Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase 2
Cell Cycle Proteins
CDC2 Protein Kinase
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase Inhibitor p27
Gene Expression Regulation, Neoplastic
Tumor Suppressor Proteins
Tumor Cells, Cultured
Cyclin-Dependent Kinase Inhibitor p16
Promoter Regions, Genetic
Proliferating Cell Nuclear Antigen
Gene Expression Regulation
E2F Transcription Factors
Cyclin-Dependent Kinase 6
Glycogen Synthase Kinase 3
Cell Transformation, Neoplastic
Tumor Suppressor Protein p53
Reverse Transcriptase Polymerase Chain Reaction
Molecular Sequence Data
RNA, Small Interfering
Proto-Oncogene Proteins c-myc
NIH 3T3 Cells
E2F1 Transcription Factor
Transcription Factor DP1
Chromosomes, Human, Pair 11
Retinoblastoma-Like Protein p107
Retinoblastoma-Binding Protein 1
Proteasome Endopeptidase Complex
S-Phase Kinase-Associated Proteins
Cell Cycle Checkpoints
Tumor Markers, Biological
Recombinant Fusion Proteins
Proto-Oncogene Proteins c-akt
Amino Acid Sequence
Chromosomes, Human, Pair 14
Cyclin-Dependent Kinase Inhibitor Proteins
Carcinoma, Squamous Cell
G1 Phase Cell Cycle Checkpoints
Mitogen-Activated Protein Kinases
Active Transport, Cell Nucleus
Cyclin-Dependent Kinase 9
E2F4 Transcription Factor
Ubiquitin-Protein Ligase Complexes
Detection of Kaposi's sarcoma herpesvirus DNA sequences in multiple myeloma bone marrow stromal cells. (1/457)Whether Kaposi's sarcoma herpesvirus (KSHV) is associated with multiple myeloma (MM) remains controversial. We assayed for KSHV DNA sequences in long-term bone marrow stromal cells (BMSCs) from 26 patients with MM and 4 normal donors. Polymerase chain reaction (PCR) using primers which amplify a KSHV gene sequence to yield a 233-bp fragment (KS330233 within open reading frame 26) was negative in all cases. Aliquots of these PCR products were used as templates in subsequent nested PCR, with primers that amplify a 186-bp product internal to KS330233. BMSCs from 24 of 26 (92%) patients with MM and 1 of 4 normal donors were KSHV PCR+. DNA sequence analyses showed interpatient specific mutations (2 to 3 bp). Both Southern blot and sequence analyses confirmed the specificity of PCR results. The presence of the KSHV gene sequences was further confirmed by amplifying T 1.1 (open reading frame [ORF] K7) and viral cyclin D (ORF 72), two other domains within the KSHV genome. Immunohistochemical studies of KSHV PCR+ MM BMSCs demonstrate expression of dendritic cell (DC) lineage markers (CD68, CD83, and fascin). Serological studies for the presence of KSHV lytic or latent antibodies were performed using sera from 53 MM patients, 12 normal donors, and 5 human immunodeficiency virus (HIV)/KSHV+ patients. No lytic or latent antibodies were present in sera from either MM patients or normal donors. Taken together, these findings show that KSHV DNA sequences are detectable in BMSCs from the majority of MM patients, but that serologic responses to KSHV are not present. Ongoing studies are defining whether the lack of antibody response is caused by the absence of ongoing infection, the presence of a novel viral strain associated with MM, or underlying immunodeficiency in these patients. (+info)
TAFII250, Egr-1, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin. (2/457)Differential display identified that gene fragment HA220 homologous to the transcriptional activator factor II 250 (TAFII250) gene, or CCG1, was increased in hypertrophied rodent heart. To determine whether TAFII250 gene expression is modified after cardiac damage, we measured TAFII250 expression in vivo in mouse hearts after injection of the cardiotoxic agent doxorubicin (DXR) and in vitro in DXR-treated isolated rat neonatal cardiomyocytes. In vivo atrial natriuretic factor (ANF), beta-myosin heavy chain (beta-MHC), Egr-1, and TAFII250 expression increased with dose and time after a single DXR injection, but only ANF and beta-MHC expression were increased after multiple injections. After DXR treatment of neonatal cardiomyocytes we found decreased ANF, alpha-MHC, Egr-1, and TAFII250 expression. Expression of the TAFII250-regulated genes, the D-type cyclins, was increased after a single injection in adult mice and was decreased in DXR-treated cardiomyocytes. Thus expression of Erg-1, TAFII250, and the D-type cyclins is modulated after cardiotoxic damage in adult and neonatal heart. (+info)
Regulation of Rb and E2F by signal transduction cascades: divergent effects of JNK1 and p38 kinases. (3/457)The E2F transcription factor plays a major role in cell cycle regulation, differentiation and apoptosis, but it is not clear how it is regulated by non-mitogenic signaling cascades. Here we report that two kinases involved in signal transduction have opposite effects on E2F function: the stress-induced kinase JNK1 inhibits E2F1 activity whereas the related p38 kinase reverses Rb-mediated repression of E2F1. JNK1 phosphorylates E2F1 in vitro, and co-transfection of JNK1 reduces the DNA binding activity of E2F1; treatment of cells with TNFalpha had a similar effect. Fas stimulation of Jurkat cells is known to induce p38 kinase and we find a pronounced increase in Rb phosphorylation within 30 min of Fas stimulation. Phosphorylation of Rb correlated with a dissociation of E2F and increased transcriptional activity. The inactivation of Rb by Fas was blocked by SB203580, a p38-specific inhibitor, as well as a dominant-negative p38 construct; cyclin-dependent kinase (cdk) inhibitors as well as dominant-negative cdks had no effect. These results suggest that Fas-mediated inactivation of Rb is mediated via the p38 kinase, independent of cdks. The Rb/E2F-mediated cell cycle regulatory pathway appears to be a normal target for non-mitogenic signaling cascades and could be involved in mediating the cellular effects of such signals. (+info)
The p21(Cip1) and p27(Kip1) CDK 'inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts. (4/457)The widely prevailing view that the cyclin-dependent kinase inhibitors (CKIs) are solely negative regulators of cyclin-dependent kinases (CDKs) is challenged here by observations that normal up-regulation of cyclin D- CDK4 in mitogen-stimulated fibroblasts depends redundantly upon p21(Cip1) and p27(Kip1). Primary mouse embryonic fibroblasts that lack genes encoding both p21 and p27 fail to assemble detectable amounts of cyclin D-CDK complexes, express cyclin D proteins at much reduced levels, and are unable to efficiently direct cyclin D proteins to the cell nucleus. Restoration of CKI function reverses all three defects and thereby restores cyclin D activity to normal physiological levels. In the absence of both CKIs, the severe reduction in cyclin D-dependent kinase activity was well tolerated and had no overt effects on the cell cycle. (+info)
DNA binding protein dbpA binds Cdk5 and inhibits its activity. (5/457)Progress in the cell cycle is governed by the activity of cyclin dependent kinases (Cdks). Unlike other Cdks, the Cdk5 catalytic subunit is found mostly in differentiated neurons. Interestingly, the only known protein that activates Cdk5 (i.e. p35) is expressed solely in the brain. It has been suggested that, besides its requirement in neuronal differentiation, Cdk5 activity is induced during myogenesis. However, it is not clear how this activity is regulated in the pathway that leads proliferative cells to differentiation. In order to find if there exists any Cdk5-interacting protein, the yeast two-hybrid system was used to screen a HeLa cDNA library. We have determined that a C-terminal 172 amino acid domain of the DNA binding protein, dbpA, binds to Cdk5. Biochemical analyses reveal that this fragment (dbpA(Cdelta)) strongly inhibits p35-activated Cdk5 kinase. The protein also interacts with Cdk4 and inhibits the Cdk4/cyclin D1 enzyme. Surprisingly, dbpA(Cdelta) does not bind Cdk2 in the two-hybrid assay nor does it inhibit Cdk2 activated by cyclin A. It could be that dbpA's ability to inhibit Cdk5 and Cdk4 reflects an apparent cross-talk between distinct signal transduction pathways controlled by dbpA on the one hand and Cdk5 or Cdk4 on the other. (+info)
A cyclin D-Cdk4 activity required for G2 phase cell cycle progression is inhibited in ultraviolet radiation-induced G2 phase delay. (6/457)Cyclin D-Cdk4 complexes have a demonstrated role in G1 phase, regulating the function of the retinoblastoma susceptibility gene product (Rb). Previously, we have shown that following treatment with low doses of UV radiation, cell lines that express wild-type p16 and Cdk4 responded with a G2 phase cell cycle delay. The UV-responsive lines contained elevated levels of p16 post-treatment, and the accumulation of p16 correlated with the G2 delay. Here we report that in UV-irradiated HeLa and A2058 cells, p16 bound Cdk4 and Cdk6 complexes with increased avidity and inhibited a cyclin D3-Cdk4 complex normally activated in late S/early G2 phase. Activation of this complex was correlated with the caffeine-induced release from the UV-induced G2 delay and a decrease in the level of p16 bound to Cdk4. Finally, overexpression of a dominant-negative mutant of Cdk4 blocked cells in G2 phase. These data indicate that the cyclin D3-Cdk4 activity is necessary for cell cycle progression through G2 phase into mitosis and that the increased binding of p16 blocks this activity and G2 phase progression after UV exposure. (+info)
Transduced p16INK4a peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G1. (7/457)Progression of cells through the G1 phase of the cell cycle requires cyclin D:Cdk4/6 and cyclin E:Cdk2 complexes; however, the duration and ordering of these complexes remain unclear. To address this, we synthesized a peptidyl mimetic of the Cdk4/6 inhibitor, p16INK4a that contained an NH2-terminal TAT protein transduction domain. Transduction of TAT-p16 wild-type peptides into cells resulted in the loss of active, hypophosphorylated pRb and elicited an early G1 cell cycle arrest, provided cyclin E:Cdk2 complexes were inactive. We conclude that cyclin D:Cdk4/6 activity is required for early G1 phase cell cycle progression up to, but not beyond, activation of cyclin E:Cdk2 complexes at the restriction point and is thus nonredundant with cyclin E:Cdk2 in late G1. (+info)
c-Myc regulates cyclin D-Cdk4 and -Cdk6 activity but affects cell cycle progression at multiple independent points. (8/457)c-myc is a cellular proto-oncogene associated with a variety of human cancers and is strongly implicated in the control of cellular proliferation, programmed cell death, and differentiation. We have previously reported the first isolation of a c-myc-null cell line. Loss of c-Myc causes a profound growth defect manifested by the lengthening of both the G1 and G2 phases of the cell cycle. To gain a clearer understanding of the role of c-Myc in cellular proliferation, we have performed a comprehensive analysis of the components that regulate cell cycle progression. The largest defect observed in c-myc-/- cells is a 12-fold reduction in the activity of cyclin D1-Cdk4 and -Cdk6 complexes during the G0-to-S transition. Downstream events, such as activation of cyclin E-Cdk2 and cyclin A-Cdk2 complexes, are delayed and reduced in magnitude. However, it is clear that c-Myc affects the cell cycle at multiple independent points, because restoration of the Cdk4 and -6 defect does not significantly increase growth rate. In exponentially cycling cells the absence of c-Myc reduces coordinately the activities of all cyclin-cyclin-dependent kinase complexes. An analysis of cyclin-dependent kinase complex regulators revealed increased expression of p27(KIP1) and decreased expression of Cdk7 in c-myc-/- cells. We propose that c-Myc functions as a crucial link in the coordinate adjustment of growth rate to environmental conditions. (+info)
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
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.
SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.
SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.
Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.
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
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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
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Cyclin Dependent Kinase Inhibitor 2D (CDKN2D) Antibody (abx005030-20) at Hölzel-Diagnostika
Human Cyclin-dependent kinase 4,CDK-4 ELISA Kit - Brogen Medikal Teknolojileri
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Inhibition of the CDK2 and Cyclin A complex leads to autophagic degradation of CDK2 in cancer cells. | Nat Commun;13(1): 2835,...
Expression of cyclin d1 and its association with disease characteristics in bladder cancer. | Gudas Lab
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The Potential Role of Cyclin-Dependent Kinase 5 in Focal Cortical Dysplasia - Nuffield Department of Clinical Neurosciences
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CCND2 gene: MedlinePlus Genetics
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Anticancer effect of involucrasin A on colorectal cancer cells by modulating the Akt/MDM2/p53 pathway
- Cyclins function as regulators of CDK kinases. (nih.gov)
- 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)
- Cyclin-dependent kinases regulate lysosomal degradation of hypoxia-inducible factor 1α to promote cell-cycle progression. (bvsalud.org)
- 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)
- 2007) The cyclin-dependent kinase inhibitor Dacapo promotes replication licensing during Drosophila endocycles. (nih.gov)
- 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)
- Here we report that HIF-1α physically and functionally interacts with cyclin-dependent kinase 1 (Cdk1) and Cdk2. (bvsalud.org)
- 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)
- 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)
- 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)
- 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)
MRNA and protein2
- Synthesis and Structure-Activity relationships of cyclin-dependent kinase 11 inhibitors based on a diaminothiazole scaffold. (harvard.edu)
- High-throughput screening identified the imidazo[1,2-a]pyridine and bisanilinopyrimidine series as inhibitors of the cyclin-dependent kinase CDK4. (rcsb.org)
- Cyclin-dependent kinase (CDK) 4/6 inhibitors have become standard of care in the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative metastatic breast cancer. (nih.gov)
- The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. (hoelzel-biotech.com)
- 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. (nih.gov)
- 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)
- Tumor necrosis factor-alpha regulates cyclin-dependent kinase 5 activity during pain signaling through transcriptional activation of p35. (nih.gov)
- 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)
- Cyclin D1 protein expression was significantly higher in non-invasive tumors than in muscle-invasive UCB (p=0.016). (cornell.edu)
- Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (nih.gov)
- 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)
- This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. (nih.gov)
- 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)
- 2006) Bruno inhibits the expression of mitotic cyclins during the prophase I meiotic arrest of Drosophila oocytes. (nih.gov)
- Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1. (harvard.edu)
- Defects in the expression of cyclin D1, a key cell-cycle regulator, have been implicated in progression of various types of cancer. (cornell.edu)
- 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)
- Detects human Cyclin B1 in direct ELISAs and Western blots. (rndsystems.com)
- Mutational mapping of receptor reveals a requirement for its N-terminal region and DNA binding domain to support cyclin G2 repression. (nih.gov)
- 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)
- 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)
- Cyclin D1 expression, cell proliferation, and clonal persistence characterize primary cutaneous CD4(+) small or medium T-cell lymphoproliferative disorder. (nih.gov)
- 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)
- The requirement for cyclin E in c-Myc overexpressing breast cancers. (harvard.edu)
- 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)
- Cyclin B1 in Human Squamous Cell Carcinoma. (rndsystems.com)
- Detection of Cyclin B1 in K562 Human Cell Line by Flow Cytometry. (rndsystems.com)
- Cyclin A transcription is cell cycle regulated and induced by cell proliferative signals. (cnrs.fr)
- A cyclin-dependent kinase that forms a complex with CYCLIN C and is active during the G1 PHASE of the CELL CYCLE. (musc.edu)
- Activation of cyclin-dependent 5 mediates orofacial mechanical hyperalgesia. (nih.gov)
- 1. The clinical significance of cyclin B1 (CCNB1) in invasive breast cancer with emphasis on its contribution to lymphovascular invasion development. (nih.gov)
- 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)
- 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)
- A specific band was detected for Cyclin B1 at approximately 52 kDa (as indicated). (rndsystems.com)
- 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)