Regulation of cell cycle re-entry by growth, survival and stress signalling pathways. (February 2000)

• Record Type: Journal Article
• Authors: Cook, S.J.; Balmanno, K.; Garner, A.; Millar, T.; Taverner, C.; Todd, D.
• Is Part Of: Biochemical Society transactions. Volume 28:Number 2(2000)
• Page Start: 233
• Page End: 240
• Publication Date: 2000-02
• Subjects: AP-, activator protein-I -- CDK, cyclin-dependent kinase -- CDKI, CDK inhibitor -- ER*, oestrogen receptor hormone-binding domain -- ERK, extracellular-signal-regulated kinase -- JNK, c-Jun N-terminal kinase -- MAPK, mitogen-activated protein kinase -- MEK, MAPK/ERK kinase -- MEKK, MEK kinase -- MKK, MAPK kinase -- PI3K, phosphoinositide 3'-kinase -- PKB, protein kinase B -- pRb, retinoblastoma tumour suppressor protein -- SAPK, stress-activated protein kinase; cyclin-dependent kinases -- MAP kinases -- stress-activated protein kinases -- Ras -- senescence; Biochemistry -- Congresses; 572
• DOI: 10.1042/bst0280233
• Languages: English
• ISSNs: 0300-5127

Abstract

Abstract : The mitogen-activated and stress-activated protein kinases transduce signals from plasma membrane signalling machinery into the nucleus to modulate gene expression. By regulating the genomic response to environmental cues (growth factors, stresses) these pathways determine whether a cell re-enters the cell cycle, undergoes cell cycle arrest, senescence or apoptosis. We are particularly interested in how these pathways integrate with each other, and interact with the cell cycle machinery to achieve these discrete biological responses.