JUNB (jun B proto-oncogene) [PDF]
, 2003 Review on JUNB (jun B proto-oncogene), with data on DNA, on the protein encoded, and where the gene is ...
Chen, F
core +1 more source
Signaling through CD44 affects cell cycle progression and c-Jun expression in acute myeloid leukemia cells [PDF]
, 2004 We present here the first evidence linking CD44 signaling to c-Jun expression and cell cycle progression in myeloid cell line models. CD44 ligation with the anti-CD44 monoclonal antibodies have been shown to induce differentiation and inhibit the ...
Peer Zada, Abdul Ali
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JNK and ERK8 as downstream effectors of receptor tyrosine kinases [PDF]
, 2006 MAP kinases are a super-family of serine-threonine protein kinases expressed in all eukaryotic cells. In mammals, there are many MAP kinases with different biological functions, grouped in distinctly regulated groups, ERK1/2 (extracellular signal related
Iavarone, Carlo
core +1 more source
Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment
Molecular Oncology, EarlyView.This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley +1 more source
Ets-2 is a target for an Akt (protein kinase B)/Jun N-terminal kinase signaling pathway in macrophages of motheaten-viable mutant mice [PDF]
, 2000 The transcription factor ets-2 was phosphorylated at residue threonine 72 in a colony-stimulating factor 1 (CSF-1)- and mitogen-activated protein kinase-independent manner in macrophages isolated from motheaten-viable (me-v) mice.
Forsthoefel, David +16 more
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Molecular Oncology, EarlyView.Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Molecular Oncology, EarlyView.Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura +19 more
wiley +1 more source
Murine c-erbB2: an oncogene that could be a target for vaccination therapy? : and the effect of HER2/c-erbB2/NeuT expression on cell signaling and milk protein formation in mouse mammary epithelial cells [PDF]
, 2006 ErbB2 is an orphan receptor tyrosine kinase which can dimerize with other ligand-activated members of the EGF receptor family to signal in pathways inducing cell proliferation. Frequently overexpressed in breast cancer and other human cancers, homologs
Noyer, Mathieu
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Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
Molecular Oncology, EarlyView.In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Molecular Oncology, EarlyView.Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source