【专题】细胞周期图片集

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【专题】细胞周期图片集

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:11

一张经典的细胞周期图片，需要打击放大才看得清楚

（缩略图，点击图片链接看原图）

天行键，君子以自强不息地势坤，君子以厚德载物

• 【求助】paper

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:15

细胞周期在G2/M期的调控机理图
The G2/M DNA damage checkpoint prevents the cell from entering mitosis (M-phase) if the genome is damaged. The cdc2-cyclin B kinase is pivotal in regulating this transition. During G2-phase, cdc2 is maintained in an inactive state by the kinases Wee1 and Myt1. As cells approach M phase, the phosphatase cdc25 is activated, perhaps by the polo-kinase Plk1. Cdc25 then activates cdc2, establishing a feedback amplification loop that efficiently drives the cell into mitosis. DNA damage activates the DNA-PK/ATM/ATR kinases, initiating two parallel cascades that inactivate cdc2-cyclin B. The first cascade rapidly inhibits progression into mitosis: the Chk kinases phosphorylate and inactivate cdc25, which can no longer activate cdc2. The second cascade is slower. Phosphorylation of p53 dissociates it from MDM2, activating its DNA binding activity. Acetylation by p300/PCAF further activates its transcriptional activity. The genes that are turned on by p53 constitute effectors of this second cascade. They include 14-3-3, which binds to the phosphorylated cdc2-cyclin B kinase and exports it from the nucleus; GADD45, which apparently binds to and dissociates the Cdc2-cyclin B kinase; and p21Cip1, an inhibitor of a subset of the cyclin-dependent kinases including Cdc2 (CDK1).

天行键，君子以自强不息地势坤，君子以厚德载物

• 【求助】paper

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:16

细胞周期G1/S检查点调控机理图
The G1/S cell cycle checkpoint controls the passage of eukaryotic cells from the first éŸap? phase (G1) into the DNA synthesis phase (S). Two cell cycle kinases, CDK4/6-cyclin D and CDK2-cyclin E, and the transcription complex that includes Rb and E2F are pivotal in controlling this checkpoint. During G1-phase, the Rb-HDAC repressor complex binds to the E2F-DP1 transcription factors, inhibiting the downstream transcription. Phosphorylation of Rb by CDK4/6 and CDK2 dissociates the Rb-repressor complex, permitting transcription of S-phase genes encoding for proteins that amplify the G1- to S-phase switch and that are required for DNA replication. Many different stimuli exert checkpoint control including TGFbeta, DNA damage, contact inhibition, replicative senescence and growth factor withdrawal. The first four act by inducing members of the INK4 or Kip/Cip families of cell cycle kinase inhibitors. TGFbeta additionally inhibits the transcription of Cdc25A, a phosphatase that activates the cell cycle kinases. Growth factor withdrawal activates GSK-3beta, which phosphorylates cyclin D, leading to its rapid ubiquitination and proteosomal degradation. Ubiquitination, nuclear export and degradation are mechanisms commonly used to rapidly reduce the concentration of cell cycle control proteins.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【求助】超声测值是大呢还是小呢？

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:17

Ras和Rho在细胞周期的G1/S转换中的作用

天行键，君子以自强不息地势坤，君子以厚德载物

• 【公告】严肃考风考纪维护公平公正

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:19

Cyclin和细胞周期调控图
The cell cycle is regulated by the interplay of many molecules. Key among these are the cyclins which are expressed and then degraded in a concerted fashion to drive the stages of the cell cycle. Cyclins combine with cyclin dependent kinases (cdks) to form activated kinases that phosphorylate targets leading to cell cycle regulation. A breakdown in the regulation of this cycle can lead to out of control growth and contribute to tumor formation. Defects in many of the molecules that regulate the cell cycle have been implicated in cancer. Key among these are p53, the cdk inhibitors (p15, p16, p18, p19, p21, p27), and Rb, all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【试题】护师资格考试试题

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:20

Cyclin E降解通路图
Cyclins are proteins that associate with cyclin-dependent protein kinases to regulate their activity and the progression of the cell cycle through specific checkpoints. Disruption of cyclin action can lead to either cell cycle arrest, or to uncontrolled cell cycle proliferation. The cyclical increase and decrease in cyclin levels is a key to cell cycle regulation. When cyclin E is abundant it interacts with the cell cycle checkpoint kinase cdk2 to activate cdk2 and allow progression of the cell cycle from G1 to S phase. One of the key targets of activated cdk2 complexed with cyclin E is the tumor suppressor Rb. When dephosphorylated in G1, Rb complexes with and blocks transcriptional activation by E2F transcription factors. When Rb is phosphorylated by cdk2/Cyclin E, it dissociates from E2f, allowing E2F to activate the transcription of genes required for S phase. One of the genes activated by E2F is cyclin E itself, leading to a positive feedback cycle as cyclin E accumulates. The decision by the cell to either remain in G1 or progress into S phase is the result in part of the balance between cyclin E production and proteolytic degradation in the proteosome. Cyclin E is targeted for destruction by the proteosome through ubiquitination when associated with a complex of proteins called the SCF or F box complex. Proteins included this complex include an F box protein that targets specific substrates such as Cyclin E for degradation. In the case of cyclin E the F box protein Fbw7, also called hCdc4, associates with phosphorylated free cyclin E to recruit it into the SCF complex for degradation. SCFFbw7 is a ubiquitin ligase recruited into the complex that specifically targets cyclin E. Cul3, skp1, and Rbx1 also are part of the complex that degrades cyclin E. There may be redundancy for some components of the complex since cul1 deletion also disrupts cyclin E degradation, and multiple F box proteins may contribute to cyclin E degradation. The interaction of multiple different factors in cyclin E accumulation integrates different signaling pathways with cell cycle regulation and may play a role in the unregulated cell cycle progression of cancer.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【资源】公卫中级考试

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:20

细胞与细胞粘附信号
http://www.bioon.com生物谷网站

Interactions between cells responsible for cell to cell adhesion also can communicate signals into the cellular interior, often involving interactions with cytoskeletal elements to produce changes in cell motility, migration, proliferation and shape. The cadherins are cell surface adhesion molecules that help form tight junctions between cells such as formation of epithelial cell layers. E-cadherin inactivation has been implicated in cancer development. In addition to mediating adhesion with other cells, cadherins transduce signals into cells through interactions with the catenins. Catenins probably affect actin cytoskeletal function through interactions with proteins like actinin and vinculin. Catenins also probably trigger changes in cell shape and motility with signals through the Rho small GTPases. Another important cell adhesion molecule is CD-31, or PECAM-1, involved in the formation of junctions between endothelial cells, cell migration, migration of lymphocytes, and regulation of lymphocyte activation. Src phosphorylates PECAM-1 on tyrosine residues causing SHP-2 association with PECAM-1. Paxillin acts as an adaptor protein between proteins involved in adhesion signaling like FAK and src and cytoskeletal elements. In addition to signals created by adhesion molecules to alter cellular responses, other signaling pathways can alter adhesion through components of the focal adhesion complex.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【活动】医考心路

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:21

细胞周期G2/M调控点信号调节
The G2/M DNA damage checkpoint prevents the cell from entering mitosis (M phase) if the genome is damaged. The Cdc2-cyclin B kinase is pivotal in regulating this transition. During G2 phase, Cdc2 is maintained in an inactive state by the kinases Wee1 and Mt1. As cells approach M phase, the phosphatase Cdc25 is activated, perhaps by the polo-kinase Pik1. Cdc25 then activates Cdc2, establishing a feedback amplification loop that efficiently drives the cell into mitosis. DNA damage activates the DNA-PK/ATM/ATR kinases, initiating two parallel cascades that inactivate Cdc2-cyclin B. The first cascade rapidly inhibits progression into mitosis: the CHK kinases phosphorylate and inactivate Cdc25, which can no longer activate Cdc2. The second cascade is slower. Phosphorylation of p53 dissociates it from MDM2, activating its DNA binding activity. Acetylation by p300/PCAF further activates its transcriptional activity. The genes that are turned on by p53 constitute effectors of this second cascade. They include 14-3-3s, which binds to the phosphorylated Cdc2-cyclin B kinase and exports it from the nucleus; GADD45, which apparently binds to and dissociates the Cdc2-cyclin B kinase; and p21Cip1, an inhibitor of a subset of the cyclin-dependent kinases including Cdc2 (CDK1).

天行键，君子以自强不息地势坤，君子以厚德载物

• 【求助】paper

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:25

细胞周期 G1/S调控点信号图
The G1/S cell cycle checkpoint controls the passage of eukaryotic cells from the first 'gap' phase (G1) into the DNA synthesis phase (S). Two cell cycle kinases, CDK4/6-cyclin D and CDK2-cyclin E, and the transcription complex that includes Rb and E2F are pivotal in controlling this checkpoint. During G1 phase, the Rb-HDAC repressor complex binds to the E2F-DP1 transcription factors, inhibiting the downstream transcription. Phosphorylation of Rb by CDK4/6 and CDK2 dissociates the Rb-repressor complex, permitting transcription of S-phase genes encoding for proteins that amplify the G1 to S phase switch and that are required for DNA replication. Many different stimuli exert checkpoint control including TGFb, DNA damage, contact inhibition, replicative senescence, and growth factor withdrawal. The first four act by inducing members of the INK4 or Kip/Cip families of cell cycle kinase inhibitors. TGFb additionally inhibits the transcription of Cdc25A, a phosphatase that activates the cell cycle kinases. Growth factor withdrawal activates GSK3b, which phosphorylates cyclin D, leading to its rapid ubiquitination and proteosomal degradation. Ubiquitination, nuclear export, and degradation are mechanisms commonly used to rapidly reduce the concentration of cell-cycle control proteins.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【转载】医生的职称是怎么制定的？

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:25

CDK调节DNA复制

Initiation of DNA replication in eukaryotes is a highly conserved, multi-step process (replication licensing) designed to restrict initiation events to once per replication origin per S phase. Its control has been uncovered by the discovery of the cyclin dependent kinases (CDKs) as master regulators of the cell cycle and the initiator proteins of DNA replication, such as the Origin Recognition Complex (ORC), Cdc6/18, Cdt1 and the mini-chromosome maintenance complex (Mcm). The proteins and the sequence of events involved in this process are conserved throughout the eukaryotic kingdom. First, the ORC comprised of six proteins binds to replication origins in the chromosomal DNA. At the end of mitosis, ORC, Cdc6/18 and Cdt1 assist the binding of Mcm proteins 2? to chromatin, and chromatin becomes licensed for replication. The activated Mcm complex functions as a replicating helicase and moves along with the replication fork to bring the origins to the unlicensed state. The cycling of CDK activity in the cell cycle regulates the two states of replication origins, the licensed state in G1-phase and the unlicensed state for the rest of the cell cycle. The restriction on licensing is relieved when CDK falls off at the completion of mitosis to allow a new round of replication.

天行键，君子以自强不息地势坤，君子以厚德载物

• 【活动】医考心路

番茄老人

医博园版主

发贴: 1919
积分: 311

得票: 42

状态: 隐身

2008-03-25 23:26

Gleevec诱导细胞增殖

The drug Gleevec (also known as imatinib mesylate or STI-571) was approved by the FDA in 2001 for the treatment of CML, chronic myeloid leukemia. While traditional cytotoxic cancer treatments such as chemotherapy or radiation therapy kill all dividing cells, Gleevec acts on a molecular target by a mechanism that is more specific to cancer cells. Traditional cytotoxic cancer agents have serious side effects such as nausea, weight loss, hair loss and severe fatigue that result from their lack of specificity in killing cells. Gleevec was designed as an inhibitor of a specific receptor associated with CML, and so produces less severe side effects than other cancer agents. CML is associated in most cases with a specific chromosomal defect, a translocation between chromosomes 9 and 22 that creates the Philadelphia chromosome. This translocation occurs at the site in the genome of a protein tyrosine kinase called abl, creating the abnormal bcr-abl protein, a fusion of the abl gene with another gene called bcr. The kinase activity of abl in the bcr-abl fusion is activated and unregulated, driving the uncontrolled cell growth observed in CML. White blood cells containing the bcr-abl mutation become able to proliferate in the absence of growth factors they normally require. Gleevec inhibits abl kinase activity, helping to reverse uncontrolled cell growth. Gleevec also inhibits the PDGF tyrosine kinase and the c-kit tyrosine kinase.
There are a variety of cellular substrates of the bcr-abl kinase that may be involved in cellular transformation. Bcr-abl is associated with the cytoplasm as part of a large signaling complex. Some of the downstream factors in bcr-abl signaling include PI3 kinase/AKT and STAT transcription factors. The activation of bcr-abl also represses apoptosis through induction of anti-apoptosis factors such as Bad, allowing transformed cells to divide. JAK2 kinase activity appears to be one target of bcr-abl. Grb-2 phosphorylation by bcr-abl may play a role in down-regulation of tyrosine kinase signaling. STAT5 may be involved in the failure of apoptosis in bcr-abl cells.
In addition to supporting the idea that cancer therapies targeting specific molecular targets should be efficacious with fewer side effects, Gleevec has also demonstrated that drugs inhibiting protein kinases can be developed successfully. Tyrosine kinases are important in a range of cellular processes, including other cancers, and will provide additional drug targets. Gleevec itself has already demonstrated potential in other cancers such as gastrointestinal stromal tumor that do not respond to existing treatments.
Although Gleevec has produced very strong clinical responses in patients with early stage CML, patients with late stage disease have had an initial response followed by a relapse of drug resistant CML cells. Cancer cells in patients with Gleevec resistant cancer either had amplification of the bcr-abl gene, or mutation of a key amino acid involved in binding drug from threonine to isoleucine.

（来自生物谷）