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Description
| - Introduction: Breast cancer is one of the most common types of cancer in women. One of the genes that were found mutated in breast cancer is casein kinase 1 epsilon (CK1 epsilon). Because CK1 epsilon is a crucial regulator of the Wnt signaling cascades, we determined how these CK1 epsilon mutations interfere with the Wnt pathway and affect the behavior of epithelial breast cancer cell lines. Results: In silico modeling and in vivo data showed that autophosphorylation at Thr 44, a site adjacent to the breast cancer point mutations in the N-terminal lobe of human CK1 epsilon, is involved in positive regulation of the CK1 epsilon activity.
- Introduction: Breast cancer is one of the most common types of cancer in women. One of the genes that were found mutated in breast cancer is casein kinase 1 epsilon (CK1 epsilon). Because CK1 epsilon is a crucial regulator of the Wnt signaling cascades, we determined how these CK1 epsilon mutations interfere with the Wnt pathway and affect the behavior of epithelial breast cancer cell lines. Results: In silico modeling and in vivo data showed that autophosphorylation at Thr 44, a site adjacent to the breast cancer point mutations in the N-terminal lobe of human CK1 epsilon, is involved in positive regulation of the CK1 epsilon activity. (en)
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Title
| - Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration.
- Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration. (en)
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skos:prefLabel
| - Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration.
- Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration. (en)
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skos:notation
| - RIV/00216224:14310/10:00067265!RIV14-MSM-14310___
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http://linked.open...avai/riv/aktivita
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http://linked.open...avai/riv/aktivity
| - P(GA204/09/0498), P(GA301/07/0814), P(GD204/09/H058), S, Z(AV0Z50040507), Z(AV0Z50040702), Z(AV0Z50070508), Z(AV0Z60220518), Z(MSM0021622430)
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http://linked.open...iv/cisloPeriodika
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http://linked.open...vai/riv/dodaniDat
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http://linked.open...aciTvurceVysledku
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http://linked.open.../riv/druhVysledku
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http://linked.open...iv/duvernostUdaju
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http://linked.open...titaPredkladatele
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http://linked.open...dnocenehoVysledku
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http://linked.open...ai/riv/idVysledku
| - RIV/00216224:14310/10:00067265
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http://linked.open...riv/jazykVysledku
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http://linked.open.../riv/klicovaSlova
| - KINASE-I-EPSILON; BETA-CATENIN; EPITHELIAL-CELLS; DISHEVELLED PHOSPHORYLATION; REGULATES GASTRULATION; SIGNALING PATHWAY; TUMOR PROGRESSION; UP-REGULATION; WNT PATHWAY; E-CADHERIN (en)
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http://linked.open.../riv/klicoveSlovo
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http://linked.open...odStatuVydavatele
| - GB - Spojené království Velké Británie a Severního Irska
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http://linked.open...ontrolniKodProRIV
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http://linked.open...i/riv/nazevZdroje
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http://linked.open...in/vavai/riv/obor
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http://linked.open...ichTvurcuVysledku
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http://linked.open...cetTvurcuVysledku
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http://linked.open...vavai/riv/projekt
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http://linked.open...UplatneniVysledku
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http://linked.open...v/svazekPeriodika
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http://linked.open...iv/tvurceVysledku
| - Bryja, Vítězslav
- Kozubík, Alois
- Krejčí, Pavel
- Tmejová, Kateřina
- Dolezal, T.
- Trantírek, Lukáš
- Bernatík, Ondřej
- Brumovská, E.
- Blankenfeldt, W.
- Foldynová-Trantírková, S.
- Sekyrová, P.
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http://linked.open...ain/vavai/riv/wos
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http://linked.open...n/vavai/riv/zamer
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issn
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number of pages
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http://bibframe.org/vocab/doi
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http://localhost/t...ganizacniJednotka
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