Cyclin-Dependent Kinase 3
Cyclin D1
Cyclin A
Cyclin E
Cyclin C
Cyclins
Cyclin-Dependent Kinases
Cyclin B
Cyclin B1
Cyclin D2
Cyclin D3
Cyclin A1
Cyclin A2
Epsilonretrovirus
Cyclin D
Cyclin G1
Cyclin G
Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)
Cell Cycle
G1 Phase
Cyclin B2
Proteolysis
Protein-Serine-Threonine Kinases
Cyclin T
Cyclin-Dependent Kinase 2
Cyclin G2
Cyclin H
Cyclin-Dependent Kinase 4
CDC2-CDC28 Kinases
Hydrogen Peroxide
Saccharomyces cerevisiae Proteins
CDC2 Protein Kinase
Phosphorylation
Cell Cycle Proteins
Transcription, Genetic
Cyclin-Dependent Kinase Inhibitor p27
S Phase
Retinoblastoma Protein
Cyclin I
RNA, Messenger
Saccharomyces cerevisiae
Oxidative Stress
Cell Wall
Mitosis
Oncogene Proteins
Genes, bcl-1
Cyclin-Dependent Kinase 6
Cyclin-Dependent Kinase Inhibitor p21
Cell Division
G2 Phase
Tumor Suppressor Proteins
E2F Transcription Factors
cdc25 Phosphatases
Molecular Sequence Data
Proto-Oncogene Proteins
Cell Nucleus
Tumor Cells, Cultured
Microtubule-Associated Proteins
Gene Expression Regulation, Neoplastic
Proliferating Cell Nuclear Antigen
F-Box Proteins
Protamine Kinase
Protein Binding
Blotting, Western
Maturation-Promoting Factor
Down-Regulation
Immunohistochemistry
Transcription Factors
Transfection
Promoter Regions, Genetic
Cyclin-Dependent Kinase Inhibitor p16
Nuclear Proteins
Gene Expression Regulation
Transcription Factor DP1
Apoptosis
Cyclin-Dependent Kinase 9
HeLa Cells
Signal Transduction
3T3 Cells
Retinoblastoma-Binding Protein 1
Tumor Suppressor Protein p53
E2F1 Transcription Factor
DNA-Binding Proteins
Retinoblastoma-Like Protein p107
Amino Acid Sequence
Base Sequence
Cells, Cultured
Protein Kinases
Ubiquitin-Protein Ligase Complexes
Mutation
Recombinant Fusion Proteins
CDC28 Protein Kinase, S cerevisiae
S-Phase Kinase-Associated Proteins
Enzyme Activation
Cyclin-Dependent Kinase Inhibitor Proteins
RNA, Small Interfering
Enzyme Inhibitors
Oocytes
Lymphoma, Mantle-Cell
Ki-67 Antigen
NIH 3T3 Cells
Fibroblasts
Reverse Transcriptase Polymerase Chain Reaction
Flow Cytometry
Meiosis
Xenopus Proteins
Cell Transformation, Neoplastic
Proto-Oncogene Proteins c-myc
Xenopus
Cyclin-Dependent Kinase 8
Precipitin Tests
Proteasome Endopeptidase Complex
Gene Expression
Cdh1 Proteins
Carrier Proteins
Proto-Oncogene Proteins c-mos
beta Catenin
Immunoblotting
Models, Biological
Interphase
Threonine
Cell Cycle Checkpoints
Up-Regulation
DNA Primers
Metaphase
Glycogen Synthase Kinase 3
RNA Interference
Neoplasm Proteins
E2F4 Transcription Factor
Ubiquitins
Positive Transcriptional Elongation Factor B
Centrosome
Anaphase
Trans-Activators
Transcriptional Activation
DNA
Cytoplasm
SKP Cullin F-Box Protein Ligases
Cell Differentiation
Purines
Tumor Markers, Biological
Ubiquitin-Protein Ligases
Immunoprecipitation
Securin
Cyclin-Dependent Kinase Inhibitor p18
Mice, Transgenic
Binding Sites
Nocodazole
Cyclin C/CDK8 and cyclin H/CDK7/p36 are biochemically distinct CTD kinases. (1/37)
Phosphorylation of the carboxyl-terminal domain (CTD) of RNA polymerase II is important for basal transcriptional processes in vivo and for cell viability. Several kinases, including certain cyclin-dependent kinases, can phosphorylate this substrate in vitro. It has been proposed that differential CTD phosphorylation by different kinases may regulate distinct transcriptional processes. We have found that two of these kinases, cyclin C/CDK8 and cyclin H/CDK7/p36, can specifically phosphorylate distinct residues in recombinant CTD substrates. This difference in specificity may be largely due to their varying ability to phosphorylate lysine-substituted heptapeptide repeats within the CTD, since they phosphorylate the same residue in CTD consensus heptapeptide repeats. Furthermore, this substrate specificity is reflected in vivo where cyclin C/ CDK8 and cyclin H/CDK7/p36 can differentially phosphorylate an endogenous RNA polymerase II substrate. Several small-molecule kinase inhibitors have different specificities for these related kinases, indicating that these enzymes have diverse active-site conformations. These results suggest that cyclin C/CDK8 and cyclin H/CDK7/p36 are physically distinct enzymes that may have unique roles in transcriptional regulation mediated by their phosphorylation of specific sites on RNA polymerase II. (+info)Two novel 14-Epi-analogues of 1,25-dihydroxyvitamin D3 inhibit the growth of human breast cancer cells in vitro and in vivo. (2/37)
The biological activity of two novel 14-epi-analogues of 1,25(OH)2D3, 19-nor-14-epi-23-yne-1,25(OH)2D3 (TX 522) and 19-nor-14,20-bisepi-23-yne-1,25(OH)2D3 (TX 527), is described. Both analogues were at least 10 times more potent than 1,25(OH)2D3 in inhibiting in vitro cell proliferation and had much lower in vivo calcemic effects than 1,25(OH)2D3. Treatment with 1,25(OH)2D3, TX 522, or TX 527 in vitro was accompanied by an accumulation of cells in the G1 phase of the cell cycle. Protein levels of cyclin C and cyclin D1 in in vitro cultures of MCF-7 cells were down-regulated to 50 and 30%, respectively, of control levels at 72 and 120 h after stimulation. Protein levels of p21 and p27 at 72 h were significantly enhanced by 1,25(OH)2D3 and TX 522 but surprisingly not by TX 527. The inability of TX 527 to up-regulate p21 seemed to be cell type specific because p21 was induced in other cell types. Diminished phosphorylation of the retinoblastoma protein after treatment with 1,25(OH)2D3, TX 522, or TX 527 may ultimately contribute to the growth inhibition caused by these compounds. According to the data presented, the induction of apoptosis seemed not to be a major mechanism responsible for the growth-inhibitory effect of 1,25(OH)2D3 and analogues. Both 14-epianalogues significantly retarded tumor progression (40% reduced compared with control mice) in an in vivo model of MCF-7 breast cancer cells established in nude mice. In conclusion, these novel analogues have the eligible profile to be tested as therapeutic agents for the treatment of hyperproliferative diseases such as breast cancer. (+info)Human cyclin C protein is stabilized by its associated kinase cdk8, independently of its catalytic activity. (3/37)
Cyclin C belongs to the cyclin family of proteins that control cell cycle transitions through activation of specific catalytic subunits, the cyclin-dependent kinases (CDKs). However, there is as yet no evidence for any role of cyclin C and its partner, cdk8, in cell cycle regulation. Rather, the cyclin C-cdk8 complex was found associated with the RNA polymerase II transcription machinery. The periodic degradation of bona fide cyclins is crucial for cell-cycle progression and depends on the catalytic activity of the associated CDK. Here we show that endogenous cyclin C protein is quite stable with a half-life of 4 h. In contrast, exogenously expressed cyclin C is very unstable (half-life 15 min) and degraded by the ubiquitin-proteasome pathway. Co-expression with its associated cdk, however, strongly stabilizes cyclin C and results in a protein half-life near that of endogenous cyclin C. In stark contrast to data reported for other members of the cyclin family, both catalytically active and inactive cdk8 induce cyclin C stabilization. Moreover, this stabilization is accompanied in both cases by phosphorylation of the cyclin, which is not detectable when unstable. Our results indicate that cyclin C has apparently diverged from other cyclins in the regulation of its stability by its CDK partner. (+info)Characterization of mediator complexes from HeLa cell nuclear extract. (4/37)
A number of mammalian multiprotein complexes containing homologs of Saccharomyces cerevisiae Mediator subunits have been described recently. High-molecular-mass complexes (1 to 2 MDa) sharing several subunits but apparently differing in others include the TRAP/SMCC, NAT, DRIP, ARC, and human Mediator complexes. Smaller multiprotein complexes (approximately 500 to 700 kDa), including the murine Mediator, CRSP, and PC2, have also been described that contain subsets of subunits of the larger complexes. To evaluate whether these different multiprotein complexes exist in vivo in a single form or in multiple different forms, HeLa cell nuclear extract was directly resolved over a Superose 6 gel filtration column. Immunoblotting of column fractions using antisera specific for several Mediator subunits revealed one major size class of high-molecular-mass (approximately 2-MDa) complexes containing multiple mammalian Mediator subunits. No peak was apparent at approximately 500 to 700 kDa, indicating that either the smaller complexes reported are much less abundant than the higher-molecular-mass complexes or they are subcomplexes generated by dissociation of larger complexes during purification. Quantitative immunoblotting indicated that there are about 3 x 10(5) to 6 x 10(5) molecules of hSur2 Mediator subunit per HeLa cell, i.e., the same order of magnitude as RNA polymerase II and general transcription factors. Immunoprecipitation of the approximately 2-MDa fraction with anti-Cdk8 antibody indicated that at least two classes of Mediator complexes occur, one containing CDK8 and cyclin C and one lacking this CDK-cyclin pair. The approximately 2-MDa complexes stimulated activated transcription in vitro, whereas a 150-kDa fraction containing a subset of Mediator subunits inhibited activated transcription. (+info)c-Myc initiates illegitimate replication of the ribonucleotide reductase R2 gene. (5/37)
The mechanisms through which the oncoprotein c-Myc initiates locus-specific gene amplification are not understood. When analysing the initiation mechanism of c-Myc-dependent amplification of the mouse ribonucleotide reductase R2 (R2) gene, we observe c-Myc-dependent initiation of illegitimate DNA replication of the R2 gene. We demonstrate multiple simultaneous c-Myc-induced R2 replication forks, whereas R2 normally replicates with a single fork. In contrast, cyclin C replicates with only a single replication fork irrespective of c-Myc deregulation. In addition to de novo replication forks, c-Myc also initiates bi-allelic replication of R2, abrogating its normal mono-allelic replication pattern. Moreover, several chromosomal regions also display c-Myc-induced illegitimate replication profiles. Thus, c-Myc can act as an illegitimate replication-licensing factor that promotes de novo replication initiation and illegitimate replication timing that adversely impacts upon genomic stability. (+info)Selenite and selenomethionine promote HL-60 cell cycle progression. (6/37)
The essential role of selenium (Se) in nutrition is well established. The elucidation of the mechanisms by which selenium regulates the cell cycle can lead to a better understanding of the nature of selenium's essentiality and its role in disease prevention. In this study, the effects of selenium deficiency or adequacy (0.25 micromol/L selenite or selenomethionine) on HL-60 cell cycle progression were examined in serum-free media. Selenium was critical for promotion of HL-60 cell growth. Cell-cycle analysis revealed that selenium deficiency caused a decrease in G1 phase cells that corresponded to an increase in G2 and sub-G1 phase cells. Gene array analysis suggested that c-Myc, cyclin C, proliferating cell nuclear antigen, cyclin-dependent kinase (cdk)1, cdk2, cdk4, cyclin B and cyclin D2 mRNA levels were lower in selenium-deficient cells than in the cells supplemented with 0.25 micromol/L selenomethionine. The decrease in the c-Myc mRNA level in selenium-deficient cells was confirmed by reverse transcription-polymerase chain reaction analysis. Furthermore, the phosphorylation state of total cellular protein was higher (57%) in selenium-supplemented cells than in selenium-deficient cells. Collectively, these results suggest a novel role for selenium at 0.25 micromol/L in up-regulation of the expression of numerous cell cycle-related genes and total cellular phosphorylated proteins in HL-60 cells in serum-free culture media. This leads to the promotion of cell cycle progression, particularly G2/M transition and/or the reduction of apoptosis, primarily in G1 cells. These observations may have additional implications for understanding the nature of selenium's essentiality. (+info)Analysis of cell cycle gene expression responding to acetoxyscirpendiol isolated from Paecilomyces tenuipes. (7/37)
Paecilomyces tenuipes is believed to contain potential oncostatic and tumor-reducing components. Molecular mechanism, however, is poorly understood concerning the potential antitumor components and their biological function. We purified acetoxyscirpendiol (ASD) from methanolic extracts (MPT) of the fungus and tested the two compounds for the molecular profile of their antitumor potential. Using a differential display protocol, cyclin C and Mad-1 were identified as candidate genes responding to MPT. When a quantitative PCR was performed on the total RNA from MCF-7 treated by MPT or ASD, gene expressions of cyclin C and Mad-1 were greatly augmented. In terms of protein expression, cyclin C level increased up to 12 folds in response to ASD as well as MPT. Similar as MPT treatments, ASD-treated cells synthesize cyclin C as 2-4 fold compared to the control treatments. In terms of Mad-1 expression in cells treated with ASD, the level of Mad-1 expression increased up to 2.5 folds by MPT treatment. Cyclin C expression was compared with non-treated cells in various cell lines. MCF-7 cell was shown highly responsive to the MPT or ASD treatment. Taken together, these results strongly indicate that MPT contains potential antitumor components which might exert their action by modulating cell cycle-related genes such as cyclin C and Mad-1 in MCF-7. The major antioncogenic component in MPT may be ASD which modulates cyclin C and Mad-1 expression. (+info)c-Myc-induced extrachromosomal elements carry active chromatin. (8/37)
Murine Pre-B lymphocytes with experimentally activated MycER show both chromosomal and extrachromosomal gene amplification. In this report, we have elucidated the size, structure, and functional components of c-Myc-induced extrachromosomal elements (EEs). Scanning electron microscopy revealed that EEs isolated from MycER-activated Pre-B+ cells are an average of 10 times larger than EEs isolated from non-MycER-activated control Pre-B- cells. We demonstrate that these large c-Myc-induced EEs are associated with histone proteins, whereas EEs of non-MycER-activated Pre B- cells are not. Immunohistochemistry and Western blot analyses using pan-histone-specific, histone H3 phosphorylation-specific, and histone H4 acetylation-specific antibodies indicate that a significant proportion of EEs analyzed from MycER-activated cells harbors transcriptionally competent and/or active chromatin. Moreover, these large, c-Myc-induced EEs carry genes. Whereas the total genetic make-up of these c-Myc-induced EEs is unknown, we found that 30.2% of them contain the dihydrofolate reductase (DHFR) gene, whereas cyclin C (CCNC) was absent. In addition, 50% of these c-Myc-activated Pre-B+ EEs incorporated bromodeoxyuridine (BrdU), identifying them as genetic structures that self-propagate. In contrast, EEs isolated from non-Myc-activated cells neither carry the DHFR gene nor incorporate BrdU, suggesting that c-Myc deregulation generates a new class of EEs. (+info)There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
The prognosis for mantle-cell lymphoma is generally poor, with a five-year survival rate of approximately 40%. Treatment options include chemotherapy, immunotherapy, and autologous stem-cell transplantation. The disease often recurs after initial therapy, and subsequent treatments may be less effective.
Mantle-cell lymphoma can be difficult to distinguish from other types of non-Hodgkin lymphoma, such as follicular lymphoma or diffuse large B-cell lymphoma, and a correct diagnosis is important for determining appropriate treatment.
Slide: Mantle Cell Lymphoma (Image courtesy of Nephron/Wikimedia Commons)
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
Cyclin
Cyclin T2
Cyclin O
Cyclin A1
Cyclin B2
Cyclin B
Cyclin E1
Cyclin D
Cyclin D2
Cyclin D1
Cyclin K
Cyclin B1
Cyclin E2
Cyclin E
Cyclin T1
Cyclin A2
Cyclin H
Cyclin A
Cyclin D3
Cyclin-dependent kinase
Cyclin-dependent kinase 1
Cyclin-dependent kinase 10
Cyclin-dependent kinase 6
Cyclin-dependent kinase 2
Cyclin-dependent kinase 7
Cyclin-dependent kinase 5
Cyclin-dependent kinase complex
Cyclin-dependent kinase 4
Cyclin-dependent kinase 9
Cyclin-dependent kinase 3
Human Cyclin B1 Antibody MAB60001-100: R&D Systems
Cyclin-Dependent Kinase 2 | Harvard Catalyst Profiles | Harvard Catalyst
Hyperactivation of MEK/ERK pathway by Ca2+ /calmodulin-dependent protein kinase kinase 2 promotes cellular proliferation by...
Go to Relief of cyclin A gene transcriptional inhibition during activation of human primary T lymphocytes via CD2 and CD28...
Cyclin' Missy: Mental Day
Cyclin-Dependent Kinase 3 | Profiles RNS
Molecular dynamics simulations reveal the determinants of cyclin-dependent kinase 2 inhibition by 5-nitrosopyrimidine...
Atypical cyclins: the extended family portrait
Non-aggregating tau phosphorylation by cyclin-dependent kinase 5 contributes to motor neuron degeneration in spinal muscular...
Cyclin Dependent Kinase Inhibitor 2D (CDKN2D) Antibody (abx005030-20) at Hölzel-Diagnostika
Human Cyclin-dependent kinase 4,CDK-4 ELISA Kit - Brogen Medikal Teknolojileri
Inhibition of the CDK2 and Cyclin A complex leads to autophagic degradation of CDK2 in cancer cells. | Nat Commun;13(1): 2835,...
Cyclin-dependent kinase-like 5 binds and phosphorylates DNA methyltransferase 1<...
Expression of cyclin d1 and its association with disease characteristics in bladder cancer. | Gudas Lab
Anti-Cyclin Dependent Kinase 2 (CDK2) | Technique alternative | 01010004187 - Antibodies, Anit-bodies, Antibody, Anti-body
The functional roles of cyclin-dependent kinase 5 in neural development - Rare & Special e-Zone
The Potential Role of Cyclin-Dependent Kinase 5 in Focal Cortical Dysplasia - Nuffield Department of Clinical Neurosciences
Role of gene signatures combined with pathology in classification of oropharynx head and neck cancer | Scientific Reports
Human Papillomavirus16 Variant E7 Gene Induces Transformation of NIH 3T3 Cells Via Up-Regulation of cdc25A and Cyclin A |...
The Arabidopsis D-type cyclin CYCD2;1 and the inhibitor ICK2/KRP2 modulate auxin-induced lateral root formation - Fingerprint
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Munin: mir-34a targets cell cycle genes CCND1 (cyclin D1) and MYCN, while mir-21 does not target PTEN and PDCD4 in neuroblastoma
HR+/HER2- Metastatic Breast Cancer: What Can You Do to Optimize Patient Access to Cyclin-dependent Kinase 4 and 6 Inhibitors? -...
Maternal cyclin B levels 'Chk' the onset of DNA replication checkpoint control in Drosophila - Fingerprint
- Research...
Ursolic Acid Regulates Cell Cycle and Proliferation in Colon
Impact of cyclins E, neutrophil elastase and proteinase 3 expression levels on clinical outcome in primary breast cancer...
CCND2 gene: MedlinePlus Genetics
Bike Snob NYC: BSNYC Friday Awkward Encounter With Someone Whose Name You Forgot!
NIOSHTIC-2 Search Results - Full View
SCOPe 2.08: Domain d2wihd2: 2wih D:310-432
Kinases7
- Because a variety of cyclin-dependent kinases (CDKs) assist the effects of EZH2 and cyclin D1, the researchers wanted to see if targeting CDKs in ATRTs with the multi-CDK inhibitor TG02 could have therapeutic effects. (physiciansweekly.com)
- To review palbociclib, a novel small-molecule inhibitor of cyclin-dependent kinases 4 and 6, and its current place in therapy for the treatment of hormone receptor (HMR)-positive, human epidermal growth factor receptor 2 (Her2)-negative advanced breast cancer. (nih.gov)
- Cyclins function as regulators of CDK kinases. (affbiotech.com)
- Regulation of cell division is orchestrated by cyclins, which bind and activate their catalytic workmates, the cyclin-dependent kinases (CDKs). (uic.es)
- The product Assay kit for Rabbit Cyclin-dependent kinases regulatory subunit 1(CKS1B) (ELISA) should be kept between two and eight degrees Celsius to ensure the retention of the stability and reactivity of the reagents included in the kit. (creatinekinases.com)
- The product Assay kit for Rabbit Cyclin-dependent kinases regulatory subunit 1(CKS1B) (ELISA) is intended to be used for research purposes only. (creatinekinases.com)
- Cyclin-dependent kinases regulate lysosomal degradation of hypoxia-inducible factor 1α to promote cell-cycle progression. (bvsalud.org)
Kinase Inhibitor1
- 2007) The cyclin-dependent kinase inhibitor Dacapo promotes replication licensing during Drosophila endocycles. (nih.gov)
CDK26
- Kinase enrichment analysis of hypo-phosphorylated proteins using the X2K Web tool identified ERK1, cyclin-dependant kinase 1 (CDK1), and CDK2 as downstream substrates of CAMKK2. (nih.gov)
- Cyclin-dependent kinase 2 (CDK2) is a kinase involved in the regulation of cell cycle, being responsible for triggering DNA synthesis. (unito.it)
- Skp2 was first identified in multi-protein complexes with cyclin A and Cdk2 in transformed cells. (yu.edu)
- We show that Skp2cyclin A interaction is separable from Skp2's ability to mediate p27 ubiquitination, but can directly protect cyclin A/Cdk2 from inhibition by p27 through competitive binding. (yu.edu)
- We also identified an eighteen-residue peptide from cyclin A binding sequences in Skp2 that can block Skp2-cyclin A/Cdk2 interaction but not p27-cyclin A/Cdk2 interaction and can therefore abolish Skp2's protective effects on cyclin A/Cdk2 activity. (yu.edu)
- Here we report that HIF-1α physically and functionally interacts with cyclin-dependent kinase 1 (Cdk1) and Cdk2. (bvsalud.org)
Phosphorylation4
- Cyclin-dependent kinase 5 modulates nociceptive signaling through direct phosphorylation of transient receptor potential vanilloid 1. (nih.gov)
- Vanadate also increased p21 and Chk1 levels and reduced Cdc25C expression, leading to phosphorylation of Cdc2 and a slight increase in cyclin B1 expression as analyzed by Western blot. (cdc.gov)
- Catalase, a specific antioxidant for H2O2, decreased vanadate-induced expression of p21 and Chk1, reduced phosphorylation of Cdc2Tyr15, and decreased cyclin B1 levels. (cdc.gov)
- Several regulatory pathways are involved: (1) activation of p21, (2) an increase of Chk1 expression and inhibition of Cdc25C, which results in phosphorylation of Cdc2 and possible inactivation of cyclin B1/Cdc2 complex. (cdc.gov)
Proteins3
- Both palbociclib and abemaciclib are, oral, highly selective inhibitors of cyclin-dependent kinase 4 and 6, which are proteins involved in cell differentiation and growth. (nih.gov)
- We demonstrated that the Skp2-cyclin A interaction is mediated by novel interaction sequences on both Skp2 and cyclin A, distinguishing it from the well-known RxL-HP interaction between cyclins and cyclin-binding proteins. (yu.edu)
- Noteworthy, the Human Genome Sequence Project unveiled the existence of several other proteins containing the "cyclin box" domain. (uic.es)
Inhibitor2
Antibody6
- PVDF membrane was probed with 0.05 µg/mL of Rabbit Anti-Human Cyclin B1 Monoclonal Antibody (Catalog # MAB60001) followed by HRP-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # HAF008 ). (rndsystems.com)
- Cyclin B1 was detected in immersion fixed paraffin-embedded sections of human squamous cell carcinoma using Rabbit Anti-Human Cyclin B1 Monoclonal Antibody (Catalog # MAB60001) at 3 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Rabbit IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC003 ). (rndsystems.com)
- K562 human chronic myelogenous leukemia cell line was stained with Rabbit Anti-Human Cyclin B1 Monoclonal Antibody (Catalog # MAB60001, filled histogram) or isotype control antibody (Catalog # AB-105-C , open histogram), followed by Phycoerythrin-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0110 ). (rndsystems.com)
- A specific band was detected for Cyclin B1 at approximately 64 kDa (as indicated) using 0.5 µg/mL of Rabbit Anti-Human Cyclin B1 Monoclonal Antibody (Catalog # MAB60001). (rndsystems.com)
- Cyclin D1 Antibody detects endogenous levels of total Cyclin D1. (affbiotech.com)
- PATIENTS AND METHODS: Tissue microarrays containing bladder cancer specimens (n=212) and adjacent normal bladder tissues (n=131) were immunostained using an antibody against cyclin D1. (cornell.edu)
MRNA and protein2
- ERβ inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein. (houstonmethodist.org)
- RESULTS: Cyclin D1 mRNA and protein expression were significantly higher in UCB compared to adjacent non-malignant bladder tissue (for mRNA p=0.003, for protein p=0.001). (cornell.edu)
CDK12
- Cyclin B1 is the major activator of CDK1. (houstonmethodist.org)
- Our findings demonstrated that unliganded ERβ causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression. (houstonmethodist.org)
Protein5
- It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. (harvard.edu)
- To understand the mechanisms underlined in this regulation in normal human cells, we have analysed in vivo protein-DNA interactions at the Cyclin A locus in primary T lymphocytes. (cnrs.fr)
- The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance throughout the cell cycle. (affbiotech.com)
- The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. (hoelzel-biotech.com)
- Cyclin D1 protein expression was significantly higher in non-invasive tumors than in muscle-invasive UCB (p=0.016). (cornell.edu)
Gene5
- Inactivation of cyclin D2 gene in prostate cancers by aberrant promoter methylation. (nih.gov)
- We investigated the epigenetic silencing of Cyclin D2 gene in prostate cancers and correlated the data with clinicopathological features. (nih.gov)
- Estrogen-occupied estrogen receptor represses cyclin G2 gene expression and recruits a repressor complex at the cyclin G2 promoter. (nih.gov)
- Because estradiol represses expression of the cyclin G2 gene, which encodes a negative regulator of the cell cycle, our aim was to understand the mechanism by which cyclin G2 is repressed by estrogen. (nih.gov)
- We show that cyclin G2 is a primary ER target gene in MCF-7 breast cancer cells that is rapidly and robustly down-regulated by estrogen. (nih.gov)
Transcriptional1
- Tumor necrosis factor-alpha regulates cyclin-dependent kinase 5 activity during pain signaling through transcriptional activation of p35. (nih.gov)
Inhibitors1
- Synthesis and Structure-Activity relationships of cyclin-dependent kinase 11 inhibitors based on a diaminothiazole scaffold. (harvard.edu)
CDKs2
- Cyclins have been traditionally defined by an oscillating (cyclic) pattern of expression and by the presence of a characteristic "cyclin box" that determines binding to the CDKs. (uic.es)
- Cyclin-dependent kinase 5 (Cdk5), a member of the Cdks family, is identified to play a critical role in the development of CNS. (edu.hk)
Degradation2
- Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (affbiotech.com)
- Mutations in the cyclin A binding domain of Skp2 significantly compromise the proliferation-stimulating activity of Skp2 without affecting its ability to cause degradation of p27 and p21. (yu.edu)
Regulates1
- Rotelli M, Policastro R, Bolling A, Killion A, Weinberg A, Dixon M, Zentner G, Walczak C, Lilly MA, Calvi B. (2019) A Cyclin A-Myb-Aurora B network regulates the choice between mitotic cycles and polyploid endoreplication cycles. (nih.gov)
Apoptosis1
- Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1. (harvard.edu)
Regulator1
- Defects in the expression of cyclin D1, a key cell-cycle regulator, have been implicated in progression of various types of cancer. (cornell.edu)
Detects1
- Detects human Cyclin B1 in direct ELISAs and Western blots. (rndsystems.com)
Repression1
- Mutational mapping of receptor reveals a requirement for its N-terminal region and DNA binding domain to support cyclin G2 repression. (nih.gov)
Methylation5
- Cyclin D2 promoter methylation was analyzed in 101 prostate cancer samples by methylation-specific PCR. (nih.gov)
- The methylation status of Cyclin D2 was correlated with the methylation of nine other tumor suppressor genes published previously from our laboratory on the same set of samples (R. Maruyama et al. (nih.gov)
- We also compared methylation of cyclin D2 with methylation of nine tumor suppressor genes [published previously from our laboratory (R. Maruyama et al. (nih.gov)
- Although the high preoperative serum prostate-specific antigen (PSA) group did not have significantly greater methylation frequency, methylation of Cyclin D2 had higher mean PSA value. (nih.gov)
- Our results indicate that methylation of Cyclin D2 in prostate cancers correlates with clinicopathological features of poor prognosis. (nih.gov)
Clinicopathological2
- In the present study, we investigated whether cyclin D1 expression is associated with clinicopathological parameters and whether it has any potential prognostic value in determining risk of UCB recurrence. (cornell.edu)
- The association between cyclin D1 and clinicopathological parameters including stage, lymph node metastasis, and disease-free survival, were evaluated. (cornell.edu)
Cancers1
- The requirement for cyclin E in c-Myc overexpressing breast cancers. (harvard.edu)
Expression5
- Expression of cyclin d1 and its association with disease characteristics in bladder cancer. (cornell.edu)
- Cyclin D1 mRNA expression data from human normal bladder (n=14) and cancer specimens (n=28) were extracted from the public Oncomine database. (cornell.edu)
- CONCLUSION: Altered expression of cyclin D1 is associated with lymph node metastasis and risk of UCB recurrence. (cornell.edu)
- Cyclin D1 expression may therefore have clinical value as a prognostic marker and potential therapeutic target. (cornell.edu)
- 2006) Bruno inhibits the expression of mitotic cyclins during the prophase I meiotic arrest of Drosophila oocytes. (nih.gov)
Regulatory1
- Following estradiol treatment of cells, chromatin immunoprecipitation analyses reveal recruitment of ER to the cyclin G2 regulatory region, dismissal of RNA polymerase II, and recruitment of a complex containing N-CoR and histone deacetylases, leading to a hypoacetylated chromatin state. (nih.gov)
Stimulation1
- Cyclin A was observed after 4 days of costimulation with anti CD2 + CD28 whereas stimulation by anti CD2 or anti CD28 alone was not effective. (cnrs.fr)
Activation1
- Activation of cyclin-dependent 5 mediates orofacial mechanical hyperalgesia. (nih.gov)
PHASE1
- A cyclin-dependent kinase that forms a complex with CYCLIN C and is active during the G1 PHASE of the CELL CYCLE. (musc.edu)
Clinical1
- 1. The clinical significance of cyclin B1 (CCNB1) in invasive breast cancer with emphasis on its contribution to lymphovascular invasion development. (nih.gov)
Human4
- Detection of Human Cyclin B1 by Western Blot. (rndsystems.com)
- Cyclin B1 in Human Squamous Cell Carcinoma. (rndsystems.com)
- Detection of Cyclin B1 in K562 Human Cell Line by Flow Cytometry. (rndsystems.com)
- Detection of Human Cyclin B1 by Simple Western TM . (rndsystems.com)
Family1
- The application of these criteria allows to systematically define, for the first time, the subfamily of atypical cyclins and enables the use of a common nomenclature for this extended family. (uic.es)
Specific1
- A specific band was detected for Cyclin B1 at approximately 52 kDa (as indicated). (rndsystems.com)
Total1
- This graph shows the total number of publications written about "Cyclin-Dependent Kinase 2" by people in Harvard Catalyst Profiles by year, and whether "Cyclin-Dependent Kinase 2" was a major or minor topic of these publication. (harvard.edu)