Begell House Inc.
Critical Reviews™ in Eukaryotic Gene Expression
CRE
1045-4403
8
1
1998
Control of Osteoclast Differentiation
1-17
10.1615/CritRevEukarGeneExpr.v8.i1.10
Sakamuri V.
Reddy
Children's Research Institute, Department of Pediatrics, Medical University of South Carolina (MUSC), Charleston, SC 29425 Department of Medicine, Division of Hematology, University of Texas Health Science Center
G. David
Roodman
Department of Medicine, Division of Hematology, University of Texas Health Science Center; Audie L. Murphy Veterans Administration Hospital, San Antonio, TX 78284
osteoclast
differentiation
hormones
cytokines
stromal cells
bone resorption
transcription factors.
The osteoclast is the primary bone-resorbing cell and is derived from the monocyte/macrophage lineage. Bipotent osteoclast precursors, which can form both osteoclasts and monocyte-macrophages, proliferate and differentiate to become unipotent post-mitotic committed osteoclast precursors. These post-mitotic committed precursors fuse to form the multinucleated osteoclast, which is then activated to resorb bone. A variety of soluble and membrane-bound factors play a critical role in regulating osteoclast formation, including growth factors, systemic hormones, and cells in the marrow microenvironment, such as osteoblasts and marrow stromal cells. Cell-to-cell interactions are important in both the formation and activity of the osteoclast. Recent molecular biological studies have identified transcription factors, such as c-fos and PU.l, which are required for osteoclast differentiation. In this review, we discuss the phenotypic changes that are induced as the cells mature from bipotent early precursors to mature osteoclasts; factors that have been identified that are involved in this process; and the role of marrow stromal cells and osteoblasts in osteoclast differentiation.
Gene Regulation by Vitamin D3
19-42
10.1615/CritRevEukarGeneExpr.v8.i1.20
Carsten
Carlberg
Institut fur Physiologische Chemie I, Heinrich-Heine-Universitat Dusseldorf, D-40001 Dusseldorf, Germany
Patsie
Polly
Institut fur Physiologische Chemie I, Heinrich-Heine-Universitat Dusseldorf, D-40001 Dusseldorf, Germany
Vitamin D response elements
vitamin D receptor
vitamin D analogues
co-factors
transcrip¬tional regulation.
The physiologically active form of vitamin D3, 1α,25-dihydroxyvitamin D3 (VD), is a nuclear hormone with pleiotropic action on the control of calcium homeostasis and bone formation, induction of cellular differentiation and apoptosis, inhibition of cellular proliferation, and other cellular signaling processes. The actions of the hormone are mediated by the vitamin D receptor (VDR), a transcription factor that is a nuclear receptor for VD and a member of the nuclear receptor superfamily. The structural relationship between the members of this transcription factor family suggests similar function in DNA binding, transactivation, and contact to other nuclear proteins. However, each nuclear receptor also demonstrates individual properties that are characteristic and not shared by its respective relatives. In this review, both common as well as individual characteristics of VDR-mediated transcriptional regulation are critically discussed.
Age-Dependent Modifications of Gene Expression in Human Fibroblasts
43-80
10.1615/CritRevEukarGeneExpr.v8.i1.30
Vincent J.
Cristofalo
Center for Gerontological Research, Allegheny University of the Health Sciences, MCP ♦ Hahnemann School of Medicine, 2900 Queen Lane, Philadelphia, PA 19129
Craig
Volker
Center for Gerontological Research, Allegheny University of the Health Sciences, MCP ♦ Hahnemann School of Medicine, 2900 Queen Lane, Philadelphia, PA 19129
Mary Kay
Francis
Center for Gerontological Research, Allegheny University of the Health Sciences, MCP ♦ Hahnemann School of Medicine, 2900 Queen Lane, Philadelphia, PA 19129
Maria
Tresini
Center for Gerontological Research, Allegheny University of the Health Sciences, MCP ♦ Hahnemann School of Medicine, 2900 Queen Lane, Philadelphia, PA 19129
aging
cell cycle
gene expression
human fibroblasts
senescence
signal transduction.
Normal human fibroblasts exhibit a limited proliferative potential in culture. When populations are serially subcultured, they grow well initially, but ultimately reach a stage when they are no longer able to proliferate in response to mitogenic stimuli. This state is designated "replicative senescence". In addition to failure to proliferate, numerous morphological and physiological changes characterize the senescent phenotype. Both stochastic and genetic mechanisms have been postulated as causal effectors of the aging process. However, the pathway leading to cellular senescence is likely to be complex with numerous changes. In this article we provide an overview of cell and molecular changes that occur during cell aging, with special emphasis on signal transduction pathways and cell cycle proteins that are likely to play key roles in determining the limited replicative life span and the changes that occur.
Regulatory Parameters of DNA Replication
81-106
10.1615/CritRevEukarGeneExpr.v8.i1.40
Maria
Zannis-Hadjopoulos
McGill Cancer Centre, McGill University, 3655 Drummond Street, Montreal, Quebec H3G 1Y6, CANADA
Gerald B.
Price
McGill Cancer Centre, McGill University, 3655 Drummond Street, Montreal, Quebec H3G 1Y6, CANADA
regulation
DNA replication
eukaryotes
origins.
One of the fundamental characteristics that help define life is the ability to propagate. At the basest level in the act of propagation is replication of the genetic information as the databank and architectural plans for each particular life form. Thus propagation of life requires the replication of the genome−for the purposes of our review, eukaryotic DNA replication. In this critical review, we have chosen to present the issues and supporting experimental evidence in question-and-answer format. Over the past 3 to 4 years, the research domain of eukaryotic DNA replication has developed a new dynamism. This new force in discovery of the fundamental elements and mechanisms for DNA replication in higher eukaryotes has been propelled by accepted methodologies for mapping (identification) of origins of DNA replication, applicable to mammalian DNA replication, and by the discovery of the origin recognition complex (ORC) in yeast, which has served as a model in the search for the mammalian equivalent.