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13 results on '"Hassel, David"'

1. Biallelic Variants in ASNA1, Encoding a Cytosolic Targeting Factor of Tail-Anchored Proteins, Cause Rapidly Progressive Pediatric Cardiomyopathy

Author

Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., van de Laar, Ingrid M.B.H., Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., and van de Laar, Ingrid M.B.H.

Published
2019

2. Biallelic Variants in ASNA1, Encoding a Cytosolic Targeting Factor of Tail-Anchored Proteins, Cause Rapidly Progressive Pediatric Cardiomyopathy

Author

Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., van de Laar, Ingrid M.B.H., Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., and van de Laar, Ingrid M.B.H.

Published
2019

3. Biallelic Variants in ASNA1, Encoding a Cytosolic Targeting Factor of Tail-Anchored Proteins, Cause Rapidly Progressive Pediatric Cardiomyopathy

Author

Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., van de Laar, Ingrid M.B.H., Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., and van de Laar, Ingrid M.B.H.

Published
2019

4. Biallelic Variants in ASNA1, Encoding a Cytosolic Targeting Factor of Tail-Anchored Proteins, Cause Rapidly Progressive Pediatric Cardiomyopathy

Author

UMC Utrecht, Pathologie Pathologen staf, Cancer, Genetica Klinische Genetica, Circulatory Health, Cardiologie patientenzorg, Child Health, Cluster C, Metabole ziekten patientenzorg, Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., van de Laar, Ingrid M.B.H., UMC Utrecht, Pathologie Pathologen staf, Cancer, Genetica Klinische Genetica, Circulatory Health, Cardiologie patientenzorg, Child Health, Cluster C, Metabole ziekten patientenzorg, Verhagen, Judith M.A., van den Born, Myrthe, van der Linde, Herma C., G J Nikkels, Peter, Verdijk, Rob M., Kivlen, Maryann H., van Unen, Leontine M.A., Baas, Annette F., Ter Heide, Henriette, van Osch-Gevers, Lennie, Hoogeveen-Westerveld, Marianne, Herkert, Johanna C., Bertoli-Avella, Aida M., van Slegtenhorst, Marjon A., Wessels, Marja W., Verheijen, Frans W., Hassel, David, Hofstra, Robert M.W., Hegde, Ramanujan S., van Hasselt, Peter M., van Ham, Tjakko J., and van de Laar, Ingrid M.B.H.

Published
2019

5. MicroRNA-10 regulates the angiogenic behavior of zebrafish and human endothelial cells by promoting vascular endothelial growth factor signaling.

Author

Hassel, David, Hassel, David, Cheng, Paul, White, Mark, Ivey, Kathryn, Kroll, Jens, Augustin, Hellmut, Katus, Hugo, Stainier, Didier, Srivastava, Deepak, Hassel, David, Hassel, David, Cheng, Paul, White, Mark, Ivey, Kathryn, Kroll, Jens, Augustin, Hellmut, Katus, Hugo, Stainier, Didier, and Srivastava, Deepak

Abstract

RATIONALE: Formation and remodeling of the vasculature during development and disease involve a highly conserved and precisely regulated network of attractants and repellants. Various signaling pathways control the behavior of endothelial cells, but their posttranscriptional dose titration by microRNAs is poorly understood. OBJECTIVE: To identify microRNAs that regulate angiogenesis. METHODS AND RESULTS: We show that the highly conserved microRNA family encoding miR-10 regulates the behavior of endothelial cells during angiogenesis by positively titrating proangiogenic signaling. Knockdown of miR-10 led to premature truncation of intersegmental vessel growth in the trunk of zebrafish larvae, whereas overexpression of miR-10 promoted angiogenic behavior in zebrafish and cultured human umbilical venous endothelial cells. We found that miR-10 functions, in part, by directly regulating the level of fms-related tyrosine kinase 1 (FLT1), a cell-surface protein that sequesters vascular endothelial growth factor, and its soluble splice variant sFLT1. The increase in FLT1/sFLT1 protein levels upon miR-10 knockdown in zebrafish and in human umbilical venous endothelial cells inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling. CONCLUSIONS: Our study provides insights into how FLT1 and vascular endothelial growth factor receptor 2 signaling is titrated in a microRNA-mediated manner and establishes miR-10 as a potential new target for the selective modulation of angiogenesis.

Published
2012

7. MicroRNA-10 regulates the angiogenic behavior of zebrafish and human endothelial cells by promoting vascular endothelial growth factor signaling.

Author

Hassel, David, Hassel, David, Cheng, Paul, White, Mark P, Ivey, Kathryn N, Kroll, Jens, Augustin, Hellmut G, Katus, Hugo A, Stainier, Didier YR, Srivastava, Deepak, Hassel, David, Hassel, David, Cheng, Paul, White, Mark P, Ivey, Kathryn N, Kroll, Jens, Augustin, Hellmut G, Katus, Hugo A, Stainier, Didier YR, and Srivastava, Deepak

Abstract

RationaleFormation and remodeling of the vasculature during development and disease involve a highly conserved and precisely regulated network of attractants and repellants. Various signaling pathways control the behavior of endothelial cells, but their posttranscriptional dose titration by microRNAs is poorly understood.ObjectiveTo identify microRNAs that regulate angiogenesis.Methods and resultsWe show that the highly conserved microRNA family encoding miR-10 regulates the behavior of endothelial cells during angiogenesis by positively titrating proangiogenic signaling. Knockdown of miR-10 led to premature truncation of intersegmental vessel growth in the trunk of zebrafish larvae, whereas overexpression of miR-10 promoted angiogenic behavior in zebrafish and cultured human umbilical venous endothelial cells. We found that miR-10 functions, in part, by directly regulating the level of fms-related tyrosine kinase 1 (FLT1), a cell-surface protein that sequesters vascular endothelial growth factor, and its soluble splice variant sFLT1. The increase in FLT1/sFLT1 protein levels upon miR-10 knockdown in zebrafish and in human umbilical venous endothelial cells inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling.ConclusionsOur study provides insights into how FLT1 and vascular endothelial growth factor receptor 2 signaling is titrated in a microRNA-mediated manner and establishes miR-10 as a potential new target for the selective modulation of angiogenesis.

Published
2012

8. MicroRNA-10 regulates the angiogenic behavior of zebrafish and human endothelial cells by promoting vascular endothelial growth factor signaling.

Author

Hassel, David, Hassel, David, Cheng, Paul, White, Mark P, Ivey, Kathryn N, Kroll, Jens, Augustin, Hellmut G, Katus, Hugo A, Stainier, Didier YR, Srivastava, Deepak, Hassel, David, Hassel, David, Cheng, Paul, White, Mark P, Ivey, Kathryn N, Kroll, Jens, Augustin, Hellmut G, Katus, Hugo A, Stainier, Didier YR, and Srivastava, Deepak

Abstract

RationaleFormation and remodeling of the vasculature during development and disease involve a highly conserved and precisely regulated network of attractants and repellants. Various signaling pathways control the behavior of endothelial cells, but their posttranscriptional dose titration by microRNAs is poorly understood.ObjectiveTo identify microRNAs that regulate angiogenesis.Methods and resultsWe show that the highly conserved microRNA family encoding miR-10 regulates the behavior of endothelial cells during angiogenesis by positively titrating proangiogenic signaling. Knockdown of miR-10 led to premature truncation of intersegmental vessel growth in the trunk of zebrafish larvae, whereas overexpression of miR-10 promoted angiogenic behavior in zebrafish and cultured human umbilical venous endothelial cells. We found that miR-10 functions, in part, by directly regulating the level of fms-related tyrosine kinase 1 (FLT1), a cell-surface protein that sequesters vascular endothelial growth factor, and its soluble splice variant sFLT1. The increase in FLT1/sFLT1 protein levels upon miR-10 knockdown in zebrafish and in human umbilical venous endothelial cells inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling.ConclusionsOur study provides insights into how FLT1 and vascular endothelial growth factor receptor 2 signaling is titrated in a microRNA-mediated manner and establishes miR-10 as a potential new target for the selective modulation of angiogenesis.

Published
2012

10. Retinoic acid catabolizing enzyme CYP26C1 is a genetic modifier in SHOX deficiency

Author

Montalbano, Antonino, Juergensen, Lonny, Roeth, Ralph, Weiss, Birgit, Fukami, Maki, Fricke-Otto, Susanne, Binder, Gerhard, Ogata, Tsutomu, Decker, Eva, Nuernberg, Gudrun, Hassel, David, Rappold, Gudrun A., Montalbano, Antonino, Juergensen, Lonny, Roeth, Ralph, Weiss, Birgit, Fukami, Maki, Fricke-Otto, Susanne, Binder, Gerhard, Ogata, Tsutomu, Decker, Eva, Nuernberg, Gudrun, Hassel, David, and Rappold, Gudrun A.

Abstract

Mutations in the homeobox gene SHOX cause SHOX deficiency, a condition with clinical manifestations ranging from short stature without dysmorphic signs to severe mesomelic skeletal dysplasia. In rare cases, individuals with SHOX deficiency are asymptomatic. To elucidate the factors that modify disease severity/penetrance, we studied a three-generation family with SHOX deficiency. The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD. The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. High levels of retinoic acid significantly decrease SHOX expression in human primary chondrocytes and zebrafish embryos. Individual morpholino knockdown of either gene shortens the pectoral fins, whereas depletion of both genes leads to a more severe phenotype. Together, our findings describe CYP26C1 as the first genetic modifier for SHOX deficiency.

Published
2016

11. Retinoic acid catabolizing enzyme CYP26C1 is a genetic modifier in SHOX deficiency

Author

Montalbano, Antonino, Juergensen, Lonny, Roeth, Ralph, Weiss, Birgit, Fukami, Maki, Fricke-Otto, Susanne, Binder, Gerhard, Ogata, Tsutomu, Decker, Eva, Nuernberg, Gudrun, Hassel, David, Rappold, Gudrun A., Montalbano, Antonino, Juergensen, Lonny, Roeth, Ralph, Weiss, Birgit, Fukami, Maki, Fricke-Otto, Susanne, Binder, Gerhard, Ogata, Tsutomu, Decker, Eva, Nuernberg, Gudrun, Hassel, David, and Rappold, Gudrun A.

Abstract

Mutations in the homeobox gene SHOX cause SHOX deficiency, a condition with clinical manifestations ranging from short stature without dysmorphic signs to severe mesomelic skeletal dysplasia. In rare cases, individuals with SHOX deficiency are asymptomatic. To elucidate the factors that modify disease severity/penetrance, we studied a three-generation family with SHOX deficiency. The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD. The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. High levels of retinoic acid significantly decrease SHOX expression in human primary chondrocytes and zebrafish embryos. Individual morpholino knockdown of either gene shortens the pectoral fins, whereas depletion of both genes leads to a more severe phenotype. Together, our findings describe CYP26C1 as the first genetic modifier for SHOX deficiency.

Published
2016

12. Stress maximum and steady extensional flow of branched polymer melts

Author

Huang, Qian, Skov, Anne Ladegaard, Rasmussen, Henrik K., Hoyle, David M., McLeish, Thomas C., Harlen, Oliver, Hassel, David, Lord, Tim D., Mackley, Malcolm R., Hassager, Ole, Huang, Qian, Skov, Anne Ladegaard, Rasmussen, Henrik K., Hoyle, David M., McLeish, Thomas C., Harlen, Oliver, Hassel, David, Lord, Tim D., Mackley, Malcolm R., and Hassager, Ole

Published
2011

13. Stress maximum and steady extensional flow of branched polymer melts

Author

Huang, Qian, Skov, Anne Ladegaard, Rasmussen, Henrik K., Hoyle, David M., McLeish, Thomas C., Harlen, Oliver, Hassel, David, Lord, Tim D., Mackley, Malcolm R., Hassager, Ole, Huang, Qian, Skov, Anne Ladegaard, Rasmussen, Henrik K., Hoyle, David M., McLeish, Thomas C., Harlen, Oliver, Hassel, David, Lord, Tim D., Mackley, Malcolm R., and Hassager, Ole

Published
2011

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