Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development. - Wikidata - wikimedia - TriplyDB

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

http://www.wikidata.org/entity/Q44691496

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The F-box protein Cdc4/Fbxw7 is a novel regulator of neural crest development in Xenopus laevis The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability The stomatin-like protein SLP-1 and Cdk2 interact with the F-Box protein Fbw7-γ The glomuvenous malformation protein Glomulin binds Rbx1 and regulates cullin RING ligase-mediated turnover of Fbw7 Parkin-dependent degradation of the F-box protein Fbw7β promotes neuronal survival in response to oxidative stress by stabilizing Mcl-1 Fbxw7 regulates lipid metabolism and cell fate decisions in the mouse liver ASB4 is a hydroxylation substrate of FIH and promotes vascular differentiation via an oxygen-dependent mechanism Phosphorylation-dependent degradation of c-Myc is mediated by the F-box protein Fbw7 Systematic analysis and nomenclature of mammalian F-box proteins Disruption of the Fbxw8 gene results in pre- and postnatal growth retardation in mice Control of cell growth by the SCF and APC/C ubiquitin ligases Isoform- and cell cycle-dependent substrate degradation by the Fbw7 ubiquitin ligase Identification of a conserved negative regulatory sequence that influences the leukemogenic activity of NOTCH1 Genetically engineered mouse models for functional studies of SKP1-CUL1-F-box-protein (SCF) E3 ubiquitin ligases Fbxw7 controls angiogenesis by regulating endothelial Notch activity Dysregulation of ubiquitin ligases in cancer FBW7 regulates endothelial functions by targeting KLF2 for ubiquitination and degradation FBXW7 mutations typically found in human cancers are distinct from null alleles and disrupt lung development Fbxw8 is essential for Cul1-Cul7 complex formation and for placental development The Fbx4 tumor suppressor regulates cyclin D1 accumulation and prevents neoplastic transformation Investigation of the atypical FBXW7 mutation spectrum in human tumours by conditional expression of a heterozygous propellor tip missense allele in the mouse intestines The canonical Notch signaling pathway: unfolding the activation mechanism.Histone deacetylase activity selectively regulates notch-mediated smooth muscle differentiation in human vascular cells.Notch inhibitors as a new tool in the war on cancer: a pathway to watch.Notch inhibition as a promising new approach to cancer therapy.Mechanistic exploration of phthalimide neovascular factor 1 using network analysis tools.Mutation analysis of hCDC4 in AML cells identifies a new intronic polymorphism.The SV40 large T antigen contains a decoy phosphodegron that mediates its interactions with Fbw7/hCdc4.Turn It Down a Notch Sent to destroy: the ubiquitin proteasome system regulates cell signaling and protein quality control in cardiovascular development and disease.Aberrant regulation of FBW7 in cancer.Fbxw7 haploinsufficiency loses its protection against DNA damage and accelerates MNU-induced gastric carcinogenesis.FBXW7 mutations in melanoma and a new therapeutic paradigm FBXW7 missense mutation: a novel negative prognostic factor in metastatic colorectal adenocarcinoma.Loss of Notch1-dependent p21(Waf1/Cip1) expression influences the Notch1 outcome in tumorigenesis.The ubiquitin ligase Fbxw7 controls adipocyte differentiation by targeting C/EBPalpha for degradation Role of Pirh2 in mediating the regulation of p53 and c-Myc.Allele-specific deletions in mouse tumors identify Fbxw7 as germline modifier of tumor susceptibility Cullins and cancer.Notch signalling in T-cell lymphoblastic leukaemia/lymphoma and other haematological malignancies.

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P2860

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

http://www.wikidata.org/entity/Q44691496

description

2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年學術文章

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2003年學術文章

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name

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@en

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@nl

type

label

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@en

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@nl

prefLabel

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@en

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development.

@nl

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Journal of Biological Chemistry

P1476

Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development

@en

P2093

Keiichi I Nakayama

http://www.w3.org/2001/XMLSchema#string

Keiko Nakayama

http://www.w3.org/2001/XMLSchema#string

Masaaki Nishiyama

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Noriko Ishida

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Ryoichiro Kageyama

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Ryosuke Tsunematsu

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Yasumasa Bessho

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Yuichi Oike

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P2860

Tetralogy of fallot and other congenital heart defects in Hey2 mutant mice

Distinct roles of the receptor tyrosine kinases Tie-1 and Tie-2 in blood vessel formation

SEL-10 is an inhibitor of notch signaling that targets notch for ubiquitin-mediated protein degradation

Members of the HRT family of basic helix-loop-helix proteins act as transcriptional repressors downstream of Notch signaling

The ubiquitin system

Notch signaling: cell fate control and signal integration in development

gridlock, an HLH gene required for assembly of the aorta in zebrafish

The F-box: a new motif for ubiquitin dependent proteolysis in cell cycle regulation and signal transduction

Archipelago regulates Cyclin E levels in Drosophila and is mutated in human cancer cell lines

Human F-box protein hCdc4 targets cyclin E for proteolysis and is mutated in a breast cancer cell line

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9417-9423

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scholarly article

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10.1074/JBC.M312337200

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P433

10

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P478

279

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Shigetsugu Hatakeyama

P577

2003-12-12T00:00:00Z

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P698

14672936

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