Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119243 | ENA |
REPOSITORIES: ENA
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Project description:CCM1 (also known as KRIT1) is critical regulator of endothelial cell biology. Mutations in CCM1 can lead to the formation of cerebral cavernous malformations (CCM). CCM lesions are frequent in the human population; however, their pathogenesis is poorly understood. This genome-wide expression analysis is aimed to unravelling novel mechanisms how CCM1 executes its functions in endothelial cells. We used human umbilical vein endothelial cells (HUVEC) as a model system to study CCM1 functions after adenoviral over expression. The results of this experiment suggest that CCM1 is a critical regulator of endothelial cell cycle control and proliferation as well as migration and angiogenesis. This fits well to the roles of CCM1 in HUVEC which indeed acts as a negative regulator of angiogenesis. Human umbilical vein endothelial cells were transduced with adenovirus expressing CCM1 or GFP as control. 48 hours after transduction total RNA was isolated from duplicates for genome-wide expression analysis biological replicate: GFP rep1, GFP rep2 biological replicate: CCM1 rep1, CCM1 rep2
2010-06-16 | E-GEOD-18014 | biostudies-arrayexpress
Project description:CCM1 (also known as KRIT1) is critical regulator of endothelial cell biology. Mutations in CCM1 can lead to the formation of cerebral cavernous malformations (CCM). CCM lesions are frequent in the human population; however, their pathogenesis is poorly understood. This genome-wide expression analysis is aimed to unravelling novel mechanisms how CCM1 executes its functions in endothelial cells. We used human umbilical vein endothelial cells (HUVEC) as a model system to study CCM1 functions after adenoviral over expression. The results of this experiment suggest that CCM1 is a critical regulator of endothelial cell cycle control and proliferation as well as migration and angiogenesis. This fits well to the roles of CCM1 in HUVEC which indeed acts as a negative regulator of angiogenesis.
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Project description:ICAP1 (also known as ITG1BP1) is a protein interaction partner of beta1-integrins and the cerebral cavernous malformation protein 1 (CCM1, also known as KRIT1). In mice Icap1 plays an important role for bone development. The function of ICAP1 in endothelial cells is poorly understood. However, the interactions with beta1-integrins and CCM1 suggest that ICAP1 should play an important role also in endothelial cells. We obtained data that ICAP1 might activate the Delta-Notch signaling cascade, a critical regulator of endothelial proliferation, migration and sprouting angiogenesis. This genome-wide expression analysis is aimed to unravelling novel mechanisms or signaling pathways how ICAP1 functions in endothelial cells. Secondly, this study aimed at defining novel target genes of Notch signaling and finally to compare the gene expression patterns of ICAP1 and NOTCH1. We used human umbilical vein endothelial cells (HUVEC) as a model system to study ICAP1 and NOTCH1 functions after adenoviral over expression in comparison to GFP over expression as control. The results of this experiment suggest that ICAP1 and NOTCH1 control a series of genes involved in cell proliferation, migration and angiogenesis. A high proportion of ICAP1-regulated genes is also regulated by NOTCH1 in a very similar manner. Human umbilical vein endothelial cells were transduced with adenovirus expressing ICAP1, NOTCH1 (only the constitutive active intracellular domain) or GFP as control. 36 hours after transduction total RNA was isolated from duplicates for genome-wide expression analysis biological replicate: GFP_1, GFP_2 biological replicate: NOTCH1_1, NOTCH1_2 biological replicate: ICAP1_1, ICAP1_2
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Project description:ICAP1 (also known as ITG1BP1) is a protein interaction partner of beta1-integrins and the cerebral cavernous malformation protein 1 (CCM1, also known as KRIT1). In mice Icap1 plays an important role for bone development. The function of ICAP1 in endothelial cells is poorly understood. However, the interactions with beta1-integrins and CCM1 suggest that ICAP1 should play an important role also in endothelial cells. We obtained data that ICAP1 might activate the Delta-Notch signaling cascade, a critical regulator of endothelial proliferation, migration and sprouting angiogenesis. This genome-wide expression analysis is aimed to unravelling novel mechanisms or signaling pathways how ICAP1 functions in endothelial cells. Secondly, this study aimed at defining novel target genes of Notch signaling and finally to compare the gene expression patterns of ICAP1 and NOTCH1. We used human umbilical vein endothelial cells (HUVEC) as a model system to study ICAP1 and NOTCH1 functions after adenoviral over expression in comparison to GFP over expression as control. The results of this experiment suggest that ICAP1 and NOTCH1 control a series of genes involved in cell proliferation, migration and angiogenesis. A high proportion of ICAP1-regulated genes is also regulated by NOTCH1 in a very similar manner.
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