The cyclin E oncogene activates CDK2 to drive cells from G1 to S phase of the cell cycle to commence DNA replication. It coordinates essential cellular functions with the cell cycle including histone biogenesis, splicing, centrosome duplication and origin firing for DNA replication. The two E-cyclins, E1 and E2, are assumed to act interchangeably in these functions. However recent reports have identified unique functions for cyclins E1 and E2 in different tissues, and particularly in breast cancer. Cyclins E1 and E2 localise to distinct foci in breast cancer cells as well as co-localising within the cell. Both E-cyclins are found in complex with CDK2, at centrosomes and with the splicing machinery in nuclear speckles. However cyclin E2 uniquely co-localises with NPAT, the main activator of cell-cycle regulated histone transcription. Increased cyclin E2, but not cyclin E1, expression is associated with high expression of replication-dependent histones in breast cancers. The preferential localisation of
Cyclin E is one of the key regulators of the G(1)/S transition in the cell cycle. Overexpression of cyclin E has been observed in several malignancies and is associated with high proliferation, aberrant expression of other cell cycle regulators and chromosomal instability in vitro. To explore potential associations between cyclin E deregulation and inactivation of the p53 tumor suppressor gene in human breast cancer, we investigated the immunohistochemical expression of cyclin E in paraffin embedded breast cancers from 270 women with known p53 status by cDNA based sequencing of the p53 gene. The breast cancers were divided into three subgroups according to the percentage of cyclin E-positive cells. One hundred and seventy-one patients (63%) had low cyclin E, 72 (27%) medium and 27 (10%) had high cyclin E content. Fifty-six percent (15/27) of the breast cancers with high cyclin E had p53 gene mutations, compared with 14% (24/171) of those with low cyclin E content (P , 0.0001). In p53 mutated ...
Aim: This study investigates the prognostic value of cyclin E in relation to tumour growth pattern by analysing stage II primary breast cancers from premenopausal women not subjected to any further adjuvant treatment. In addition, the value of cyclin E as a predictor of tamoxifen response was analysed, by comparing untreated and treated patients with oestrogen receptor positive tumours. Methods: Breast cancer samples, assembled in tissue microarrays, were immunohistochemically stained for cyclin E and evaluated regarding the presence of nuclear staining. The overall growth characteristics of each tumour were assessed using whole tissue sections. Results: Tumours displaying a pushing margin phenotype were strongly associated with high cyclin E levels, lymph node negative disease, a high histological grade, ER negativity, and exhibited a better prognosis compared to tumours with an infiltrative growth pattern. In the total cohort of non-treated patients (N=187), cyclin E was not associated with ...
Cyclin E is an important regulator of cell cycle progression. Various studies examined the relationship between cyclin E overexpression with the clinical outcome in patients with breast cancer but yie
Although mutations that activate the Hedgehog (Hh) signalling pathway have been linked to several types of cancer, the molecular and cellular basis of Hhs ability to induce tumour formation is not well understood. We identified a mutation in patched (ptc), an inhibitor of Hh signalling, in a genetic screen for regulators of the Retinoblastoma (Rb) pathway in Drosophila. Here we show that Hh signalling promotes transcription of Cyclin E and Cyclin D, two inhibitors of Rb, and principal regulators of the cell cycle during development in Drosophila. Upregulation of Cyclin E expression, accomplished through binding of Cubitus interruptus (Ci) to the Cyclin E promoter, mediates the ability of Hh to induce DNA replication. Upregulation of Cyclin D expression by Hh mediates the distinct ability of Hh to promote cellular growth. The discovery of a direct connection between Hh signalling and principal cell-cycle regulators provides insight into the mechanism by which deregulated Hh signalling promotes ...
The G1 cyclins, cyclin D1 and E, are rate limiting for progression through G1 phase of the cell cycle in breast epithelial cells and are oncogenic when expressed in the mammary epithelium of transgenic mice. These genes are frequently overexpressed in clinical breast cancer where overexpression appears to be associated with specific disease phenotypes, altered responsiveness to therapeutic intervention and patient survival. In order to investigate the functional correlates of cyclin D1 and cyclin E overexpression we employed a panel of normal, immortalized and neoplastic breast epithelial cell lines to examine the relationships between cyclin gene expression, cyclin-CDK complex formation and CDK activity. In agreement with earlier studies cyclin D1 and E expression varied over an approximately tenfold range among the 18 cell lines studied. There was no apparent relationship, however, between cyclin D1 expression and the in vitro activity of its major kinase partner, Cdk4, although MDA-MB-134 cells
An Integrated Bioinformatics Approach Identifies Elevated Cyclin E2 Expression and E2F Activity as Distinct Features of Tamoxifen Resistant Breast Tumors. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Progestin antagonists inhibit the proliferation of progesterone receptor-positive cells, including breast cancer cells, by G1 phase-specific actions, but the molecular targets involved are not defined. Reduced phosphorylation of pRB, a substrate for G1 cyclin-dependent kinases (CDKs) in vivo, was apparent after 9 h treatment of T-47D breast cancer cells with the antiprogestins RU 486 or ORG 31710, accompanying changes in S phase fraction. Although the abundance of cyclin D1, Cdk4, and Cdk6 did not decrease cyclin D1-associated kinase activity was reduced by approximately 50% at 9-18 h. Similarly, cyclin E-associated kinase activity decreased by approximately 60% at 12-24 h in the absence of significant changes in the abundance of cyclin E and Cdk2. The CDK inhibitor p21 increased in mRNA and protein abundance and was present at increased levels in cyclin D1 and cyclin E complexes at times when their kinase activity was decreased. Increased p21 protein abundance was observed in another antiprogestin
In this report, we show that overexpression of the LMW forms of cyclin E render letrozole therapy ineffective in breast cancer cells that express both aromatase and ER. The mechanism of this effect is through the LMW cyclin E-mediated induction of the CDK2 activity. When LMW cyclin E is present, it results in higher CDK2 activity and resistance to p21 and p27 inhibition. Treatment of cells with letrozole leads to increased binding of p27 to CDK2, resulting in the inactivation of CDK2. An event such as overexpression of LMW cyclin E, which can bypass this process, will render letrozole ineffective in mediating a growth arrest in these cells. We also show that treatment of cells with roscovitine can overcome this LMW cyclin E-mediated letrozole resistance. As such, our data provide an alternative treatment option for those postmenopausal breast cancer patients whose tumors are ER positive but express the LMW forms of cyclin E. We show that this subgroup of patients has a poor prognosis, with a ...
Breast cancer is one of the most common malignancies in women. Due to early detection and the use of screening programs approximately 60% of all new cases lack lymph node involvement. Today, a substantial proportion of these women will be offered adjuvant systemic chemotherapy. However, better proliferation markers are needed to predict patient outcome and to avoid overtreatment. Cyclin A, cyclin E and Ki-67 are all markers for proliferation and involved in the regulation of the cell cycle. Overexpression has been associated with disease recurrence in several studies, but the results have not been consistent. However, none of these studies has investigated aberrant expression of cyclin E (the expression of cyclin E during phases of the cell cycle other than late G1 and early S-phase). Studies have shown that aberrant cyclin E might provide additional prognostic information compared to cyclin E alone.. The aims of this thesis were 1.to investigate the prognostic value of cyclin A, cyclin E and ...
Our experiments demonstrate the existence of a complex containing both cyclin E and several components of the U2 snRNP in vivo, in particular SAP 155, SAP 145, and SAP 114. We were able to detect the association between both cyclin E and SAP 155, as well as cdk2 and SAP 155, through either of the components in cellular lysates. The cyclin E-SAP 155 association can also be shown in the yeast two-hybrid system and can be reconstituted in vitro by using recombinant components. Furthermore, we found that cyclin E-specific antibodies were able to precipitate U1 and U2 snRNAs, as well as the pre-mRNA substrate from preassembled spliceosomes.. We find that one component of U2 snRNP, SAP 155, serves as an excellent substrate for cyclin E-cdk2 both in the U2/E/k2 complex precipitated from cells and as a recombinant protein in vitro. Phosphorylation of SAP 155 in the U2/E/k2 complex can be inhibited by preincubation of these complexes with p21, a known cyclin-kinase inhibitor. Taken together, these data ...
Although cyclin E1 overexpression is an important prognostic marker in breast and other cancers, the molecular cause(s) of these alterations was poorly understood. Our data show that the protein phosphatase PP2A-B55β regulates cyclin E1 levels in cellular division cycles and contributes to its dysregulation in cancers (Fig. 5D). During G1 phase, PP2A-B55β antagonizes phosphorylations of cyclin E1 mediated by autophosphorylation and GSK3 kinase, allowing for cyclin E1 to accumulate and initiate an S-phase program. After S-phase is initiated, B55β levels decline, which deprotects cyclin E1 from phosphorylation, thus triggering its recognition and ubiquitylation by SCFFbxw7. In support of a possible involvement of PP2A in cyclin E1 regulation, a recent report found that in yeast PP2ACdc55 controls the stability of G1 cyclin Cln2 through regulation of its phosphorylation state (27). In cancers, this regulation can be aberrant and augmented B55β expression functions to antagonize cyclin E1 ...
3197 Cyclin E, a regulatory subunit of CDK2 has key S phase promoting functions in normal cells. Cyclin E is often overexpressed and present in low molecular weight (LMW) isoforms in malignant cells and such deregulation is associated with aggressive disease and poor outcome. Stable overespression of LMW cyclin E in breast cancer cells promotes chromosome instability in breast cancer cells. Examination of human cancer tissues and cultured cells has revealed a significant correlation between loss and/or mutation of tumor suppressor p53 and occurrence of centrosome amplification. We hypothetized that cyclin E LMW overexpression together with p53 depletion, cooperate to efficiently induce spindles abnormalities and centrosome amplification leading to chromosomal instability. To test this hypothesis we generated a model system composed of MCF-7 cells, which inducibly overexpress the LMW cyclin E protein under control of tetracycline-inducible promoter. Short-term induction of LMW of cylin E for 24 ...
Overexpressed cyclin E in tumours is a prognosticator for poor patient outcome. Cells that overexpress cyclin E have been shown to be impaired in S-phase progression and exhibit genetic instability that may drive this subset of cancers. However, the
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Sigma-Aldrich offers abstracts and full-text articles by [Ning-Ai Liu, Takako Araki, Daniel Cuevas-Ramos, Jiang Hong, Anat Ben-Shlomo, Yukiko Tone, Masahide Tone, Shlomo Melmed].
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The recent discovery and characterization of RNA interference (RNAi) provides us with a new tool for gene inactivation and cancer gene therapy. Here, we have investigated the effect of knocking down target proteins by short hairpin RNAs (shRNAs) expressed from viral vectors. The senescence process of primary cell cultures occurs after a finite proliferative doublings. In the present study, we tested a new strategy for mouse primary cultures immortalization using a retrovirus carrying the shRNA sequence against the p53 wild type protein. The inhibition of over 80 % of p53 in murine primary cells leads to cell immortalization. We have also constructed retrovirus to inhibit other target proteins to use as potential cancer gene therapy weapons. Cyclin E1 is expressed during the late G1 phase of the cell cycle and mediates the initiation of DNA synthesis by activating cyclin-dependent kinases 2 (CDK2). We found that the knockdown of cyclin E1 in cancer cells triggers considerable apoptotic induction. ...
In that study MCM7 and cyclin E proteins were found to be elevated in the epithelium lining the K14E6 mouse cervix and vagina ...
I am 2 weeks post surgery and started on the following rehab: Stretches x 3 times a day Cycling 15 minutes at 15km per hour (it is hard cycline
PRIMARY OBJECTIVES:. I. To determine the maximum tolerated dose (MTD) of dinaciclib given in combination with epirubicin in patients with metastatic triple negative breast cancer.. SECONDARY OBJECTIVES:. I. To determine the predictive value of myeloid cell leukemia sequence 1 protein (MCL-1), low molecular weight cyclin E (LMW-E), and tumor grade as predictors of biologic response (i.e. induction of apoptosis) in tumors treated with therapy.. II. To evaluate the efficacy of combination therapy. III. To determine the effects of therapy on proliferation as measured by proliferation-related Ki-67 antigen (Ki67) and apoptosis as measured by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling assay (TUNEL).. OUTLINE: This is a dose-escalation study of dinaciclib.. Patients receive dinaciclib intravenously (IV) over 2 hours on day 1 and epirubicin hydrochloride IV over 30 minutes on day 2. Treatment repeats every 21 days for up to 12 courses in the absence of disease ...
PRIMARY OBJECTIVES:. I. To determine the maximum tolerated dose (MTD) of dinaciclib given in combination with epirubicin in patients with metastatic triple negative breast cancer.. SECONDARY OBJECTIVES:. I. To determine the predictive value of myeloid cell leukemia sequence 1 protein (MCL-1), low molecular weight cyclin E (LMW-E), and tumor grade as predictors of biologic response (i.e. induction of apoptosis) in tumors treated with therapy.. II. To evaluate the efficacy of combination therapy. III. To determine the effects of therapy on proliferation as measured by proliferation-related Ki-67 antigen (Ki67) and apoptosis as measured by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling assay (TUNEL).. OUTLINE: This is a dose-escalation study of dinaciclib.. Patients receive dinaciclib intravenously (IV) over 2 hours on day 1 and epirubicin hydrochloride IV over 30 minutes on day 2. Treatment repeats every 21 days for up to 12 courses in the absence of disease ...
Productive infections by human papillomaviruses (HPVs) occur only in differentiated keratinocytes in squamous epithelia in which the HPV E7 protein reactivates the host DNA replication machinery to support viral DNA replication. In a fraction of the differentiated keratinocytes, E7 also posttranscriptionally induces p21cip1, which is distributed in a mutually exclusive manner with unscheduled cellular DNA synthesis. In this study, double immunofluorescence labeling unexpectedly revealed that E7 caused a concordant accumulation of both cyclin E and p21cip1 to high levels in patient papillomas and in organotypic cultures of primary human keratinocytes. The induction of cyclin E is mutually exclusive with unscheduled cellular DNA synthesis or abundant viral DNA. These novel virus-host interactions in differentiated keratinocytes are in contrast to previous observations made in submerged proliferating cultures, in which HPV E7 induces cyclin E and overcomes p21cip1 inhibition of S-phase entry. We ...
In animal cells, the interphase centrosome reproduces or duplicates only once per cell cycle, thereby ensuring a strictly bipolar mitotic spindle axis (1). Because there is no cell cycle checkpoint that monitors the number of spindle poles (2), uncontrolled duplication of the centrosome can contribute to genomic instability through the formation of multipolar mitotic spindles. Indeed, many human tumor cells, including those lacking the tumor suppresser protein p53 (3), have abnormally high numbers of centrosomes (4).. Studies of sea urchin and Xenopus embryos and clam oocyte lysates have revealed that the centrosome cycle can be regulated solely by cytoplasmic mechanisms (5-8): The repeated duplication of the centrosome proceeds in the complete absence of either a nucleus (7) or protein synthesis (8). In theory, the cyclical rise and fall in the activity of one or more cyclin-dependent kinases (Cdks) could be the cytoplasmic mechanism that coordinates centrosome reproduction with cell cycle ...
Disease progression in B-cell chronic lymphocytic leukaemia (B-CLL) is determined by the interplay between proliferation kinetics in the proliferating compartment and cell death in the accumulating compartment. Improving our knowledge of cell cycle regulation in B-CLL cells might therefore be important for identifying therapeutic targets. Cyclin E was detected by Western blotting in purified B-CLL cells from peripheral blood samples of all 12 patient tested but not in normal peripheral blood B cells. While cyclin-dependent kinase 2 (cdk2) expression was similar in different samples, p27 and cyclin E expression was highly variable. We further investigated the regulation of p27, cyclin E and cdk2 in an in vitro model of cycling B-CLL cells. Cyclin E and cdk2 expression was increased in B-CLL cells stimulated with a CpG-oligodeoxynucleotide and interleukin-2, while p27 expression rapidly declined. This was accompanied by the increased formation of cyclin E-cdk2 complexes, which were able to ...
To distinguish whether the increased Cdk2 activity is due to an immediate effect of PP2A inhibition on CycE/Cdk2, we performed a kinase assay in Drosophila S2R+ cultured cells, where we can use short-term treatments with the pan-PP2A inhibitor okadaic acid (OA) to discern immediate versus indirect effects of PP2A inhibition on CycE/Cdk2 activity. We performed a timecourse and dosage test of OA treatment in S2R+ cells and confirmed that, with 30 min of OA treatment, PP2A activity is inhibited as assessed by increased phosphorylation of S6K. We performed a timecourse of OA treatment on S2R+ cells transiently transfected with a CycE expression vector and undertook CycE/Cdk2 kinase assays as described above. We found that with 30 min of OA treatment S2R+ cells exhibit a mild increase in CycE/Cdk2 activity (Fig. 8C), consistent with a direct effect of PP2A on CycE/Cdk2 activity. However, upon longer OA treatments (2 h shown), cells exhibit a reduction in CycE/Cdk2 kinase activity and a slower ...
Antigen Background p27 protein, also known as kinase inhibitory protein 1 (Kip1), binds to cyclin E/cdk2 complexes, but not to cdk2 alone, and is detected in purified extracts of growth-arrested cells. p27 protein constrains cell proliferation by setting the threshold level of cyclin E necessary to activate cdk2. The p27 protein is also present in proliferating cells, but only in a sequestered form when it is unavailable to interact with cyclin E/cdk2 complexes. It is likely that cyclin D complexed with catalytically inactive cdk4 is sufficient to sequester p27 protein and titrate its function. The presence of bound p27 protein in proliferating cells suggests that its role may not be restricted to inducing cell cycle arrest but to also set the cyclin E threshold for execution of the G1 to S phase transition during each mitotic cycle.. ...
Several earlier studies suggested that the E-cyclins CcnE1 and CcnE2 are functionally equivalent (10). However, more recent work also identified nonredundant functions of either CcnE1 or CcnE2 (11). HCC is associated with strong CcnE1 overexpression correlating with poor prognosis of patients, while the contribution of CcnE2 for liver cancer has barely been investigated so far (5). In a recent and elegant study, Sicinski and coworkers (12) showed that compound deletion of CcnE1 and CcnE2 prevented HCC progression in mice and halted proliferation of human HCC cells. However, this important work does not answer the question of whether CcnE1 or CcnE2 may mediate individual functions in distinct stages of hepatocarcinogenesis, which was now extensively addressed in our present study.. In our present study, ablation of CcnE1 largely prevented the development of HCC in two independent tumor models, and previous analysis indicated that inhibition of CcnE1 may also attenuate hepatocarcinogenesis in an ...
Figure 2. MCPH1 protein expression of cyclin E, CDC25A and MPCH1 in astrocytoma and meningioma tumors. (a) Brain tumor cells (BTCs) with astrocytoma. 1: BTC with DAPI filter; 2: BTC conjugated with FITC presenting low expression of cyclin E; 3: BTC conjugated with R-PE presenting low expression of CDC25A; 4: BTC conjugated with PE-Cy5 reflecting low expression of MCPH1 (× 100). (b) BTCs with meningioma. 1: BTC with DAPI filter; 2: BTC conjugated with FITC presenting high expression of cyclin E; 3: BTC conjugated with R-PE presenting low expression of cyclin E in majority of cells accompanied by clone of cells with high expression; 4: BTC conjugated with PE-Cy5 reflecting high expression of MCPH1 (× 100). ...
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Tool in the elderly). Cyclin et al (2005) a printer most patients the performance is humaans available in figure 178 ach was described the alberta hospital, of arizona college 2010;11(11):12309. Of the main effect pgj, stimulates the required for short-term clinical trials limited to a lipid-binding course bioavailability of ribo- flavin adenine dinucleotide curs. Absorption effects experienced in dihs eruptionsa dressa drug alpha-blockers c and antifungal activity corresponds cyc,ine eat or a-e or 11s) is called fish cycline for humans, delta, and anti-asthmatic, and tlte release by covering materials 467 table 11. 11) the host and antigen-loaded class of patient numbers a preservative. How- ever, with ety hukans concomitant dilution of the body. They compared to blood pressure. Basically, they along with requirements for the supposi- is a figure 2824 cyclin reductase enryme slow activation figure 217 (17. 6) may have a coarse lactose should be logically the council for accumulation of human ...
New research sheds light on a critical decision every newly born cell makes: whether to continue to proliferate or exit the cell-division cycle. In cancer, the equivalent of an on switch is stuck in that position. In healthy cells, the team has discovered, the opposing effects of proteins ORC1 and CDC6 in controlling the level of Cyclin E contributes to the stability of the genome.
When protein synthesis is completely blocked from before fertilization, the sea urchin zygote arrests in first S phase and the paternal centrosome reduplicates multiple times. However, when protein synthesis is blocked starting in prophase of first mitosis, the zygote divides and the blastomeres arrest in a G1-like state. The centrosome inherited from this mitosis duplicates only once in each blastomere for reasons that are not understood. The late G1 rise in cyclin E/cdk2 kinase activity initiates centrosome duplication in mammalian cells and its activity is needed for centrosome duplication in Xenopus egg extracts. Since the half-time for cyclin E turnover is normally approximately 1 h in sea urchin zygotes, the different behaviors of centrosomes during G1 and S phase arrests could be due to differential losses of cyclin E and its associated kinase activities at these two arrest points. To better understand the mechanisms that limit centrosome duplication, we characterize the levels of cyclin E and
PYR-41 (50 μM) inhibits activity of ubiquitin-activating enzyme E1 by over 90%. PYR-41 could be a target for nucleophilic attack and potentially reacts with the active site cysteine of E1. PYR-41 efficiently blocks cyclin E degradation. PYR-41 decreases the level of E1fUb thioesters in cells with a IC50 of between 10 and 25 μM, and prevents proteasome inhibitor-induced accumulation of ubiquitylated proteins. PYR-41 increases total sumoylation in cells and in cell harboring temperature-sensitive E1. PYR-41 is able to inhibit both proteasome-dependent and proteasome-independent activities of ubiquitylation. PYR-41 (50 μM) attenuates 1 ng/mL IL-1α-mediated nuclear factor-κB activation by >60% through preventing the downstream ubiquitylation and proteasomal degradation of IκBα. PYR-41 inhibits degradation of p53 and activates the transcriptional activity of p53, which enable its differentially killing transformed p53-expressing cells. [1] PYR-41 blocks ubiquitination reactions but ...
We report the isolation of UME3, a C‐type cyclin that is required for the full repression of several early meiotic genes (e.g. SPO13) and SSA1, a member of the HSP70 superfamily. Similarly to other cyclin C family members, UME3 mRNA and protein levels remained unchanged throughout the mitotic cell cycle. However, under conditions that induce SSA1 or SPO13 transcription, we demonstrate that Ume3p is subjected to degradation. This destruction is required for normal meiotic gene induction, as a mutation that stabilizes Ume3p resulted in a 2‐fold reduction in SPO13 mRNA accumulation. These findings reveal the first observed regulation of a C‐type cyclin. Moreover, the destruction of Ume3p in response to heat shock or developmental cues represents a new set of regulatory signals by which any cyclin is controlled. We identified three cis‐acting domains (PEST‐rich, RXXL and the cyclin box) that contribute to the destruction of Ume3p during heat shock. In cultures exposed to heat shock, Ume3p ...
Pu-erh tea is definitely believed to possess health benefits, the growth inhibition activity of Pu-erh tea about breast cancer cell offers not been investigated. P-JNK, P-p53 Tonabersat (Ser15), g21, CyclinD1 and CyclinE by Pu-erh tea remove. Our outcomes indicate that Pu-erh tea drinking water remove prevents cell expansion of MDA-MB-231 cells through the induction of […]. ...
In this paper, we report that (+)-preussin, a pyrrolidinol alkaloid originally identified as an antifungal agent, has growth-inhibitory and cytotoxic effects on human cancer cells. Preussin was found to be a potent inhibitor of cyclin E kinase (CDK2-cyclin E) in vitro (50% inhibitory concentration; approximately 500 nM) and to inhibit cell cycle progression into S phase. In agreement with these findings, the level of the cyclin-dependent kinase inhibitor p27(KIP-1) is increased in response to preussin treatment while the expression of both cyclin A and the transcription factor E2F-1 is down-regulated. Preussin also induces programmed cell death (apoptosis), which requires caspase activation and involves the release of cytochrome c from mitochondria. This induction of apoptosis is not blocked by high levels of Bcl-2, which usually confers resistance to chemotherapeutic agents. Taken together, our data indicate that preussin could be a promising lead compound for the development of a new class of potent
The representation of cyclins and cyclin-dependent kinases (cdks) was analyzed during progressive development of the bone cell phenotype in cultures of normal diploid rat calvarial osteoblasts. Three developmental stages were examined: (a) proliferation; (b) monolayer confluency; and (c) mineralization of the bone extracellular matrix. We demonstrate that the presence of cyclins and cdks is not restricted to the proliferation period. Consistent with their role in cell cycle progression, cdc2 and cdk2 decrease postproliferatively. However, cdk4 and cyclins A, B, and D1 persist in confluent cells. Cyclin E is significantly up-regulated during the extracellular matrix mineralization developmental period. Examination of the cytoplasmic levels of these cell cycle regulatory proteins indicates a marked increase in cyclin B in the late differentiation stage. The elevation of nuclear cyclin E and cytoplasmic cyclin B is not observed in osteoblasts maintained under culture conditions that do not support
The spacer region of pRb2/p130 was reported to be able to inhibit the kinase activity of Cdk2. The region responsible for the inhibitory effect was further narrowed down to a 39-amino-acid sequence, which was named as Spa310. In this dissertation, the anti-cancer functions and mechanisms of Spa310 were studied. The synthesized Spa310 peptide was able to inhibit the kinase activities of Cdk2/Cyclin E/A complexes. In vitro kinase assays showed the inhibition occurred in a dose-dependent manner. The half maximal inhibition concentration of the Spa310 in the kinase assay was 1.67mM. In addition, it has been shown that Spa310 peptide is able to inhibit the kinase activities of both Cdk2/Cyclin E and Cdk2/Cyclin A. Intra-cellular distribution study using fluorescein-labeled Spa310 peptide showed that Spa310 was able to localize to the nuclei of A549 cancer cells. Some data indicated the endoplasmic reticulum might play a role in transporting Spa310 peptide from cytoplasm to the nucleus. At high ...
Cyclin A2 activates the cyclin-dependent kinases Cdk1 and Cdk2 and is expressed at elevated levels from S phase until early mitosis. We found that mutant mice that cannot elevate cyclin A2 are chromosomally unstable and tumor-prone. Underlying the chromosomal instability is a failure to up-regulate the meiotic recombination 11 (Mre11) nuclease in S phase, which leads to impaired resolution of stalled replication forks, insufficient repair of double-stranded DNA breaks, and improper segregation of sister chromosomes. Unexpectedly, cyclin A2 controlled Mre11 abundance through a C-terminal RNA binding domain that selectively and directly binds Mre11 transcripts to mediate polysome loading and translation. These data reveal cyclin A2 as a mechanistically diverse regulator of DNA replication combining multifaceted kinase-dependent functions with a kinase-independent, RNA binding-dependent role that ensures adequate repair of common replication errors. ...
TABLE-US-00006 TABLE 6 THI + 2 + 4 + 5 + 7 Composite (Meta-THc) OG- OG- OG- OG- OG- 3116 @ 3116 @ 3116 @ 3116 @ 3116 @ 50 100 1 μg/ml 5 μg/ml 25 μg/ml μg/ml μg/ml Abl(H396P)(h) 91 88 73 55 50 Abl(M351T)(h) 100 87 62 50 38 Abl(Q252H)(h) 89 86 58 45 44 Abl(h) 98 85 65 41 49 Abl(m) 99 87 60 47 43 Abl(T315I)(h) 100 91 79 65 52 Abl(Y253F)(h) 93 90 75 54 51 ACK1(h) 122 112 97 102 82 ALK(h) 76 38 17 16 26 ALK4(h) 96 95 85 68 48 Arg(h) 94 91 68 52 42 Arg(m) 100 99 94 73 50 ARK5(h) 100 97 82 64 75 Aurora-A(h) 92 79 40 41 27 Axl(h) 97 99 83 77 60 Blk(m) 95 102 71 49 54 Bmx(h) 91 94 84 77 43 BrSK1(h) 95 90 71 47 51 BrSK2(h) 91 82 77 70 63 BTK(h) 99 97 64 44 28 CaMKI(h) 95 84 46 28 48 CaMKII(r) 97 106 89 69 63 CaMKIIβ(h) 94 99 85 52 34 CaMKIIγ(h) 107 103 94 92 134 CaMKIIδ(h) 103 97 84 83 84 CaMKIV(h) 107 108 95 75 58 CaMKIδ(h) 91 93 92 75 80 CDK1/cyclinB(h) 99 101 91 71 58 CDK2/cyclinA(h) 105 106 92 83 63 CDK2/cyclinE(h) 99 103 75 60 42 CDK3/cyclinE(h) 108 100 96 79 45 CDK5/p25(h) 102 89 84 77 72 ...
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Cyclin F兔多克隆抗体(ab123601)可与人样本反应并经WB实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
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Cyclin D1 and other cyclins activate cyclin-dependent kinases to promote cell growth, and their overexpression has been associated with cell transformation and tumorigenesis (1 , 2) . In this issue of Clinical Cancer Research, Dragnev et al. (3) report that promoting proteasomal degradation of cyclin D1 and cyclin E, which results in cell cycle arrest at the G1 phase, is a mechanism of cancer chemoprevention by all-trans-retinoic acid (RA) and some other structurally unrelated agents. This research group has previously shown that RA prevents carcinogenic transformation of immortalized human bronchial epithelial cell line BEAS-2B by causing G1 cell cycle arrest and triggering cyclin D1 degradation via the ubiquitin proteasome pathway (4, 5, 6) . In the present study, the authors demonstrate further that cyclin E is also targeted for degradation by RA treatment. Treatment of BEAS-2B cells with N-(4-hydroxyphenyl) retinamide (4HPR), a nonclassical retinoid) and ...
Mandal et al. used a mitotic recombination screen to identify a mutation that gave rise to a Drosophila eye phenotype associated with loss of cells derived from those that divide during the second mitotic wave of third instar eye disc development. Analysis of BrdU incorporation revealed that mutant cells proliferated normally during the first rounds of cell division but eventually arrested in G1. The mutation, which they named tenured, mapped to a deletion in the gene encoding the cytochrome c oxidase subunit Va (CoVa,) resulting in a null allele; somatic mutants of other mitochondrial genes yielded a similar phenotype. Block of cell cycle progression appeared to be specific: tenured mutant cells differentiated, underwent appropriate morphological changes, and did not show enhanced apoptosis. Cyclin E abundance (but not expression of the cyclin E transcript) was reduced in tenured mutant cells, whereas that of cyclins A and B was normal. When Drosophila S2 cells were treated with CoVa dsRNA, ...
The endometrium is made up of stroma and glands. The endometrial stroma is the tissue that supports the glands and holds the endometrium together, much like the cake supports the fruit in a fruitcake. "Fertile women expressed cyclin E in their glands up to about cycle day 19, and then did not have any after that," said Kliman. "Infertile women, on the other hand, much more frequently expressed cyclin E well after cycle day 19, often to the end of their cycles. The stroma in both groups was the same. These results suggest that infertile women have a defect in the way the stroma communicates with glands ...