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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
H L Ford, A B Pardee
{"title":"The S phase: beginning, middle, and end: a perspective.","authors":"H L Ford,&nbsp;A B Pardee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Events in the S phase of the cell cycle have been investigated to a relatively limited extent in comparison with those in G1 and M phases. Four aspects of S are briefly discussed in this report: (1) the final biochemical step permitting initiation of DNA synthesis, (2) determination of replication timing of individual genes and its mechanism, (3) S phase processes that lead to the onset of M phase, and (4) resetting the S-phase machinery.</p>","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800181","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
Communication between the cell membrane and the nucleus: role of protein compartmentalization. 细胞膜与细胞核之间的通讯:蛋白质区隔化的作用。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<250::aid-jcb31>3.3.co;2-v
S. Lelièvre, M. Bissell
{"title":"Communication between the cell membrane and the nucleus: role of protein compartmentalization.","authors":"S. Lelièvre, M. Bissell","doi":"10.1002/(sici)1097-4644(1998)72:30/31+<250::aid-jcb31>3.3.co;2-v","DOIUrl":"https://doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<250::aid-jcb31>3.3.co;2-v","url":null,"abstract":"Understanding how the information is conveyed from outside to inside the cell is a critical challenge for all biologists involved in signal transduction. The flow of information initiated by cell-cell and cell-extracellular matrix contacts is mediated by the formation of adhesion complexes involving multiple proteins. Inside adhesion complexes, connective membrane skeleton (CMS) proteins are signal transducers that bind to adhesion molecules, organize the cytoskeleton, and initiate biochemical cascades. Adhesion complex-mediated signal transduction ultimately directs the formation of supramolecular structures in the cell nucleus, as illustrated by the establishment of multi complexes of DNA-bound transcription factors, and the redistribution of nuclear structural proteins to form nuclear subdomains. Recently, several CMS proteins have been observed to travel to the cell nucleus, suggesting a distinctive role for these proteins in signal transduction. This review focuses on the nuclear translocation of structural signal transducers of the membrane skeleton and also extends our analysis to possible translocation of resident nuclear proteins to the membrane skeleton. This leads us to envision the communication between spatially distant cellular compartments (i.e., membrane skeleton and cell nucleus) as a bidirectional flow of information (a dynamic reciprocity) based on subtle multilevel structural and biochemical equilibria. At one level, it is mediated by the interaction between structural signal transducers and their binding partners, at another level it may be mediated by the balance and integration of signal transducers in different cellular compartments.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 22","pages":"250-63"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637239","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 RB family of cell cycle regulatory factors. 细胞周期调节因子RB家族。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(SICI)1097-4644(1998)72:30/31+<30::AID-JCB5>3.0.CO;2-J
P. Stiegler, M. Kasten, A. Giordano
{"title":"The RB family of cell cycle regulatory factors.","authors":"P. Stiegler, M. Kasten, A. Giordano","doi":"10.1002/(SICI)1097-4644(1998)72:30/31+<30::AID-JCB5>3.0.CO;2-J","DOIUrl":"https://doi.org/10.1002/(SICI)1097-4644(1998)72:30/31+<30::AID-JCB5>3.0.CO;2-J","url":null,"abstract":"The intense investigation of the retinoblastoma \"tumor suppressor family\" members, pRb, pRb2/p130, and p107, has revealed impressive mechanisms evolved to safeguard development and homeostasis in higher eukaryotes. Members of the retinoblastoma family are involved in implementing and controlling three major aspects of cellular life: (1) proliferative growth, (2) differentiation, and (3) apoptosis. The activities of these proteins are highly regulated, enabling them to precisely establish control. The pRb protein is well understood in its regulatory abilities and is considered a classical tumor suppressor. The role of pRb2/p130 protein in growth suppression and its potential as a tumor suppressor have been established during the last few years. The p107 protein, structurally and functionally similar to, but yet distinctive from, pRb2/p130, is characterized at a more rudimentary level. In this report, we review the latest data on the retinoblastoma protein family and its web of regulatory mechanisms.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 10","pages":"30-6"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637604","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: 81
Control of bone formation and resorption: biological and clinical perspective. 骨形成和骨吸收的控制:生物学和临床观点。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(SICI)1097-4644(1998)72:30/31+<55::AID-JCB9>3.0.CO;2-R
G. Rodan
{"title":"Control of bone formation and resorption: biological and clinical perspective.","authors":"G. Rodan","doi":"10.1002/(SICI)1097-4644(1998)72:30/31+<55::AID-JCB9>3.0.CO;2-R","DOIUrl":"https://doi.org/10.1002/(SICI)1097-4644(1998)72:30/31+<55::AID-JCB9>3.0.CO;2-R","url":null,"abstract":"Bone is subject to continuous breakdown (resorption) by osteoclasts and rebuilding (formation) by osteoblasts in order to fulfill its functions. Most bone diseases including osteoporosis are due to excessive bone resorption relative to formation. Recent research has generated new insights into the regulation of osteoclast and osteoblast differentiation and function and the interaction between the two cell types. There is increased awareness of the role of mechanical stimuli in bone homeostasis and by inference the function of bone cells. This information can lead to new therapeutic modalities for maintaining a healthy skeleton into old age.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 16","pages":"55-61"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637736","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: 53
The ongoing saga of osteoporosis treatment. 正在进行的骨质疏松症治疗传奇。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01
B S Komm, P V Bodine
{"title":"The ongoing saga of osteoporosis treatment.","authors":"B S Komm,&nbsp;P V Bodine","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"277-83"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800007","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
DNA replication machinery of the mammalian cell. 哺乳动物细胞的DNA复制机制。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(SICI)1097-4644(1998)72:30/31+<18::AID-JCB4>3.0.CO;2-0
L. Malkas
{"title":"DNA replication machinery of the mammalian cell.","authors":"L. Malkas","doi":"10.1002/(SICI)1097-4644(1998)72:30/31+<18::AID-JCB4>3.0.CO;2-0","DOIUrl":"https://doi.org/10.1002/(SICI)1097-4644(1998)72:30/31+<18::AID-JCB4>3.0.CO;2-0","url":null,"abstract":"The process of DNA replication in mammalian cells is highly complex and has several unique features that distinguish it from simpler prokaryotic systems. The study of mammalian DNA replication lagged behind that of prokaryotes for many years. This was because of the lack of a reliable and efficient mammalian cell-based in vitro DNA replication system. In 1984, the first mammalian-based DNA replication system that initiated DNA synthesis successfully in vitro was developed. The employment of the mammalian in vitro DNA replication system has led to the identification of several DNA replication proteins. This article describes the current knowledge regarding the proteins mediating mammalian DNA replication, as well as how they are proposed to function during DNA synthesis. There is also a discussion of the role the mammalian cell nuclear architecture plays in DNA replication. The evidence for the existence of an organized DNA replication machine in mammalian cells is also presented.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 19","pages":"18-29"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637056","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: 22
Checking on the cell cycle. 检查细胞周期。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01 DOI: 10.1002/(sici)1097-4644(1998)72:30/31+<50::aid-jcb8>3.3.co;2-
W. Mercer
{"title":"Checking on the cell cycle.","authors":"W. Mercer","doi":"10.1002/(sici)1097-4644(1998)72:30/31+<50::aid-jcb8>3.3.co;2-","DOIUrl":"https://doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<50::aid-jcb8>3.3.co;2-","url":null,"abstract":"Cell cycle checkpoint controls play a major role in preventing the development of cancer [see Sherr, 1994, for a more detailed discussion]. Major checkpoints occur at the G1 to S phase transition and at the G2 to M phase transitions. Cancer is a genetic disease that arises from defects in growth-promoting oncogenes and growth-suppressing tumor suppressor genes. The p53 tumor suppressor protein plays a role in both the G1/S phase and G2/M phase checkpoints. The mechanism for this activity at the G1/S phase checkpoint is well understood, but its mechanism of action at the G2/M phase checkpoint remains to be elucidated. The p53 protein is thought to prevent chromosomal replication specifically during the cell cycle if DNA damage is present. In addition, p53 can induce a type of programmed cell death, or apoptosis, under certain circumstances. The general goal of p53 appears to be the prevention of cell propagation if mutations are present. The p53 protein acts as a transcription factor by binding to certain specific genes and regulating their expression. One of these, WAF1 or Cip1, is activated by p53 and is an essential downstream mediator of p53-dependent G1/S phase checkpoint control. The function of p53 can be suppressed by another gene, MDM2, which is overexpressed in certain tumorigenic mouse cells and binds to p53 protein, thus inhibiting its transcriptional activation function. Other cellular proteins have been found to bind to p53, but the significance of the associations is not completely understood in all cases. The large number of human cancers in which the p53 gene is altered makes this gene a good candidate for cancer screening approaches.","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":" 23","pages":"50-4"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50637729","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
Checking on the cell cycle. 检查细胞周期。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01
W E Mercer
{"title":"Checking on the cell cycle.","authors":"W E Mercer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cell cycle checkpoint controls play a major role in preventing the development of cancer [see Sherr, 1994, for a more detailed discussion]. Major checkpoints occur at the G1 to S phase transition and at the G2 to M phase transitions. Cancer is a genetic disease that arises from defects in growth-promoting oncogenes and growth-suppressing tumor suppressor genes. The p53 tumor suppressor protein plays a role in both the G1/S phase and G2/M phase checkpoints. The mechanism for this activity at the G1/S phase checkpoint is well understood, but its mechanism of action at the G2/M phase checkpoint remains to be elucidated. The p53 protein is thought to prevent chromosomal replication specifically during the cell cycle if DNA damage is present. In addition, p53 can induce a type of programmed cell death, or apoptosis, under certain circumstances. The general goal of p53 appears to be the prevention of cell propagation if mutations are present. The p53 protein acts as a transcription factor by binding to certain specific genes and regulating their expression. One of these, WAF1 or Cip1, is activated by p53 and is an essential downstream mediator of p53-dependent G1/S phase checkpoint control. The function of p53 can be suppressed by another gene, MDM2, which is overexpressed in certain tumorigenic mouse cells and binds to p53 protein, thus inhibiting its transcriptional activation function. Other cellular proteins have been found to bind to p53, but the significance of the associations is not completely understood in all cases. The large number of human cancers in which the p53 gene is altered makes this gene a good candidate for cancer screening approaches.</p>","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"50-4"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800109","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
Control of bone formation and resorption: biological and clinical perspective. 骨形成和骨吸收的控制:生物学和临床观点。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01
G A Rodan
{"title":"Control of bone formation and resorption: biological and clinical perspective.","authors":"G A Rodan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bone is subject to continuous breakdown (resorption) by osteoclasts and rebuilding (formation) by osteoblasts in order to fulfill its functions. Most bone diseases including osteoporosis are due to excessive bone resorption relative to formation. Recent research has generated new insights into the regulation of osteoclast and osteoblast differentiation and function and the interaction between the two cell types. There is increased awareness of the role of mechanical stimuli in bone homeostasis and by inference the function of bone cells. This information can lead to new therapeutic modalities for maintaining a healthy skeleton into old age.</p>","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"55-61"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800110","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
Osteopontin expression and function: role in bone remodeling. 骨桥蛋白的表达和功能:在骨重塑中的作用。
Journal of cellular biochemistry. Supplement Pub Date : 1998-01-01
D T Denhardt, M Noda
{"title":"Osteopontin expression and function: role in bone remodeling.","authors":"D T Denhardt,&nbsp;M Noda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The cytokine and cell attachment protein osteopontin (OPN) is not necessary for the development and survival of mice in a clean animal facility. The primary role of OPN appears to be that of facilitating recovery of the organism after injury or infection, which generally causes an increase in its expression. It also is essential for some forms of bone remodeling. OPN stimulates cellular signaling pathways via various receptors found on most cell types and can encourage cell migration. OPN modulates immune and inflammatory responses and possibly negatively regulates Ras signaling pathways. Its apparent ability to enhance cell survival by inhibiting apoptosis may explain why the metastatic proficiency of tumor cells increases with increased OPN expression.</p>","PeriodicalId":77196,"journal":{"name":"Journal of cellular biochemistry. Supplement","volume":"30-31 ","pages":"92-102"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20800114","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
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