Journal of cellular biochemistry. Supplement最新文献_第2页

Regulation and regulatory parameters of histone modifications. 组蛋白修饰的调控和调控参数。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<203::aid-jcb25>3.3.co;2-w

J. Davie, D. N. Chadee

{"title":"Regulation and regulatory parameters of histone modifications.","authors":"J. Davie, D. N. Chadee","doi":"10.1002/(sici)1097-4644(1998)72:30/31+<203::aid-jcb25>3.3.co;2-w","DOIUrl":"https://doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<203::aid-jcb25>3.3.co;2-w","url":null,"abstract":"Histone acetylation and phosphorylation destablizes nucleosome and chromatin structure. Relaxation of the chromatin fiber facilitates transcription. Coactivator complexes with histone acetyltransferase activity are recruited by transcription factors bound to enhancers or promoters. The recruited histone acetyltransferases may acetylate histone or nonhistone chromosomal proteins, resulting in the relaxation of chromatin structure. Alternatively, repressors recruit corepressor complexes with histone deacetylase activity, leading to condensation of chromatin. This review highlights the recent advances made in our understanding of the roles of histone acetyltransferases, histone deacetylases, histone kinases, and protein phosphatases in transcriptional activation and repression. Exciting reports revealing mechanistic connections between histone modifying activities and the RNA polymerase II machinery, the coupling of histone deacetylation and DNA methylation, the possible involvement of histone deacetylases in the organization of nuclear DNA, and the role of chromatin modulators in oncogenesis are discussed.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 5","pages":"203-13"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637112","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}

引用次数: 3

Tissue engineering: the first decade and beyond. 组织工程:第一个十年及以后。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<297::aid-jcb36>3.3.co;2-y

L. Bonassar, C. Vacanti

引用次数: 62

Macromolecular exchanges between the nucleus and cytoplasm. 细胞核和细胞质之间的大分子交换。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

C M Feldherr

引用次数: 0

In search of cellular control: signal transduction in context. 在寻找细胞控制:信号转导的背景。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

D Ingber

{"title":"In search of cellular control: signal transduction in context.","authors":"D Ingber","doi":"","DOIUrl":"","url":null,"abstract":"The field of molecular cell biology has experienced enormous advances over the last century by reducing the complexity of living cells into simpler molecular components and binding interactions that are amenable to rigorous biochemical analysis. However, as our tools become more powerful, there is a tendency to define mechanisms by what we can measure. The field is currently dominated by efforts to identify the key molecules and sequences that mediate the function of critical receptors, signal transducers, and molecular switches. Unfortunately, these conventional experimental approaches ignore the importance of supramolecular control mechanisms that play a critical role in cellular regulation. Thus, the significance of individual molecular constituents cannot be fully understood when studied in isolation because their function may vary depending on their context within the structural complexity of the living cell. These higher-order regulatory mechanisms are based on the cell's use of a form of solid-state biochemistry in which molecular components that mediate biochemical processing and signal transduction are immobilized on insoluble cytoskeletal scaffolds in the cytoplasm and nucleus. Key to the understanding of this form of cellular regulation is the realization that chemistry is structure and hence, recognition of the the importance of architecture and mechanics for signal integration and biochemical control. Recent work that has unified chemical and mechanical signaling pathways provides a glimpse of how this form of higher-order cellular control may function and where paths may lie in the future.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"232-7"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800003","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}

引用次数: 0

Intranuclear targeting of DNA replication factors. DNA复制因子的核内靶向。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

H Leonhardt, H P Rahn, M C Cardoso

引用次数: 0

Translocations, fusion genes, and acute leukemia. 易位，融合基因和急性白血病。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

V Saha, B D Young, P S Freemont

{"title":"Translocations, fusion genes, and acute leukemia.","authors":"V Saha, B D Young, P S Freemont","doi":"","DOIUrl":"","url":null,"abstract":"Genes involved in chromosomal translocations, associated with the formation of fusion proteins in leukemia, are modular in nature and regulatory in function. It is likely that they are involved in the initiation and maintenance of normal hematopoiesis. A conceptual model is proposed by which disruption of these different genes leads to the development of acute leukemia. Central to this model is the functional interaction between the mammalian trithorax and polycomb group protein complexes. Many of the genes identified in leukemia-associated translocations are likely upstream regulators, co-participators or downstream targets of these complexes. In the natural state, these proteins interact with each other to form multimeric higher-order structures, which sequentially regulate the development of the normal hematopoietic state, either through HOX gene expression or other less defined pathways. The novel interaction domains acquired by the chimaeric fusion products subvert normal cellular control mechanisms, which result in both a failure of cell maturation and activation of anti-apoptotic pathways. The mechanisms by which these translocation products are able to affect these processes are thought to lie at the level of chromatin-mediated transcriptional activation and/or repression. The stimuli for proliferation and development of clinically overt disease may require subsequent mutations in more than one oncogene or tumor suppressor gene, or both. A more comprehensive catalogue of mutation events in malignant cells is therefore required to understand the key regulatory networks that serve to maintain multipotentiality and in particular the modifications which initiate and coordinate commitment in differentiating hematopoietic cells. We propose a model in which common pathways for leukemogenesis lie along the cell cycle control of chromatin structure in terms of transcriptional activation or repression. A clearer understanding of this cascade will provide opportunities for the design and construction of novel biological agents that are able to restore normal regulatory mechanisms.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"264-76"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800006","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}

引用次数: 0

Signal transduction by transforming growth factor-beta: a cooperative paradigm with extensive negative regulation. 转化生长因子- β的信号转导:具有广泛负调控的合作范式。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

M E Engel, P K Datta, H L Moses

{"title":"Signal transduction by transforming growth factor-beta: a cooperative paradigm with extensive negative regulation.","authors":"M E Engel, P K Datta, H L Moses","doi":"","DOIUrl":"","url":null,"abstract":"Transforming growth factor-beta (TGF-beta) represents an evolutionarily conserved family of secreted factors that mobilize a complex signaling network to control cell fate by regulating proliferation, differentiation, motility, adhesion, and apoptosis. TGF-beta promotes the assembly of a cell surface receptor complex composed of type I (T beta RI) and type II (T beta RII) receptor serine/threonine kinases. In response to TGF-beta binding, T beta RII recruits and activates T beta RI through phosphorylation of the regulatory GS-domain. Activated T beta RI then initiates cytoplasmic signaling pathways to produce cellular responses. SMAD proteins together constitute a unique signaling pathway with key roles in signal transduction by TGF-beta and related factors. Pathway-restricted SMADs are phosphorylated and activated by type I receptors in response to stimulation by ligand. Once activated, pathway-restricted SMADs oligomerize with the common-mediator Smad4 and subsequently translocate to the nucleus. Genetic analysis in Drosophila melanogaster and Caenorhabditis elegans, as well as T beta RII and SMAD mutations in human tumors, emphasizes their importance in TGF-beta signaling. Mount ng evidence indicates that SMADs cooperate with ubiquitous cytoplasmic signaling cascades and nuclear factors to produce the full spectrum of TGF-beta responses. Operating independently, these ubiquitous elements may influence the nature of cellular responses to TGF-beta. Additionally, a variety of regulatory schemes contribute temporal and/or spatial restriction to TGF-beta responses. This report reviews our current understanding of TGF-beta signal transduction and considers the importance of a cooperative signaling paradigm to TGF-beta-mediated biological responses.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"111-22"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800116","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}

引用次数: 0

Steroid receptors at the nexus of transcriptional regulation. 类固醇受体在转录调控的关系。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01

T J Barrett, T C Spelsberg

{"title":"Steroid receptors at the nexus of transcriptional regulation.","authors":"T J Barrett, T C Spelsberg","doi":"","DOIUrl":"","url":null,"abstract":"During the past few years, our understanding of nuclear receptor action has dramatically improved as a result of the identification and functional analysis of co-regulators such as factors involved in chromatin remodeling, transcription intermediary factors (co-repressors and co-activators), and direct interactions with the basal transcriptional machinery. Furthermore, the elucidation of the crystal structures of the empty ligand-binding domains of the nuclear receptor and of complexes formed by the nuclear receptor's ligand-binding domain bound to agonists and antagonists has contributed significantly to our understanding of the early events of nuclear receptor action. However, the picture of hormone- and hormone receptor-mediated mechanisms of gene regulation remain incomplete and extremely complicated when one also considers the \"nontraditional\" interactions of hormone-activated nuclear receptors, for example, interactions between the activated steroid receptors and components of the chromatin/nuclear matrix; and finally the nongenomic effects that steroid hormones can exhibit with other signaling pathways. In this prospectus on steroid receptors, we discuss the implications of various steroid hormone and nuclear receptor interactions and potential future directions of investigation.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"185-93"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800124","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}

引用次数: 0

The S phase: beginning, middle, and end: a perspective. S阶段:开始、中间和结束:一个透视图。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<1::aid-jcb2>3.3.co;2-5

H. Ford, A. Pardee

引用次数: 0

Signal transduction by transforming growth factor-beta: a cooperative paradigm with extensive negative regulation. 转化生长因子- β的信号转导:具有广泛负调控的合作范式。

Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<111::aid-jcb15>3.3.co;2-x

M. Engel, P. Datta, H. Moses

{"title":"Signal transduction by transforming growth factor-beta: a cooperative paradigm with extensive negative regulation.","authors":"M. Engel, P. Datta, H. Moses","doi":"10.1002/(sici)1097-4644(1998)72:30/31+<111::aid-jcb15>3.3.co;2-x","DOIUrl":"https://doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<111::aid-jcb15>3.3.co;2-x","url":null,"abstract":"Transforming growth factor-beta (TGF-beta) represents an evolutionarily conserved family of secreted factors that mobilize a complex signaling network to control cell fate by regulating proliferation, differentiation, motility, adhesion, and apoptosis. TGF-beta promotes the assembly of a cell surface receptor complex composed of type I (T beta RI) and type II (T beta RII) receptor serine/threonine kinases. In response to TGF-beta binding, T beta RII recruits and activates T beta RI through phosphorylation of the regulatory GS-domain. Activated T beta RI then initiates cytoplasmic signaling pathways to produce cellular responses. SMAD proteins together constitute a unique signaling pathway with key roles in signal transduction by TGF-beta and related factors. Pathway-restricted SMADs are phosphorylated and activated by type I receptors in response to stimulation by ligand. Once activated, pathway-restricted SMADs oligomerize with the common-mediator Smad4 and subsequently translocate to the nucleus. Genetic analysis in Drosophila melanogaster and Caenorhabditis elegans, as well as T beta RII and SMAD mutations in human tumors, emphasizes their importance in TGF-beta signaling. Mount ng evidence indicates that SMADs cooperate with ubiquitous cytoplasmic signaling cascades and nuclear factors to produce the full spectrum of TGF-beta responses. Operating independently, these ubiquitous elements may influence the nature of cellular responses to TGF-beta. Additionally, a variety of regulatory schemes contribute temporal and/or spatial restriction to TGF-beta responses. This report reviews our current understanding of TGF-beta signal transduction and considers the importance of a cooperative signaling paradigm to TGF-beta-mediated biological responses.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 7","pages":"111-22"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50636983","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}

引用次数: 18