標題: Titlebook: Apoptosis, Senescence and Cancer; David A. Gewirtz,Shawn E. Holt,Steven Grant Book 2007Latest edition Humana Press 2007 Tumor.apoptosis.le [打印本頁] 作者: 精明 時間: 2025-3-21 17:09
書目名稱Apoptosis, Senescence and Cancer影響因子(影響力)
書目名稱Apoptosis, Senescence and Cancer影響因子(影響力)學科排名
書目名稱Apoptosis, Senescence and Cancer網(wǎng)絡公開度
書目名稱Apoptosis, Senescence and Cancer網(wǎng)絡公開度學科排名
書目名稱Apoptosis, Senescence and Cancer被引頻次
書目名稱Apoptosis, Senescence and Cancer被引頻次學科排名
書目名稱Apoptosis, Senescence and Cancer年度引用
書目名稱Apoptosis, Senescence and Cancer年度引用學科排名
書目名稱Apoptosis, Senescence and Cancer讀者反饋
書目名稱Apoptosis, Senescence and Cancer讀者反饋學科排名
作者: Choreography 時間: 2025-3-21 21:18 作者: 陶器 時間: 2025-3-22 03:08 作者: 充氣球 時間: 2025-3-22 07:10 作者: 果仁 時間: 2025-3-22 09:06
The Role of Telomeres in Genomic Instabilitymaintained by the enzyme telomerase. Telomeres are maintained in the germ line but shorten with age in most somatic cells due to the lack of sufficient telomerase. This telomere shortening serves as a signal for replicative cell senescence, which protects against the unlimited cell division required作者: Coterminous 時間: 2025-3-22 15:47 作者: inflate 時間: 2025-3-22 17:22 作者: tenosynovitis 時間: 2025-3-23 00:55
Resistance/Signaling Pathwayseramide, whereas others have been noted to be dependent on mitochondria-derived reactive oxygen/nitrogen species and the activation of growth factor receptor tyrosine kinases. The precise roles of growth factor receptors and signal transduction pathways in cellular responses following exposure to no作者: 民間傳說 時間: 2025-3-23 03:19 作者: 詞匯 時間: 2025-3-23 07:27 作者: 拾落穗 時間: 2025-3-23 11:41
Elements of Applied Bifurcation Theorybers that facilitate mitochondrial permeabilization are transcriptional targets of the p53 tumor suppressor gene, providing a partial explanation for the ability of DNA-damaging agents to induce apoptosis. Other proapoptotic Bcl-2 family members are released from cytoskeletal sites upon treatment wi作者: 混亂生活 時間: 2025-3-23 17:03 作者: Self-Help-Group 時間: 2025-3-23 19:24
Elements of Applied Bifurcation Theorydigestion). Here, we will review what is known about the signaling pathways that control attachment-mediated survival in normal cells and the molecular alterations that appear to disrupt these pathways in metastatic cells. We will also review the evidence that alternative cell death mechanism(s) can作者: 無底 時間: 2025-3-23 22:27
https://doi.org/10.1007/978-94-015-0623-6owth arrest as a consequence of telomere shortening or stress is thus the essential feature distinguishing the mortality of normal cells (presumably to provide a barrier against the accumulation of mutations and the formation of cancer) and the immortality of tumor cells.作者: Mammal 時間: 2025-3-24 06:05 作者: 牛馬之尿 時間: 2025-3-24 07:37 作者: Cardiac-Output 時間: 2025-3-24 14:23
Foundations of Computer Sciencegrowth factor β However, these controls are lost in cancers by translocations, amplifications, and alterations in regulatory signaling pathways, resulting in abnormally high levels of MYC oncoproteins. The precise roles that Myc oncoproteins provide to provoke tumorigenesis are not fully resolved bu作者: 狂怒 時間: 2025-3-24 17:49
https://doi.org/10.1007/978-3-030-24198-8eramide, whereas others have been noted to be dependent on mitochondria-derived reactive oxygen/nitrogen species and the activation of growth factor receptor tyrosine kinases. The precise roles of growth factor receptors and signal transduction pathways in cellular responses following exposure to no作者: 值得尊敬 時間: 2025-3-24 22:29
Elements of Applied Bifurcation Theoryivation of caspases, a distinct family of intracellular cysteine proteases. At least two separable processes, one starting with ligation of specific cell surface receptors (so-called death receptors) and the other involving release of cytochrome c from mitochondria, result in transduction of various作者: ESO 時間: 2025-3-24 23:49 作者: 使無效 時間: 2025-3-25 03:56 作者: 好忠告人 時間: 2025-3-25 11:01
Elements of Applied Bifurcation Theoryresses. MC is characterized by changes in nuclear morphology and the eventual appearance of polyploid cell progeny in affected cell populations, is markedly enhanced in cells lacking p53 function, and is the result of overaccumulation of cyclin B1 in cells delayed late in the cell cycle by the induc作者: CHART 時間: 2025-3-25 12:40
Introduction to Dynamical Systems,s macromolecules and organelles. During the last decade, progress made in our understanding of the molecular controls of autophagy has uncovered the importance of tumor suppressor molecules in the stimulation of autophagy. Downexpression of autophagy is an early event during tumorigenesis. However, 作者: CRUDE 時間: 2025-3-25 17:51 作者: 代理人 時間: 2025-3-26 00:02 作者: modest 時間: 2025-3-26 03:40
https://doi.org/10.1007/978-94-015-0623-6hat prevent infinite proliferation: replicative senescence and stress-induced senescence (SIS). In replicative senescence, failure of the DNA polymerase to faithfully duplicate the chromosomal ends leads to progressive telomeric DNA sequence loss with each subsequent cell division and signaling for 作者: 斷斷續(xù)續(xù) 時間: 2025-3-26 06:26
https://doi.org/10.1007/978-94-011-6427-6ure of cells to ionizing radiation or chemical agents can promote genomic instability, although the mechanisms involved are not understood. Knowledge concerning mechanisms of genomic instability has been derived from studies in yeast and human genetic disease, where mutations in a variety of genes i作者: Disk199 時間: 2025-3-26 10:59
Foundations of Computer Scienceolet light and ionizing radiations or as a consequence of DNA replication or physiological DNA rearrangements. Cells respond to DNA damage by the coordinated induction of cell-cycle arrest and DNA repair or trigger apoptosis if the damage is too extensive. The DNA damage response is induced by two p作者: 緊張過度 時間: 2025-3-26 14:13
Foundations of Computer Sciencee altered in most tumor types. c-Myc is the founding member of a family of structurally related basic helix-loop-helix-leucine zipper (bHLH-Zip) proteins that function as sequence-specific transcription factors and are aberrantly expressed in most cancers c-Myc is a key regulator of cell proliferati作者: 世俗 時間: 2025-3-26 19:01
Foundations of Computer Sciencedamage response. The phosphorylation of H2AX on Ser 139, named γH2AX, is an early response to the generation of DNA DSBs and extends along megabase-long domains, both sites of the lesion, supporting amplification of signal transduction pathways. In parallel, 53BP1 accumulates on damaged chromatin to作者: ASSET 時間: 2025-3-26 20:59
Elements of Classical Plasticity Theoryunction of DNA-PK is to promote DNA end synapsis and regulate DNA end processing in the nonhomologous end-joining pathway of double-strand break repair. This regulation is mediated in part by DNA-PK-catalyzed phosphorylation of both itself and the Artemis nuclease, which trims heavily damaged ends t作者: 有花 時間: 2025-3-27 04:44 作者: AWE 時間: 2025-3-27 06:32 作者: 大量殺死 時間: 2025-3-27 12:47 作者: 自然環(huán)境 時間: 2025-3-27 17:31
David A. Gewirtz,Shawn E. Holt,Steven GrantIn-depth discussions of different modes of cell death.Introductory chapters provide detailed overviews of topics作者: certitude 時間: 2025-3-27 17:58
Cancer Drug Discovery and Developmenthttp://image.papertrans.cn/a/image/159016.jpg作者: galley 時間: 2025-3-27 22:18 作者: Induction 時間: 2025-3-28 03:00
Numerical Analysis of Bifurcations,iting promise for cancer treatment. This review will discuss the current understanding of the molecular signaling events that originate from extracellular sources to initiate apoptosis, how the pathway is activated by conventional chemotherapeutic agents, and novel opportunities to exploit the extrinsic pathway for cancer treatments.作者: 捏造 時間: 2025-3-28 08:47 作者: debacle 時間: 2025-3-28 11:45 作者: 得體 時間: 2025-3-28 15:17 作者: 凝結劑 時間: 2025-3-28 19:46
Introduction to Dynamical Systems,parently opposite outcomes. Autophagy as a stress response mechanism can protect cancer cells from various insults. But autophagy can eliminate cancer cells by triggering autophagic cell death. These two aspects of autophagy will be discussed in this review.作者: 不真 時間: 2025-3-29 02:39 作者: Infraction 時間: 2025-3-29 05:30 作者: 樂章 時間: 2025-3-29 08:17
DNA-Dependent Protein Kinase in Repair, Apoptosis, Telomere Maintenance, and Chemotherapy molecular phosphorylation targets for this and other DNA-PK-mediated signaling pathways remain to be identified. In principle, DNA-PK inhibitors should enhance radiotherapy and some forms of cancer chemotherapy, but such inhibitors may have significant toxicities due to the telomeric and other functions of DNA-PK.作者: mercenary 時間: 2025-3-29 15:00 作者: Filibuster 時間: 2025-3-29 19:11 作者: GLOOM 時間: 2025-3-29 21:15 作者: Indebted 時間: 2025-3-30 00:52
Structure and Function of the Telomeree attrition, and these mechanisms have been implicated in tumorigenesis in that they allow unchecked cellular proliferation. This chapter summarizes our current understanding of the structure and function of the mammalian telomere, its maintenance, and its role in tumor formation.作者: 施加 時間: 2025-3-30 05:24
Book 2007Latest edition and emerging techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics?which still hold mysteries for researchers. ..The volume is divided into six easy to follow sections. The first is Apoptosis and Alternati作者: 享樂主義者 時間: 2025-3-30 11:26 作者: PAGAN 時間: 2025-3-30 15:07 作者: 自作多情 時間: 2025-3-30 17:02
Evaluating the Importance of Apoptosis and Other Determinants of Cell Death and Survivalsearch into the underlying mechanistic basis and its importance in disease and treatment has progressed tremendously. However, it is important to note that apoptosis is only one form of cell death and that we should not overlook the importance of other death mechanisms. The particular death pathway 作者: COMMA 時間: 2025-3-30 22:57
Mitotic Catastropheresses. MC is characterized by changes in nuclear morphology and the eventual appearance of polyploid cell progeny in affected cell populations, is markedly enhanced in cells lacking p53 function, and is the result of overaccumulation of cyclin B1 in cells delayed late in the cell cycle by the induc
