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標(biāo)題: Titlebook: Cell Cycle Deregulation in Cancer; Greg H. Enders Book 2010 Springer Science+Business Media, LLC 2010 DNA.biology.cancer.cancer therapy.ce [打印本頁]

作者: 不友善    時(shí)間: 2025-3-21 17:29
書目名稱Cell Cycle Deregulation in Cancer影響因子(影響力)




書目名稱Cell Cycle Deregulation in Cancer影響因子(影響力)學(xué)科排名




書目名稱Cell Cycle Deregulation in Cancer網(wǎng)絡(luò)公開度




書目名稱Cell Cycle Deregulation in Cancer網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Cell Cycle Deregulation in Cancer被引頻次




書目名稱Cell Cycle Deregulation in Cancer被引頻次學(xué)科排名




書目名稱Cell Cycle Deregulation in Cancer年度引用




書目名稱Cell Cycle Deregulation in Cancer年度引用學(xué)科排名




書目名稱Cell Cycle Deregulation in Cancer讀者反饋




書目名稱Cell Cycle Deregulation in Cancer讀者反饋學(xué)科排名





作者: EVICT    時(shí)間: 2025-3-21 21:07
https://doi.org/10.1007/978-94-017-6766-8feration is a fundamental feature of all types of cancer. One of the key regulators of cell proliferation is the E2F transcription factor. E2F controls the expression of many genes that are required for cells to divide and elevated E2F activity is found in most tumor cells. The activation and inacti
作者: Criteria    時(shí)間: 2025-3-22 03:33
https://doi.org/10.1007/978-94-017-6766-8tiation of DNA replication, and virtually all components of the pre-RC are regulated by complex mechanisms that center around the activity of cyclin-dependent kinases (CDKs). CDK/cyclin complexes both positively and negatively regulate pre-RC components, including their expression, activity, stabili
作者: Legion    時(shí)間: 2025-3-22 05:48

作者: 依法逮捕    時(shí)間: 2025-3-22 10:21

作者: inflame    時(shí)間: 2025-3-22 15:58
The Essence of Acts of Empathy,apoptosis. Recently, both of these proteins were found to be intimately tied to metabolic pathways and to play surprising roles in autophagy. Autophagy (“self-eating”) is a critical response of eukaryotic cells to stress. During this process, portions of the cytosol, including cytoplasmic organelles
作者: inflame    時(shí)間: 2025-3-22 20:45
https://doi.org/10.1007/978-94-017-7402-4 the biological organization of tumours. These cells, named tumour-initiating cells (TICs), or cancer stem cells (CSCs), share phenotypic and functional characteristics with normal stem cells, most notably their ability to self-renew. Here we discuss regulation of self-renewal in normal haematopoiet
作者: transdermal    時(shí)間: 2025-3-23 00:55

作者: Canyon    時(shí)間: 2025-3-23 02:12

作者: ANTI    時(shí)間: 2025-3-23 07:41
https://doi.org/10.1007/978-94-017-9984-3rogression to fully fledged cancer would allow for chemoprevention or therapeutic interventions; however in most cases, IEN remains undetected and the exact mechanisms for progression remain unknown. Barrett’s oesophagus, the premalignant stage of oesophageal adenocarcinoma, is the perfect model to
作者: 過度    時(shí)間: 2025-3-23 11:02

作者: STAT    時(shí)間: 2025-3-23 17:12
https://doi.org/10.1007/978-1-4419-1770-6DNA; biology; cancer; cancer therapy; cell; esophagus; research; senescence; tumor; tumorigenesis
作者: Brochure    時(shí)間: 2025-3-23 18:22

作者: 脫毛    時(shí)間: 2025-3-23 23:11
Greg H. Endersoutlines major cell cycle perturbations that drive tumorigenesis and considers the prospects for using such knowledge in cancer therapy..Includes supplementary material:
作者: Pillory    時(shí)間: 2025-3-24 03:56

作者: menopause    時(shí)間: 2025-3-24 06:49

作者: 模范    時(shí)間: 2025-3-24 12:31
https://doi.org/10.1007/978-94-017-6766-8Furthermore, deregulation of pre-RC components and CDK/cyclins is observed in a multitude of human cancers. Thus, regulation of pre-RC assembly is a critical facet of normal cell biology that has profound implications related to cancer etiology and diagnosis.
作者: insincerity    時(shí)間: 2025-3-24 18:21

作者: conspicuous    時(shí)間: 2025-3-24 19:38
The Senescence Secretome and Its Impact on Tumor Suppression and Cancers includes increased production of cytokines, matrix metalloproteases, and altered production of many growth factors. This review discusses these factors, their mechanism of regulation in senescent cells, and their contribution to the senescent phenotype and its role in tumor suppression.
作者: 口味    時(shí)間: 2025-3-25 03:08
https://doi.org/10.1007/978-94-017-7127-6kpoints. Failure of cells to undergo mitotic catastrophe is believed to contribute to tumorigenesis. Furthermore, mitotic catastrophe is exploited as a strategy to induce cell death in cancer treatments.
作者: sterilization    時(shí)間: 2025-3-25 04:06
The Essence of Acts of Empathy,on-specific degradation process allows the cell to adapt to its bioenergetic needs and to prolong survival. The following sections will outline the evidence for a role of p53 and ARF in autophagy, the role of this pathway in cancer, and what questions remain to be answered.
作者: 總    時(shí)間: 2025-3-25 11:28

作者: Glower    時(shí)間: 2025-3-25 15:31

作者: 合唱隊(duì)    時(shí)間: 2025-3-25 16:36
p53, ARF, and the Control of Autophagyon-specific degradation process allows the cell to adapt to its bioenergetic needs and to prolong survival. The following sections will outline the evidence for a role of p53 and ARF in autophagy, the role of this pathway in cancer, and what questions remain to be answered.
作者: profligate    時(shí)間: 2025-3-25 22:48
Maintenance of Telomeres in Cancerrves as a cellular clock that limits proliferation potential. In this chapter I will review the mechanisms that allow the proper function of telomeres in normal cells as well as the mechanisms employed by cancer cells to bypass their normal regulation.
作者: Bucket    時(shí)間: 2025-3-26 03:27
Changzhi Wu,Xiangyu Wang,Jiang Lins includes increased production of cytokines, matrix metalloproteases, and altered production of many growth factors. This review discusses these factors, their mechanism of regulation in senescent cells, and their contribution to the senescent phenotype and its role in tumor suppression.
作者: 沒有希望    時(shí)間: 2025-3-26 06:48
2199-2584 ludes supplementary material: .Cancer is fundamentally a disease of abnormal cell proliferation: Cancer cells multiply when and where they should not. This proliferation entails escape from normal bounds imposed by the tissue environment, the internal biology of the cell (DNA damage, chromosomal imb
作者: Defense    時(shí)間: 2025-3-26 10:58
https://doi.org/10.1007/978-94-017-7402-4al characteristics with normal stem cells, most notably their ability to self-renew. Here we discuss regulation of self-renewal in normal haematopoietic and leukaemic stem cells, focusing on the role of cell quiescence and inhibitors of the cell cycle.
作者: Bumptious    時(shí)間: 2025-3-26 15:53

作者: ARM    時(shí)間: 2025-3-26 18:42
Book 2010cape from normal bounds imposed by the tissue environment, the internal biology of the cell (DNA damage, chromosomal imbalances, disorganized mitotic spindles), and the proliferative history of the cell (normal generational times). Some of the key oncogenic events in cancer directly perturb proteins
作者: COMMA    時(shí)間: 2025-3-26 22:08
Escape from Cellular Quiescencerm refers to a state of dormancy as opposed to a proliferative state. However, quiescent cells are in any other regard metabolically active. In many tissues with relative fast cell renewal rates the primary function of a small group of undifferentiated cells is limited to self-renewal (stem cells).
作者: projectile    時(shí)間: 2025-3-27 03:51
Interplay Between Cyclin-Dependent Kinases and E2F-Dependent Transcriptionferation is a fundamental feature of all types of cancer. One of the key regulators of cell proliferation is the E2F transcription factor. E2F controls the expression of many genes that are required for cells to divide and elevated E2F activity is found in most tumor cells. The activation and inacti
作者: lattice    時(shí)間: 2025-3-27 06:09

作者: calorie    時(shí)間: 2025-3-27 13:20
Mitotic Checkpoint and Chromosome Instability in Cancerly change gene expression patterns on a global scale and provides a mechanism that promotes genetic and biochemical diversity that is used by cells to achieve a transformed state or to survive suboptimal growth conditions. The mitotic checkpoint is a fail-safe mechanism that monitors the fidelity of
作者: JUST    時(shí)間: 2025-3-27 15:53

作者: nepotism    時(shí)間: 2025-3-27 20:01
p53, ARF, and the Control of Autophagyapoptosis. Recently, both of these proteins were found to be intimately tied to metabolic pathways and to play surprising roles in autophagy. Autophagy (“self-eating”) is a critical response of eukaryotic cells to stress. During this process, portions of the cytosol, including cytoplasmic organelles
作者: mettlesome    時(shí)間: 2025-3-27 22:29
Regulation of Self-Renewing Divisions in Normal and Leukaemia Stem Cells the biological organization of tumours. These cells, named tumour-initiating cells (TICs), or cancer stem cells (CSCs), share phenotypic and functional characteristics with normal stem cells, most notably their ability to self-renew. Here we discuss regulation of self-renewal in normal haematopoiet
作者: 偽造者    時(shí)間: 2025-3-28 02:10
Maintenance of Telomeres in Cancera cancer cell of origin. Fortunately, this event is made infrequent by the evolution of mechanisms able to preserve genomic stability and to limit the proliferation potential of somatic cells. A crucial role in both of these processes is played by the nucleoproteins that localize to the tips of our
作者: 多樣    時(shí)間: 2025-3-28 06:15

作者: 意外的成功    時(shí)間: 2025-3-28 13:45
Cell Cycle Deregulation in Pre-neoplasia: Case Study of Barrett’s Oesophagusrogression to fully fledged cancer would allow for chemoprevention or therapeutic interventions; however in most cases, IEN remains undetected and the exact mechanisms for progression remain unknown. Barrett’s oesophagus, the premalignant stage of oesophageal adenocarcinoma, is the perfect model to
作者: 盡責(zé)    時(shí)間: 2025-3-28 16:01

作者: tenuous    時(shí)間: 2025-3-28 20:13

作者: Fermentation    時(shí)間: 2025-3-29 02:02

作者: 枯燥    時(shí)間: 2025-3-29 06:16

作者: intertwine    時(shí)間: 2025-3-29 08:18

作者: thalamus    時(shí)間: 2025-3-29 13:27
https://doi.org/10.1007/978-94-017-9984-3y an accumulation of abnormally expressed growth factors and oncogenes. Furthermore, the abnormally high level of duodeno-gastro-oesophageal acid reflux bathing the distal oesophagus contributes further to increasing proliferation. The real challenge for future research will be to identify causal ev
作者: 矛盾    時(shí)間: 2025-3-29 17:04
Occupying Disability: An Introductionkpoint control and repair, suggesting promise for chemotherapy/cdk inhibitor combinations. Further preclinical mechanistic experiments, as well as pharmacodynamic assessments accompanying clinical trials, will be necessary to establish cdk inhibition as an anti-cancer strategy.
作者: Obstreperous    時(shí)間: 2025-3-29 22:37

作者: Limerick    時(shí)間: 2025-3-30 03:17

作者: hurricane    時(shí)間: 2025-3-30 07:03
Interplay Between Cyclin-Dependent Kinases and E2F-Dependent Transcription of E2F-dependent phenotypes was ., a kinase that had not previously been linked to E2F. In this review, we summarize the effects of CDKs on E2F1 activity and describe a model that may explain the role of CDK8–CycC in E2F regulation. Since CDKs can both increase and decrease E2F activity, understand
作者: 松緊帶    時(shí)間: 2025-3-30 10:11
Mitotic Checkpoint and Chromosome Instability in Cancerpromoting complex/cyclosome (APC/C). The CIN phenotype of many cancer cell lines may be attributed to the lack of a robust mitotic checkpoint as these cells fail to arrest in response to microtubule inhibitors such as taxol and nocodazole. Interestingly, mutations in the essential mitotic checkpoint




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