Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B. - Wikidata - wikimedia - TriplyDB

Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.

Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.

http://www.wikidata.org/entity/Q39647760

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Structure and function of human DnaJ homologue subfamily a member 1 (DNAJA1) and its relationship to pancreatic cancer Rewired ERK-JNK signaling pathways in melanoma Cap-Independent Translational Control of Carcinogenesis The significance of genetics for cholangiocarcinoma development Role of immune escape mechanisms in Hodgkin's lymphoma development and progression: a whole new world with therapeutic implications TGF-β1-induced EMT promotes targeted migration of breast cancer cells through the lymphatic system by the activation of CCR7/CCL21-mediated chemotaxis To NFκB or not to NFκB: The Dilemma on How to Inhibit a Cancer Cell Fate Regulator Triptolide inhibits the proliferation of prostate cancer cells and down-regulates SUMO-specific protease 1 expression Identification of Biomarker and Co-Regulatory Motifs in Lung Adenocarcinoma Based on Differential Interactions Global gene profiling of spontaneous hepatocellular carcinoma in B6C3F1 mice: similarities in the molecular landscape with human liver cancer P19 H-ras induces G1/S phase delay maintaining cells in a reversible quiescence state Pathobiology of hodgkin lymphoma.Emerging roles of ATF2 and the dynamic AP1 network in cancer.CARMA1-mediated NF-kappaB and JNK activation in lymphocytes.Cell transformation by v-Rel reveals distinct roles of AP-1 family members in Rel/NF-kappaB oncogenesis.The heat shock protein-90 co-chaperone, Cyclophilin 40, promotes ALK-positive, anaplastic large cell lymphoma viability and its expression is regulated by the NPM-ALK oncoprotein.HLXB9 activates IL6 in Hodgkin lymphoma cell lines and is regulated by PI3K signalling involving E2F3.Mapping of transcription factor motifs in active chromatin identifies IRF5 as key regulator in classical Hodgkin lymphoma Molecular biology of Hodgkin's and Reed/Sternberg cells in Hodgkin's lymphoma.Profiling of Hodgkin's lymphoma cell line L1236 and germinal center B cells: identification of Hodgkin's lymphoma-specific genes.The molecular pathogenesis of Hodgkin lymphoma.Critical role of SHP2 (PTPN11) signaling in germinal center-derived lymphoma.Cop1 constitutively regulates c-Jun protein stability and functions as a tumor suppressor in mice.Jun-regulated genes promote interaction of diffuse large B-cell lymphoma with the microenvironment.Mechanisms of indomethacin-induced alterations in the choline phospholipid metabolism of breast cancer cells.B-cell-intrinsic hepatitis C virus expression leads to B-cell-lymphomagenesis and induction of NF-κB signalling.The IkappaB kinase complex and NF-kappaB act as master regulators of lipopolysaccharide-induced gene expression and control subordinate activation of AP-1.Chemokine receptor 7 (CCR7) gene expression is regulated by NF-κB and activator protein 1 (AP1) in metastatic squamous cell carcinoma of head and neck (SCCHN).c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B-lymphoma cells CARMA1 controls Th2 cell-specific cytokine expression through regulating JunB and GATA3 transcription factors.Constitutive AP-1 activity and EBV infection induce PD-L1 in Hodgkin lymphomas and posttransplant lymphoproliferative disorders: implications for targeted therapy.The AP1-dependent secretion of galectin-1 by Reed Sternberg cells fosters immune privilege in classical Hodgkin lymphoma.C-Jun recruits the NSL complex to regulate its target gene expression by modulating H4K16 acetylation and promoting the release of the repressive NuRD complex What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?HP1a/KDM4A is involved in the autoregulatory loop of the oncogene gene c-Jun.Constitutive control of AKT1 gene expression by JUNB/CJUN in ALK+ anaplastic large-cell lymphoma: a novel crosstalk mechanism.Aberrant expression of c-Jun in glioblastoma by internal ribosome entry site (IRES)-mediated translational activation Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cells.c-FLIP mediates resistance of Hodgkin/Reed-Sternberg cells to death receptor-induced apoptosis.

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Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.

http://www.wikidata.org/entity/Q39647760

description

2002 nî lūn-bûn

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

@en

Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

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type

label

Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

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Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

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prefLabel

Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

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Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B.

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The EMBO Journal

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Aberrantly expressed c-Jun and ...... and synergize with NF-kappa B

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Andreas Lietz

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

Bernd Dörken

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Claus Scheidereit

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Harald Stein

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Ioannis Anagnostopoulos

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Kurt Bommert

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Stephan Mathas

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P2860

The Hallmarks of Cancer

Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin's disease

c-Jun regulates cell cycle progression and apoptosis by distinct mechanisms

Regulation of IL-4 expression by the transcription factor JunB during T helper cell differentiation

UV-Induced stabilization of c-fos and other short-lived mRNAs

ATF-2 is preferentially activated by stress-activated protein kinases to mediate c-jun induction in response to genotoxic agents

Control of cell cycle progression by c-Jun is p53 dependent

Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity

Mammalian MAP kinase signalling cascades

Up-regulation of the chemokine receptor CCR7 in classical but not in lymphocyte-predominant Hodgkin disease correlates with distinct dissemination of neoplastic cells in lymphoid organs

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4104-4113

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10.1093/EMBOJ/CDF389

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15

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21

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Franziska Jundt

Fatima Mechta-Grigoriou

Daniel Krappmann

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2002-08-01T00:00:00Z

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277470824

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12145210

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126136

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