The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy. - Test2 - elhamkhani - TriplyDB

The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy.

The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy.

http://www.wikidata.org/entity/Q34202686

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The structure and regulation of Cullin 2 based E3 ubiquitin ligases and their biological functions Novel strategies to target the ubiquitin proteasome system in multiple myeloma SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer Cullin family proteins and tumorigenesis: genetic association and molecular mechanisms Targeting the ubiquitin pathway for cancer treatment Building and remodelling Cullin-RING E3 ubiquitin ligases Genetically engineered mouse models for functional studies of SKP1-CUL1-F-box-protein (SCF) E3 ubiquitin ligases E2 enzyme inhibition by stabilization of a low-affinity interface with ubiquitin E2-binding surface on Uba3 β-grasp domain undergoes a conformational transition From Proteomic Analysis to Potential Therapeutic Targets: Functional Profile of Two Lung Cancer Cell Lines, A549 and SW900, Widely Studied in Pre-Clinical Research Mutations in UBA3 confer resistance to the NEDD8-activating enzyme inhibitor MLN4924 in human leukemic cells NEDDylation is essential for Kaposi's sarcoma-associated herpesvirus latency and lytic reactivation and represents a novel anti-KSHV target Ubiquitin E3 ligase CRL4(CDT2/DCAF2) as a potential chemotherapeutic target for ovarian surface epithelial cancer Targeting Cullin-RING ligases by MLN4924 induces autophagy via modulating the HIF1-REDD1-TSC1-mTORC1-DEPTOR axis.Inactivation of SAG/RBX2 E3 ubiquitin ligase suppresses KrasG12D-driven lung tumorigenesis Dissection of DNA damage responses using multiconditional genetic interaction maps Cul4B regulates neural progenitor cell growth.Phase I Study of the Novel Investigational NEDD8-Activating Enzyme Inhibitor Pevonedistat (MLN4924) in Patients with Relapsed/Refractory Multiple Myeloma or Lymphoma.Endothelial deletion of Sag/Rbx2/Roc2 E3 ubiquitin ligase causes embryonic lethality and blocks tumor angiogenesis.The molecular determinants for distinguishing between ubiquitin and NEDD8 by USP2.Targeting the neddylation pathway to suppress the growth of prostate cancer cells: therapeutic implication for the men's cancer.MLN4924 (Pevonedistat), a protein neddylation inhibitor, suppresses proliferation and migration of human clear cell renal cell carcinoma Targeting Cullin-RING E3 ubiquitin ligases for drug discovery: structure, assembly and small-molecule modulation.Targeting cullin-RING ligases for cancer treatment: rationales, advances and therapeutic implications.The ubiquitin-proteasome system: opportunities for therapeutic intervention in solid tumors Neddylation dysfunction in Alzheimer's disease.Oncogenic function of SCCRO5/DCUN1D5 requires its Neddylation E3 activity and nuclear localization.Neddylation pathway is up-regulated in human intrahepatic cholangiocarcinoma and serves as a potential therapeutic target Pevonedistat (MLN4924), a First-in-Class NEDD8-activating enzyme inhibitor, in patients with acute myeloid leukaemia and myelodysplastic syndromes: a phase 1 study.A phase I study of the investigational NEDD8-activating enzyme inhibitor pevonedistat (TAK-924/MLN4924) in patients with metastatic melanoma.Targeting Neddylation pathways to inactivate cullin-RING ligases for anticancer therapy A microarray-based gene expression analysis to identify diagnostic biomarkers for unknown primary cancer Phage display to identify Nedd8-mimicking peptides as inhibitors of the Nedd8 transfer cascade.The neddylation-cullin 2-RBX1 E3 ligase axis targets tumor suppressor RhoB for degradation in liver cancer.Rictor Undergoes Glycogen Synthase Kinase 3 (GSK3)-dependent, FBXW7-mediated Ubiquitination and Proteasomal Degradation.The Cullin 4A/B-DDB1-Cereblon E3 Ubiquitin Ligase Complex Mediates the Degradation of CLC-1 Chloride Channels DNA damage-induced activation of CUL4B targets HUWE1 for proteasomal degradation.Synergistic inhibition of autophagy and neddylation pathways as a novel therapeutic approach for targeting liver cancer.Targeting the mTOR-DEPTOR pathway by CRL E3 ubiquitin ligases: therapeutic application Suppression of glioblastoma by targeting the overactivated protein neddylation pathway.

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The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy.

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年学术文章

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2010年學術文章

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The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy.

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The NEDD8 Conjugation Pathway and Its Relevance in Cancer Biology and Therapy.

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James E Brownell

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Lawrence R Dick

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Michael A Milhollen

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Peter G Smith

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Teresa A Soucy

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P2860

Cullin-RING ubiquitin ligases: global regulation and activation cycles

Identification of the activating and conjugating enzymes of the NEDD8 conjugation pathway

The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the S-M checkpoint and causes apoptosis in neurons

Structure of the Cul1-Rbx1-Skp1-F boxSkp2 SCF ubiquitin ligase complex

Merlin/NF2 suppresses tumorigenesis by inhibiting the E3 ubiquitin ligase CRL4(DCAF1) in the nucleus

Conservation in the mechanism of Nedd8 activation by the human AppBp1-Uba3 heterodimer

A unique E1-E2 interaction required for optimal conjugation of the ubiquitin-like protein NEDD8

Prophase destruction of Emi1 by the SCF(betaTrCP/Slimb) ubiquitin ligase activates the anaphase promoting complex to allow progression beyond prometaphase

Two E3 ubiquitin ligases, SCF-Skp2 and DDB1-Cul4, target human Cdt1 for proteolysis.

Regulation of nucleolar signalling to p53 through NEDDylation of L11

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