Alpha interferon suppresses the cyclin D3 and cdc25A genes, leading to a reversible G0-like arrest
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Summary
The delayed pattern of cyclin reexpression provides evidence that alpha-interferon signaling imposes a G0-like state on this system and represents a novel mechanism through which an external inhibitory cytokine interacts with the cell cycle machinery.
- Type
- article
- Published
- 1996-07-01
- Cited by
- 141
- References
- 42
- Access
- Open access
- OpenAlex
- https://openalex.org/W2169747575
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:35607287
Keywords
Biology, Cyclin A, Cyclin B, Cyclin E, Cyclin D
References
- Cell cycle regulation of CDK2 activity by phosphorylation of Thr160 and Tyr15.
- Recessive genetic deregulation abrogates c-myc suppression by interferon and is implicated in oncogenesis
- Isolation of monoclonal antibodies specific for human c-myc proto-oncogene product
- Activation of the phosphatase activity of human cdc25A by a cdk2‐cyclin E dependent phosphorylation at the G1/S transition.
- Cdc25A is a novel phosphatase functioning early in the cell cycle.
- Purification of the major protein-tyrosine-phosphatases of human placenta.
- Cyclin A is required at two points in the human cell cycle.
- Complementation by wild-type p53 of interleukin-6 effects on M1 cells: induction of cell cycle exit and cooperativity with c-myc suppression
- Transforming growth factor beta 1 inhibition of p34cdc2 phosphorylation and histone H1 kinase activity is associated with G1/S-phase growth arrest
- Acceleration of the G1/S phase transition by expression of cyclins D1 and E with an inducible system.
- Tumor necrosis factor reduces c-myc expression and cooperates with interferon-gamma in HeLa cells.
- Association of human cyclin E with a periodic G1-S phase protein kinase.
- The retinoblastoma tumor suppressor protein.
- Cloning of p27Kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals.
- pl5INK4B is a potentia| effector of TGF-β-induced cell cycle arrest
- Cyclin E/cdk2 and cyclin A/cdk2 kinases associate with p107 and E2F in a temporally distinct manner.
- The role of p34 kinases in the G1 to S-phase transition.
- An alternative pathway of T-cell activation: a functional role for the 50 kd T11 sheep erythrocyte receptor protein.
- Close link between reduction of c-myc expression by interferon and G0/G1 arrest
- Cdk inhibitors: on the threshold of checkpoints and development.
Cited by
- Mechanisms of interferon action.
- A rate limiting function of cdc25A for S phase entry inversely correlates with tyrosine dephosphorylation of Cdk2
- Cell cycle control, checkpoint mechanisms, and genotoxic stress.
- Cdk6-cyclin D3 complex evades inhibition by inhibitor proteins and uniquely controls cell's proliferation competence
- Interferon- : an overview of signals, mechanisms and functions
- Apoptosis and interferons: Role of interferon-stimulated genes as mediators of apoptosis
- Basic fibroblast growth factor-stimulates cytosolic phospholipase A2, phospholipase C-γ1 and phospholipase D through distinguishable signaling mechanisms
- Cell cycle regulation by the Cdc25 phosphatase family.
- Prolonged STAT1 activation related to the growth arrest of malignant lymphoma cells by interferon-alpha.
- Biologic Therapy of Leukemia
- Protein-protein conjugation using interferon
- Gene Therapy with Interferon Alpha and the Angiogenic Inhibitor, Vasostatin, in Neuroendocrine Tumors of the Digestive System
- Regulation of the STAT1 by the Epstein-Barr virus.
- Pathogenesis and targeted therapy of T-cell lymphoma
- Suppression of ovarian carcinoma cell growth in vivo by the interferon-inducible plasma membrane protein, phospholipid scramblase 1.
- Oxidative stress and cell cycle checkpoint function.
- Interferon-alpha inhibits Stat5 DNA-binding in IL-2 stimulated primary T-lymphocytes.
- Interferon regulatory factor 5, a novel mediator of cell cycle arrest and cell death.
- New therapeutic approaches in PV
- DAP-5, a novel homolog of eukaryotic translation initiation factor 4G isolated as a putative modulator of gamma interferon-induced programmed cell death
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