Ets factors and regulation of the extracellular matrix.
Ets factors are critical mediators of extracellular matrix (ECM) remodelling. As the spectrum of Ets-regulated target genes widens, so does their role in various pathological and physiological processes. Regulation of matrix degrading proteases by Ets factors in tumor invasion and metastasis is well established. Emerging evidence suggests that they may also play a role in the pathology of autoimmune diseases. Newly characterized Ets target genes such as tenascin-C and collagen type I suggest their role in diseases characterized by aberrant collagen deposition (fibrosis). Ets function is also critical in bone and cartilage development. There is increasing knowledge of the complex regulatory mechanisms involved in transcription of Ets target genes. Ets factors may function as activators or as repressors via association with specific cofactors depending on the promoter context. Signaling pathways can modulate the activation status of Ets factors and their transcriptional partners. Precise understanding of the role of Ets factors in the complex cellular network governing the expression of ECM proteins and the enzymes that degrade them will be a focus of future studies.
Trojanowska
M
M
Division of Rheumatology and Immunology, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston South Carolina, SC 29401, USA.
D016475:3T3 Cells; D000818:Animals; D001327:Autoimmune Diseases / Q000378:metabolism; D001842:Bone and Bones / Q000196:embryology / Q000378:metabolism; D002356:Cartilage / Q000196:embryology; D002642:Chick Embryo; D003094:Collagen / Q000378:metabolism; D004268:DNA-Binding Proteins; D004790:Enzyme Induction / Q000235:genetics; D005109:Extracellular Matrix / Q000378:metabolism*; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D008666:Metalloendopeptidases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D005810:Multigene Family; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology; D009389:Neovascularization, Pathologic / Q000235:genetics / Q000378:metabolism; D015513:Oncogene Proteins / Q000235:genetics / Q000502:physiology; D010012:Osteogenesis / Q000235:genetics; D010641:Phenotype; D050787:Proto-Oncogene Protein c-ets-2; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D050783:Proto-Oncogene Proteins c-ets; D016755:Proto-Oncogene Proteins c-jun / Q000502:physiology; D012097:Repressor Proteins; D015398:Signal Transduction / Q000235:genetics; D016329:Sp1 Transcription Factor; D019063:Tenascin / Q000378:metabolism; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology*; D000071230:Transcriptional Regulator ERG; D014407:Tumor Cells, Cultured; D014945:Wound Healing / Q000235:genetics
D004268:DNA-Binding Proteins; C107465:ERF protein, human; C072312:ERG protein, human; C494069:ETS2 protein, human; C494070:Ets2 protein, mouse; D016326:Extracellular Matrix Proteins; D009363:Neoplasm Proteins; D015513:Oncogene Proteins; D050787:Proto-Oncogene Protein c-ets-2; D011518:Proto-Oncogene Proteins; D050783:Proto-Oncogene Proteins c-ets; D016755:Proto-Oncogene Proteins c-jun; D012097:Repressor Proteins; D016329:Sp1 Transcription Factor; D019063:Tenascin; D015534:Trans-Activators; D014157:Transcription Factors; D000071230:Transcriptional Regulator ERG; D003094:Collagen; D008666:Metalloendopeptidases