes. The compact sperm genome contains compartments with actively transcribed genes but no fine-scale topological domains, concomitant with the presence of protamines. 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Structurally conserved lamina-associated domains (LADs) are formed by genomic regions that contact the NL. Lamins are also found in the nucleoplasm, with a yet unknown function. Here we map the genome-wide localization of lamin B1 in an euchromatin-enriched fraction of the mouse genome and follow its dynamics during the epithelial-to-mesenchymal transition (EMT). Lamin B1 associates with actively expressed and open euchromatin regions, forming dynamic euchromatin lamin B1-associated domains (eLADs) of about 0.3 Mb. Hi-C data link eLADs to the 3D organization of the mouse genome during EMT and correlate lamin B1 enrichment at topologically associating domain (TAD) borders with increased border strength. Having reduced levels of lamin B1 alters the EMT transcriptional signature and compromises the acquisition of mesenchymal traits. 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During epithelial to mesenchymal transition (EMT), loss of epithelial markers is mediated by transcriptional repressors such as SNAIL, SLUG, or ZEB1/2 that bind to E-box promoter sequences of specific genes. The effect of these repressors on SDC-1 expression remains unknown. Here, we demonstrated that SNAIL, SLUG and ZEB1 expressions are increased in advanced PCa, contrarily to SDC-1. SNAIL, SLUG and ZEB1 also showed an inversion to SDC-1 in prostate cell lines. ZEB1, but not SNAIL or SLUG, represses SDC-1 as demonstrated by experiments of ectopic expression in epithelial prostate cell lines. Inversely, expression of ZEB1 shRNA in PCa cell line increased SDC-1 expression. The effect of ZEB1 is transcriptional since ectopic expression of this gene represses SDC-1 promoter activity and ZEB1 binds to the SDC-1 promoter as detected by ChIP assays. An epigenetic mark associated to transcription repression H3K27me3 was bound to the same sites that ZEB1. In conclusion, this study identifies ZEB1 as a key repressor of SDC-1 during PCa progression and point to ZEB1 as a potentially diagnostic marker for PCa.</p>', 'date' => '2018-07-31', 'pmid' => 'http://www.pubmed.gov/30065348', 'doi' => '10.1038/s41598-018-29829-1', 'modified' => '2019-04-17 15:32:57', 'created' => '2019-04-16 12:25:30', 'ProductsPublication' => array( [maximum depth reached] ) ), (int) 4 => array( 'id' => '2852', 'name' => 'ClpX stimulates the mitochondrial unfolded protein response (UPRmt) in mammalian cells', 'authors' => 'Al-Furoukh N, Ianni A, Nolte H, Hölper S, Krüger M, Wanrooij S, Braun T', 'description' => '<p>Proteostasis is crucial for life and maintained by cellular chaperones and proteases. One major mitochondrial protease is the ClpXP complex, which is comprised of a catalytic ClpX subunit and a proteolytic ClpP subunit. Based on two separate observations, we hypothesized that ClpX may play a leading role in the cellular function of ClpXP. Therefore, we analyzed the effect of ClpX overexpression on a myoblast proteome by quantitative proteomics. ClpX overexpression results in the upregulation of markers of the mitochondrial proteostasis pathway, known as the "mitochondrial unfolded protein response" (UPRmt). Although this pathway is described in detail in Caenorhabditis elegans, it is not clear whether it is conserved in mammals. Therefore, we compared features of the classical nematode UPRmt with our mammalian ClpX-triggered UPRmt dataset. We show that they share the same retrograde mitochondria-to-nucleus signaling pathway that involves the key UPRmt transcription factor CHOP (also known as Ddit3, CEBPZ or GADD153). In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. 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These beads are intended for isolation of immune complexes (chromatin and specific antibody) in ChIP experiments. The beads are suitable for immunoprecipitation of rabbit polyclonal Abs, mouse IgG2a, IgG2b and IgA, guinea pig IgG, dog IgG, pig IgG. The beads should be washed before use.</span></p>', 'label1' => '', 'info1' => '', 'label2' => '', 'info2' => '', 'label3' => '', 'info3' => '', 'format' => '880 µl', 'catalog_number' => 'C03020004', 'old_catalog_number' => 'kch-503-880', 'sf_code' => 'C03020004-', 'type' => 'REF', 'search_order' => '04-undefined', 'price_EUR' => '80', 'price_USD' => '105', 'price_GBP' => '75', 'price_JPY' => '12530', 'price_CNY' => '', 'price_AUD' => '262', 'country' => 'ALL', 'except_countries' => 'None', 'quote' => false, 'in_stock' => false, 'featured' => false, 'no_promo' => false, 'online' => true, 'master' => true, 'last_datasheet_update' => '0000-00-00', 'slug' => 'unblocked-protein-a-beads-880-ul-880-ul', 'meta_title' => 'Unblocked protein A beads, 880 µl', 'meta_keywords' => '', 'meta_description' => 'Unblocked protein A beads, 880 µl', 'modified' => '2015-07-28 15:00:47', 'created' => '2015-06-29 14:08:20', 'ProductsGroup' => array( 'id' => '415', 'product_id' => '1916', 'group_id' => '359' ) ) $label = '<img src="/img/banners/banner-customizer-back.png" alt=""/>' $document = array( 'id' => '280', 'name' => 'Datasheet Unblocked Protein A beads kch-503', 'description' => 'Datasheet description', 'image_id' => null, 'type' => 'Datasheet', 'url' => 'files/products/reagents/Datasheet_Unblocked_Protein_A_beads_kch-503.pdf', 'slug' => 'datasheet-unblocked-protein-a-beads-kch-503', 'meta_keywords' => null, 'meta_description' => null, 'modified' => '2015-07-07 11:47:43', 'created' => '2015-07-07 11:47:43', 'ProductsDocument' => array( 'id' => '985', 'product_id' => '1915', 'document_id' => '280' ) ) $sds = array( 'id' => '1828', 'name' => 'Unblocked Protein A beads SDS ES es', 'language' => 'es', 'url' => 'files/SDS/A_beads/SDS-C03020002_C03020003_C03020004-Unblocked_Protein_A_beads-ES-es-GHS_1_0.pdf', 'countries' => 'ES', 'modified' => '2021-09-30 13:03:02', 'created' => '2021-09-30 13:03:02', 'ProductsSafetySheet' => array( 'id' => '3194', 'product_id' => '1915', 'safety_sheet_id' => '1828' ) ) $publication = array( 'id' => '2852', 'name' => 'ClpX stimulates the mitochondrial unfolded protein response (UPRmt) in mammalian cells', 'authors' => 'Al-Furoukh N, Ianni A, Nolte H, Hölper S, Krüger M, Wanrooij S, Braun T', 'description' => '<p>Proteostasis is crucial for life and maintained by cellular chaperones and proteases. One major mitochondrial protease is the ClpXP complex, which is comprised of a catalytic ClpX subunit and a proteolytic ClpP subunit. Based on two separate observations, we hypothesized that ClpX may play a leading role in the cellular function of ClpXP. Therefore, we analyzed the effect of ClpX overexpression on a myoblast proteome by quantitative proteomics. ClpX overexpression results in the upregulation of markers of the mitochondrial proteostasis pathway, known as the "mitochondrial unfolded protein response" (UPRmt). Although this pathway is described in detail in Caenorhabditis elegans, it is not clear whether it is conserved in mammals. Therefore, we compared features of the classical nematode UPRmt with our mammalian ClpX-triggered UPRmt dataset. We show that they share the same retrograde mitochondria-to-nucleus signaling pathway that involves the key UPRmt transcription factor CHOP (also known as Ddit3, CEBPZ or GADD153). In conclusion, our data confirm the existence of a mammalian UPRmt that has great similarity to the C. elegans pathway. Furthermore, our results illustrate that ClpX overexpression is a good and simple model to study the underlying mechanisms of the UPRmt in mammalian cells.</p>', 'date' => '2015-10-01', 'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26142927', 'doi' => '10.1016/j.bbamcr.2015.06.016', 'modified' => '2016-03-14 10:20:09', 'created' => '2016-03-14 10:20:09', 'ProductsPublication' => array( 'id' => '534', 'product_id' => '1915', 'publication_id' => '2852' ) ) $externalLink = ' <a href="http://www.ncbi.nlm.nih.gov/pubmed/26142927" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 ProductsController::slug() - APP/Controller/ProductsController.php, line 1052 ReflectionMethod::invokeArgs() - [internal], line ?? Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
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