Cyclin-Dependent Kinase Inhibitor p27: A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.

Cyclin-Dependent Kinase Inhibitor p27: A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.

Essential component of the SCF (SKP1-CUL1-F-box protein) ubiquitin ligase complex, which mediates the ubiquitination of proteins involved in cell cycle progression, signal transduction and transcription. In the SCF complex, serves as an adapter that links the F-box protein to CUL1 (By similarity).

Opens the Highlight Feature Bar and highlights feature annotations from the FEATURES table of the record. The Highlight Feature Bar can be used to navigate to and highlight other features and provides links to display the highlighted region separately. Links in the FEATURES table will also highlight the corresponding region of the sequence. More... ...

MicroRNA-200b and microRNA-200c (miR-200b/c) are 2 of the most frequently upregulated oncomiRs in intestines cancer cells. cell lines. Additionally, we confirmed that dominance of RECK by miR-200b/c therefore brought about SKP2 (S-phase kinase-associated proteins 2) level and g27Kip1 (also known as cyclin-dependent kinase inhibitor 1B) destruction in intestines cancers cells, which promotes cancer cell proliferation […]. Read More ». ...

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Plant S-phase kinase-associated protein 1 (SKP1) genes play crucial roles in plant development and differentiation. However, the role of SKP1 in citrus is unclear. Herein, we described a novel SKP1-like gene, designated as CrWSKP1, from

S-phase kinase-associated protein 2 (424 aa, ~48 kDa) is encoded by the human SKP2 gene. This protein is involved in the regulation of protein-protein interactions that govern the cell cycle.

The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.

cGMP Dependent Kinase Inhibitor Peptide chemical properties, What are the chemical properties of cGMP Dependent Kinase Inhibitor Peptide 82801-73-8, What are the physical properties of cGMP Dependent Kinase Inhibitor Peptide ect.

https://www.databridgemarketresearch.com/toc/?dbmr=global-cell-cycle-inhibitors-market. Competitive Landscape and Global Cell Cycle Inhibitors Market Share Analysis. Cell cycle inhibitors market competitive landscape provides details by competitor. Details included are company overview, company financials, revenue generated, market potential, investment in research and development, new market initiatives, global presence, production sites and facilities, company strengths and weaknesses, product launch, clinical trials pipelines, product approvals, patents, product width and breath, application dominance, technology lifeline curve. The above data points provided are only related to the companies focus related to cell cycle inhibitors market.. Global Cell Cycle Inhibitors Market Country Level Analysis. The countries covered in the cell cycle inhibitors market report are U.S., Canada, Mexico in North America, Brazil, Argentina, Peru, Rest of South America, as part of South America, Germany, ...

Background 14-3-3 is a p53-mediated cell-cycle inhibitor in epithelial cells. those of additional cell-cycle inhibitor genes, CDKN2A and ARF. Results The manifestation levels of 14-3-3 mRNA in almost all cell lines were low and comparable to those in normal hematopoietic cells except for 2 B-cell lines. On the contrary, 14-3-3 mRNA was aberrantly overexpressed regularly in mature lymphoid malignancies (30 of 93, 32.3%) and rarely in acute leukemia (3 of 35, 8.6%). 14-3-3 protein was readily detectable and roughly reflected the mRNA level. In contrast to epithelial tumors, methylation status of the 14-3-3 gene was not associated with manifestation in hematological malignancies. Mutations of p53 were recognized in 12 individuals and associated with lower manifestation of 14-3-3. The manifestation levels of 14-3-3, CDKN2A and ARF were not correlated with but rather reciprocal to one another, suggesting that simultaneous overexpression of any two of them is definitely incompatible with tumor growth. ...

Disruption of the cyclin-dependent kinase-inhibitory domain of p27 enhances growth of mice. Growth is attributed to an increase in cell number, due to increased cell proliferation, most obviously in tissues that ordinarily express p27 at the highest levels. Disruption of p27 function leads to nodula …

Harrison, T.A., Smith Adams, L.B., Moore, P.D., Perna, M.K., Sword, J.D.and Defoe, D. M.. Accelerated turnover of taste bud cells in mice deficient for the cyclin-dependent kinase inhibitor p27Kip1.BMC Neuroscience 2011, 12:34 ...

BCL6 interacts with the transcription factor Miz-1 to suppress the cyclin-dependent kinase inhibitor p21 and cell cycle arrest in germinal center B cells ...

Substituted guanines and pyrimidines were tested as inhibitors of cyclin B1/CDK1 and cyclin A3/CDK2 and soaked into crystals of monomeric CDK2. O6-Cyclohexylmethylguanine (NU2058) was a competitive inhibitor of CDK1 and CDK2 with respect to ATP (Ki values: CDK1, 5 +/- 1 microM; CDK2, 12 +/- 3 microM …

The KOMP Repository Collection is located at the MMRRC at the University of California, Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...

1OIT: Imidazo[1,2-A]Pyridines: A Potent and Selective Class of Cyclin-Dependent Kinase Inhibitors Identified Through Structure-Based Hybridisation

2VTN: Identification of N-(4-Piperidinyl)-4-(2,6-Dichlorobenzoylamino)-1H-Pyrazole-3-Carboxamide (at7519), a Novel Cyclin Dependent Kinase Inhibitor Using Fragment-Based X-Ray Crystallography and Structure Based Drug Design.

The p57(Kip2) cyclin-dependent kinase inhibitor (CDKi) has been implicated in embryogenesis, stem-cell senescence and pathologies, but little is known of its role in cell cycle control. Here, we show that p57(Kip2) is ...

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These effects are mediated by nuclear accumulation of the p27(Kip1) inhibitor induced by the downregulation of the p45(Skp2) and Cks1 proteins, which target p27(Kip1) for degradation ...

The cortactin oncoprotein is frequently overexpressed in head and neck squamous cell carcinoma (HNSCC), often due to amplification of the encoding gene (CTTN). While cortactin overexpression enhances invasive potential, recent research indicates that it also promotes cell proliferation, but how cortactin regulates the cell cycle machinery is unclear. In this article we report that stable short hairpin RNA-mediated cortactin knockdown in the 11q13-amplified cell line FaDu led to increased expression of the Cip/Kip cyclin-dependent kinase inhibitors (CDKIs) p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) and inhibition of S-phase entry. These effects were associated with increased binding of p21(WAF1/Cip1) and p27(Kip1) to cyclin D1- and E1-containing complexes and decreased retinoblastoma protein phosphorylation. Cortactin regulated expression of p21(WAF1/Cip1) and p27(Kip1) at the transcriptional and posttranscriptional levels, respectively. The direct roles of p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) ...

Sustained activation of extracellular signal-regulated kinase (ERK) has been detected previously in numerous tumors in the absence of RAS-activating mutations. However, the molecular mechanisms responsible for ERK-unrestrained activity independent of RAS mutations remain unknown. Here, we evaluated the effects of the functional interactions of ERK proteins with dual-specificity phosphatase 1 (DUSP1), a specific inhibitor of ERK, and S-phase kinase-associated protein 2 (SKP2)/CDC28 protein kinase 1b (CKS1) ubiquitin ligase complex in human hepatocellular carcinoma (HCC). Levels of DUSP1, as assessed by real-time reverse transcription-PCR and Western blot analysis, were significantly higher in tumors with better prognosis (as defined by the length of patients survival) when compared with both normal and nontumorous surrounding livers, whereas DUSP1 protein expression sharply declined in all HCC with poorer prognosis. In the latter HCC subtype, DUSP1 inactivation was due to either ...

Mammalian taste buds contain several specialized cell types that coordinately respond to tastants and communicate with sensory nerves. While it has long been appreciated that these cells undergo continual turnover, little is known concerning how adeq

The cyclin-dependent kinase (CDK) inhibitor p27Kip1 has been shown to regulate cellular proliferation via inhibition of CDK activities. routine and g27Kip1 (hereafter g27) can regulate CDK actions.1-3 The p27 protein was originally known as an inhibitor of CDK activities for things containing CDK2 and shown to inhibit cyclin E and cyclin A activities which regulate G1 and S phase traverse.4-6 In addition to CDK inhibition, g27 provides other multifarious connections with cyclin N/cdk4 processes putatively.7 Since cellular amounts of g27 are elevated in response to high cell thickness, serum deprival, and TGF, it was hypothesized g27 brought cells into quiescence and held them in G0 through the inhibition of CDK actions.8 Numerous reviews have got characterized the control of p27 including the control of its transcription,9,10 translation,11,12 post-translational adjustments.7,13,14 cellular localization15-19 and balance.20-23 The regulations of its stability has a main role in adjusting mobile ...

MicroRNAs (miRNA) have tumor suppressive and oncogenic potential in human cancer, but whether and how miRNAs control cell cycle progression is not understood. To address this question, we carried out a comprehensive analysis of miRNA expression during serum stimulation of quiescent human cells. Time course analyses revealed that four miRNAs are up-regulated and |100 miRNAs are down-regulated, as cells progress beyond the G(1)-S phase transition. We analyzed the function of two up-regulated miRNAs (miR-221 and miR-222) that are both predicted to target the cell growth suppressive cyclin-dependent kinase inhibitors p27 and p57. Our results show that miR-221 and miR-222 both directly target the 3 untranslated regions of p27 and p57 mRNAs to reduce reporter gene expression, as well as diminish p27 and p57 protein levels. Functional studies show that miR-221 and miR-222 prevent quiescence when elevated during growth factor deprivation and induce precocious S-phase entry, thereby triggering cell death. Thus,

Transforming growth factor-β (TGF-β) plays an important role in regulating hematopoiesis, inhibiting proliferation while stimulating differentiation when appropriate. We previously demonstrated that the type III TGF-β receptor (TβRIII, or betaglycan) serves as a novel suppressor of cancer progression in epithelial tumors; however, its role in hematologic malignancies is unknown. Here we demonstrate that TβRIII protein expression is decreased or lost in the majority of human multiple myeloma specimens. Functionally, restoring TβRIII expression in myeloma cells significantly inhibited cell growth, proliferation, and motility, largely independent of its ligand presentation role. In a reciprocal fashion, shRNA-mediated silencing of endogenous TβRIII expression enhanced cell growth, proliferation, and motility. Although apoptosis was not affected, TβRIII inhibited proliferation through induction of the cyclin-dependent kinase inhibitors p21 and p27. TβRIII further regulated myeloma cell ...

Transforming Growth Factor-β (TGF-β) regulates a variety of biological effects, including cellular proliferation, dependent on the cellular context. There is growing evidence that TGF-β regulates numerous pathways independent of Smad, including the PI3K/Akt pathway. Therefore, since FoxO is downstream of PI3K/Akt, we examined the role of TGF-β on the post-translational regulation of FoxO family members. It was found that TGF-β increased the phosphorylation of FoxO1, 3a, and 4, as well as the cytoplasmic localization of FoxO1 in fibroblasts via the PI3K/Akt pathway. In addition, since Akt and FoxO members can induce phosphorylation and transcription of p27ᵏⁱᵖ¹ (a cyclin dependent kinase inhibitor), respectively, we examined both the post-translational and transcriptional regulation of p27ᵏⁱᵖ¹ by TGF-β in fibroblasts. p27ᵏⁱᵖ¹ phosphorylation increased following TGF-β addition, resulting in cytoplasmic localization in fibroblasts over time. p27ᵏⁱᵖ¹ mRNA expression ...

Cyclin-dependent Kinase Inhibitor (CKI); Inhibitor Of Cdc28-Clb Kinase Complexes That Controls G1/S Phase Transition, Preventing Premature S Phase And Ensuring Genomic Integrity; Phosphorylated By Clb5/6-Cdk1 And Cln1/2-Cdk1 Kinase Which Regulate Timing Of Sic1p Degradation; Phosphorylation Targets Sic1p For SCF(CDC4)-dependent Turnover; Functional Homolog Of Mammalian Kip1

CDKN2A / p14ARF antibody (cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)) for ICC/IF, IHC, IHC-Fr, IHC-P, WB. Anti-CDKN2A / p14ARF pAb (GTX23642) is tested in Human samples. 100% Ab-Assurance.

BEZ235 (NVP-BEZ235) is a dual ATP-competitive PI3K and mTOR inhibitor for p110α/γ/δ/β and mTOR(p70S6K) with IC50 of 4 nM /5 nM /7 nM /75 nM /6 nM, respectively. Inhibits ATR with IC50 of 21 nM, whileshown to be a poor inhibitor to Akt and PDK1. Phase 2. ...

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W. Petrich, K.B. Lewandrowski, J.B. Muhlestein, M.E.H. Hammond, J.L. Januzzi, E.L. Lewandrowski, R.R. Pearson, B. Dolenko, J. Fr h, M. Haass, M.M. Hirschl, W. K hler, R. Mischler, J. M cks, J. Ordóñez-Llanos, O. Quarder, R. Somorjai, A. Staib, C. Sylvक़, G. Werner, R. ...

Cutaneous T cell lymphomas (CTCLs) represent a heterogeneous group of non-Hodgkin lymphomas that affect the skin. The pathogenesis of these conditions is poorly understood. For example, the signaling mechanisms contributing to the dysregulated growth of the neoplastic T cells are not well defined. Here, we demonstrate that loss of nuclear localization of pro-IL-16 facilitates CTCL cell proliferation by causing a decrease in expression of the cyclin dependent-kinase inhibitor p27Kip1. The decrease in p27Kip1 expression was directly attributable to an increase in expression of S-phase kinase-associated protein 2 (Skp2). Regulation of Skp2 is in part attributed to the nuclear presence of the scaffold protein pro-IL-16. T cells isolated from 11 patients with advanced CTCL, but not those from healthy controls or patients with T cell acute lymphocytic leukemia (T-ALL), demonstrated reduction in nuclear pro-IL-16 levels. Sequence analysis identified the presence of mutations in the 5ι end of the PDZ1 ...

Although the androgen receptor (AR) has been implicated in the promotion of apoptosis in testicular cells (TSCs), the molecular pathway underlying AR-mediated apoptosis and its sensitivity to environmental hormones in TSCs and induced pluripotent stem cells (iPSCs) remain unclear. We generated the iPSCs from bovine TSCs via the electroporation of OCT4. The established iPSCs were supplemented with leukemia inhibitory factor and bone morphogenetic protein 4 to maintain and stabilize the expression of stemness genes and their pluripotency. Apoptosis signaling was assessed after exposure to mono-(2-ethylhexyl) phthalate (MEHP), the active metabolite of di-(2-ethylhexyl) phthalate. Here, we report that iPSCs were more resistant to MEHP-induced apoptosis than were original TSCs. MEHP also repressed the expression of AR and inactivated WNT signaling, and then led to the commitment of cells to apoptosis via the cyclin dependent kinase inhibitor p21CIP1. The loss of the frizzed receptor 7 and the gain of p21CIP

TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1

The retinoblastoma (RB) and cyclin-dependent kinase inhibitor 2/multiple tumor suppressor gene 1 (CDKN2/MTS1) tumor suppressor genes play important roles in the regulation of the cell cycle. The protein products of these two genes, pRB and p16INK4A (p16), respectively, inhibit progression from G1 to S phase. Moreover, p16 has been shown to exert its function through inhibition of CDK4-mediated phosphorylation of pRB. Both genes have been found to be mutated or deleted in a wide range of primary human tumors and tumor cell lines. However, the presence of CDKN2/MTS1 containing nonneoplastic elements in every tumor specimen may contribute to the apparent lower deletion detection rate in resected neoplasms compared to cell lines. We have developed an immunohistochemical assay that allows us to assess p16 expression in formalin-fixed, paraffin-embedded tissues. As controls, we used paraffin-embedded pellets of cell lines with well-defined p16 status (four positive and four negative lines), as well ...

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Background Over the last decade a number of species, from farm animals to rodents, have been cloned using somatic cell nuclear transfer technology (SCNT). This technique has the potential to revolutionize the way that genetically modified animals are made. In its current state, the process of SCNT is very inefficient (|5% success rate), with several technical and biological hurdles hindering development. Yet, SCNT provides investigators with powerful advantages over other approaches, such as allowing for prescreening for the desired level of transgene expression and eliminating the excess production of undesirable wild-type animals. The rat plays a significant role in biomedical research, but SCNT has been problematic for this species. In this study, we address one aspect of the problem by evaluating methods of activation in artificially constructed rat embryos. Principal Findings We demonstrate that treatment with a calcium ionophore (ionomycin) combined with a variety of cyclin-dependent kinase

We have previously shown that Nodal and ALK7 are expressed in human placenta (Roberts et al., 2003) and that Nodal signalling through ALK7 inhibits trophoblast cell proliferation (Munir et al., 2004), migration and invasion (Nadeem et al., 2011). In this study, we provided evidence that p27 is a key mediator of Nodal signalling in trophoblast cells. We found that Nodal not only upregulated p27 expression, but also induced p27 and CDK2 translocation to the cytoplasm, leading to inhibition of cell proliferation and migration/invasion.. The present study demonstrates that Nodal upregulates p27 mRNA and protein levels through multiple mechanisms. First, we found that in the presence of a transcription inhibitor, Nodal slowed down the decay of p27 mRNA. Second, we observed that Nodal increased p27 levels over a long period of time and this effect was still evident when protein translation was inhibited, suggesting that Nodal increases the p27 protein stability. This notion is further supported by the ...

The myc oncogene is overexpressed in almost half of all breast and ovarian cancers, but attempts at therapeutic interventions against myc have proven to be challenging. Additionally, studies utilizing a xenograft model shown that nanoparticle-mediated delivery of miR-124 could reduce tumor growth and sensitize cells to etoposide, suggesting a medical software of miRNAs as therapeutics to target the practical effect of myc on tumor growth. Intro The manifestation and activity of myc transcription element is definitely regularly deregulated in malignancy and attempts to target it have been demanding.1 Myc has an important regulatory part in multiple pathways, including cell cycle,2, 3 rate of metabolism4, 5 and cellular architecture;6, 7 however, its part in the cell cycle is directly related to the proliferative capacity of malignancy cells. The cell proliferative effect of myc can become coupled to changes buy 50-07-7 in levels and activity of the cyclin-dependent kinase inhibitor p27/kip, ENAH ...

ECM accumulation and ASMC proliferation are hallmarks in the development of intimal thickenings associated with the development of atherosclerotic lesions.61 Our recent work has shown that insertion of decorin-overexpressing cells into injured arteries causes a decrease in intimal volume.30 This decrease is due primarily to a decrease in ECM volume rather than a change in cell number within the intima. The results of the present in vitro study support these in vivo observations and, furthermore, suggest that the effects of decorin overexpression may involve the modulation of TGF-β activity.. An initial decrease in DNA synthesis by decorin-overexpressing cells was observed during the first 24 hours after plating, but this relative decrease disappeared at later time points. The relative decrease in LDSN cells of [3H]thymidine incorporation and increase of cyclin-dependent kinase inhibitors p21 and p27 at 24 hours after plating are similar to the effects that were reported in studies of human ...

Synonyms: Regulation of Nuclear Pre-MRNA Domain Containing 1A, RPRD1A, P15RS, Cyclin-Dependent Kinase 2B-Inhibitor-Related Protein, Cyclin-Dependent Kinase Inhibitor 2B-Related Protein (P15INK4B-Related Protein), P15INK4B-Related Protein, HsT3101, Regulation of Nuclear Pre-MRNA Domain-Containing Protein 1A, Cyclin-Dependent Kinase Inhibitor 2B-Related Protein, FLJ10656.. ...

Substituted guanines and pyrimidines were tested as inhibitors of cyclin B1/CDK1 and cyclin A3/CDK2 and soaked into crystals of monomeric CDK2. O6-Cyclohexylmethylguanine (NU2058) was a competitive inhibitor of CDK1 and CDK2 with respect to ATP (Ki values: CDK1, 5 +/- 1 microM; CDK2, 12 +/- 3 microM) and formed a triplet of hydrogen bonds (i.e., NH-9 to Glu 81, N-3 to Leu 83, and 2-NH2 to Leu 83). The triplet of hydrogen bonding and CDK inhibition was reproduced by 2,6-diamino-4-cyclohexylmethyloxy-5-nitrosopyrimidine (NU6027, Ki values: CDK1, 2.5 +/- 0.4 microM; CDK2, 1.3 +/- 0.2 microM). Against human tumor cells, NU2058 and NU6027 were growth inhibitory in vitro (mean GI50 values of 13 +/- 7 microM and 10 +/- 6 microM, respectively), with a pattern of sensitivity distinct from flavopiridol and olomoucine. These CDK inhibition and chemosensitivity data indicate that the distinct mode of binding of NU2058 and NU6027 has direct consequences for enzyme and cell growth inhibition.

Recombinant human CDKN1B protein, fused to His-tag at N-terminus, was expressed in E. coli and purified by using conventional chromatography. MW: 24.2 kDa.

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Supplementary Materialscancers-12-01563-s001. MHC-I-negative murine tumor cell genes and lines from the IFN- transduction sign pathway are participating. Fhit-transfected tumor cells demonstrated immunogenic extremely, being rejected with a T lymphocyte-mediated immune system response. Strikingly, this immune Vitamin A system rejection was even more regular in females than in men. The immune system response generated secured hosts against the tumor development of non-transfected cells and against various other tumor cells inside our murine tumor PEPCK-C model. Finally, we also noticed a Vitamin A direct relationship between FHIT appearance and HLA-I surface area expression in individual breasts tumors. Recovery of Fhit appearance on MHC course I harmful tumor cells could be a good immunotherapeutic strategy and could even become an individualized immunotherapeutic vaccine. 0.05. A two-tailed Learners 0.05. A two-tailed Learners 0.001, Fisher check) (Body 3A; Body S7A). Small male ...

2vtp: Identification of N-(4-piperidinyl)-4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxamide (AT7519), a novel cyclin dependent kinase inhibitor using fragment-based X-ray crystallography and structure based drug design.

https://astx.com/wp-content/uploads/2019/11/logo_white.png 0 0 webadmin https://astx.com/wp-content/uploads/2019/11/logo_white.png webadmin2010-11-29 12:06:482016-11-29 12:06:57Cho et al. 4-(Pyrazol-4-yl)-pyrimidines as Selective Inhibitors of Cyclin-Dependent Kinase 4/6. Journal of Medicinal Chemistry 53, no. 22 2010: 7938-7957. DOI: 10.1021/jm100571n. ...

Results: In vitro studies showed a pronounced growth inhibitory and pro-apoptotic effect of LBH589 on both HCC cell lines at low micromolar concentrations (IC50 approx. 0.1 µM). Interstingly, the pro-apoptotic effect of Panobinostat was not paralleled by a breakdown of ΔΨm. p53wt HepG2 cells were more sensitive than the p53-/- Hep3B cells. Quantitative PCR and western blotting showed an involvement of the cell cycle regulators p21cip1/waf1 and Chek1 but not the bax/bcl-2 system. Panobinostat regulated the expression of p21cip1/waf1 via a transcriptional upregulation as evidenced by ChIP ...

Dr. Li studies the intracellular pathways related to IL-7s effects on T cell apoptosis and proliferation. She found that IL-7 promotes T cell survival and division by blocking degradation of Mcl-1 and inducing degradation of the cell cycle inhibitor p27kip1. Her current work focuses on identifying the ubiquitination pathways that IL-7 uses to control the stability of Mcl-1

CDKN1C - CDKN1C Mutant (L33R), Myc-DDK-tagged ORF clone of Homo sapiens cyclin-dependent kinase inhibitor 1C (p57, Kip2) (CDKN1C), transcript variant 1 as transfection-ready DNA available for purchase from OriGene - Your Gene Company.

CDKN2A - CDKN2A (untagged)-Human cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) (CDKN2A), transcript variant 4 available for purchase from OriGene - Your Gene Company.

Raje N, Hideshima T, Mukherjee S, Raab M, Vallet S, Chhetri S, Cirstea D, Pozzi S, Mitsiades C, Rooney M, Kiziltepe T, Podar K, Okawa Y, Ikeda H, Carrasco R, Richardson PG, Chauhan D, Munshi NC, Sharma S, Parikh H, Chabner B, Scadden D, Anderson KC. Preclinical activity of P276-00, a novel small-molecule cyclin-dependent kinase inhibitor in the therapy of multiple myeloma. Leukemia. 2009 May; 23(5):961-70 ...

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NU2058 (O6-(Cyclohexylmethyl)guanine) is a potent, competitive and guanine-based CDK inhibitor with IC50s of 17 μM and 26 μM for CDK2 and CDK1. NU2058 has anti-cancer activity. - Mechanism of Action & Protocol.

p21 C/P 1/El and p 2 7K/P 1 are cyclin-dependant kinase inhibitors that fonn an integral part of the cell cycle process. These proteins function as cell-cycle inhibitors, and are able to induce cell cycle arrest by binding ...

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KIP2 deletion affects Bik1 localization at cMT +tips. (A) Bik1 localization in WT (GFP-TUB1) and kip2Δ mutant. In the mutant, Bik1 accumulation is reduced or a

AZD5438 is a potent inhibitor of CDK1/2/9 with IC50 of 16 nM/6 nM/20 nM. It is less potent to CDK5/6 and also inhibits GSK3β. Phase 1.Quality confirmed by NMR & HPLC. See customer reviews, validations & product citations.

SKP2兔多克隆抗体(ab68455)可与小鼠, 大鼠, 人样本反应并经WB, IP, IHC, ICC实验严格验证，被3篇文献引用并得到1个独立的用户反馈。所有产品均提供质保服务，中国75%以上现货。

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