Pub Date : 1990-11-01DOI: 10.1111/j.1574-6968.1990.tb03520.x
H U Bernard
Papillomaviruses cause neoplasia of epithelia and subepidermal fibroblasts which may progress to certain forms of malignancies. During the viral life cycle, papillomavirus genomes receive, process and generate signals. Transcription factors binding to their enhancer carry information about tissue specificity and hormonal regulation, while other factors in the cornified layer of the epidermis activate capsid protein production. Furthermore, products of the viral E2 and E1 genes constitute feedback signals that modulate viral transcription and replication. Proteins derived from the genes E5, E6 and E7 modulate cellular homeostasis so as to induce neoplatic transformation. A molecular understanding of these regulatory events may form a prerequisite for a causal therapy of papillomavirus-induced malignancies.
{"title":"Controls in the papillomavirus life cycle.","authors":"H U Bernard","doi":"10.1111/j.1574-6968.1990.tb03520.x","DOIUrl":"https://doi.org/10.1111/j.1574-6968.1990.tb03520.x","url":null,"abstract":"<p><p>Papillomaviruses cause neoplasia of epithelia and subepidermal fibroblasts which may progress to certain forms of malignancies. During the viral life cycle, papillomavirus genomes receive, process and generate signals. Transcription factors binding to their enhancer carry information about tissue specificity and hormonal regulation, while other factors in the cornified layer of the epidermis activate capsid protein production. Furthermore, products of the viral E2 and E1 genes constitute feedback signals that modulate viral transcription and replication. Proteins derived from the genes E5, E6 and E7 modulate cellular homeostasis so as to induce neoplatic transformation. A molecular understanding of these regulatory events may form a prerequisite for a causal therapy of papillomavirus-induced malignancies.</p>","PeriodicalId":77129,"journal":{"name":"FEMS microbiology immunology","volume":"2 4","pages":"201-5"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1574-6968.1990.tb03520.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13332082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1990-11-01DOI: 10.1111/j.1574-6968.1990.tb03519.x
A G Porter
Tumour necrosis factor-alpha (TNF-alpha) and lymphotoxin (LT or TNF-beta) are cytokines, best known for their cytotoxic or cytostatic effects on some tumour cells. They are structurally related, compete for a common receptor, and are potent inducers of similar biological responses. TNF-alpha and LT appear to have distinct three-dimensional structures because they differ greatly in their sensitivity to various proteases and chemical agents, and antibodies raised against one cytokine do not cross-react with the other cytokine. The closely linked TNF-alpha and LT genes are independently regulated since many cell types produce only TNF-alpha or LT. Expression of the TNF-alpha gene can be controlled either at the transcriptional or at the post-transcriptional level. In some cell types, TNF-alpha and LT induce qualitatively or quantitatively different biological responses, and LT can antagonize the action of TNF-alpha. The disparate biological activities of TNF-alpha and LT may be related to their different interactions with a common receptor. It is possible that TNF-alpha and LT have different physiological roles.
{"title":"Human tumour necrosis factors-alpha and -beta: differences in their structure, expression and biological properties.","authors":"A G Porter","doi":"10.1111/j.1574-6968.1990.tb03519.x","DOIUrl":"https://doi.org/10.1111/j.1574-6968.1990.tb03519.x","url":null,"abstract":"<p><p>Tumour necrosis factor-alpha (TNF-alpha) and lymphotoxin (LT or TNF-beta) are cytokines, best known for their cytotoxic or cytostatic effects on some tumour cells. They are structurally related, compete for a common receptor, and are potent inducers of similar biological responses. TNF-alpha and LT appear to have distinct three-dimensional structures because they differ greatly in their sensitivity to various proteases and chemical agents, and antibodies raised against one cytokine do not cross-react with the other cytokine. The closely linked TNF-alpha and LT genes are independently regulated since many cell types produce only TNF-alpha or LT. Expression of the TNF-alpha gene can be controlled either at the transcriptional or at the post-transcriptional level. In some cell types, TNF-alpha and LT induce qualitatively or quantitatively different biological responses, and LT can antagonize the action of TNF-alpha. The disparate biological activities of TNF-alpha and LT may be related to their different interactions with a common receptor. It is possible that TNF-alpha and LT have different physiological roles.</p>","PeriodicalId":77129,"journal":{"name":"FEMS microbiology immunology","volume":"2 4","pages":"193-9"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1574-6968.1990.tb03519.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13435498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}