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1. Full Text Targeting cyclin-dependent kinase 1 (CDK1) but not CDK4/6 or CDK2 is selectively lethal to MYC-dependent human breast cancer cells
by Kang, Jian and Sergio, C M and Sutherland, Robert L and Musgrove, Elizabeth A
BMC Cancer, ISSN 1471-2407, 01/2014, Volume 14, Issue 1, p. 32
Background: Although MYC is an attractive therapeutic target for breast cancer treatment, it has proven challenging to inhibit MYC directly, and clinically... 
Cyclin-dependent kinase | Breast cancer | Synthetic lethality | MYC | SYNTHETIC LETHAL | C-MYC | TUMOR-CELLS | PROLIFERATION | INHIBITION | GENE | ONCOLOGY | PATHWAY | ESTROGEN | THERAPEUTIC TARGETS | EXPRESSION | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Phosphorylation | Cyclin-Dependent Kinase 4 - genetics | Humans | Molecular Targeted Therapy | CDC2 Protein Kinase - metabolism | Dose-Response Relationship, Drug | Breast Neoplasms - enzymology | Transfection | Bcl-2-Like Protein 11 | RNA Interference | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Cell Death - drug effects | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins - metabolism | Cyclin-Dependent Kinase 2 - metabolism | CDC2 Protein Kinase - genetics | CDC2 Protein Kinase - antagonists & inhibitors | Cyclin-Dependent Kinase 6 - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase 2 - genetics | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Apoptosis Regulatory Proteins - metabolism | Breast Neoplasms - genetics | Signal Transduction - drug effects | Breast Neoplasms - pathology | Cell Cycle Checkpoints - drug effects | Cell Line, Tumor | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Care and treatment | Patient outcomes | Cancer cells | Physiological aspects | Genetic aspects | Research | Risk factors | Cyclins
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2. Full Text TEAD4-YAP interaction regulates tumoral growth by controlling cell-cycle arrest at the G1 phase
by Takeuchi, Shin and Kasamatsu, Atsushi and Yamatoji, Masanobu and Nakashima, Dai and Endo-Sakamoto, Yosuke and Koide, Nao and Takahara, Toshikazu and Shimizu, Toshihiro and Iyoda, Manabu and Ogawara, Katsunori and Shiiba, Masashi and Tanzawa, Hideki and Uzawa, Katsuhiro
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 04/2017, Volume 486, Issue 2, pp. 385 - 390
TEA domain transcription factor 4 (TEAD4), which has critical functions in the process of embryonic development, is expressed in various cancers. However, the... 
TEA domain transcription factor 4 | Human oral squamous cell carcinoma | Yes-associated protein (YAP) | TARGET | BIOMARKER | BIOCHEMISTRY & MOLECULAR BIOLOGY | HIPPO PATHWAY | YAP | FAMILY | BIOPHYSICS | DNA | PROGNOSTIC MARKER | EXPRESSION | RNA, Small Interfering - genetics | Cell Proliferation | Carcinoma, Squamous Cell - pathology | Humans | Middle Aged | Male | Cyclin E - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Muscle Proteins - antagonists & inhibitors | Transcription, Genetic | Mouth Neoplasms - genetics | Cyclin-Dependent Kinase 2 - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Cyclin-Dependent Kinase 2 - genetics | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Muscle Proteins - genetics | Cell Nucleus - genetics | Cyclin D1 - genetics | Mouth Neoplasms - surgery | Cell Line, Tumor | RNA, Small Interfering - metabolism | Cyclin D1 - metabolism | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Cyclin-Dependent Kinase 4 - genetics | Gene Expression Regulation, Neoplastic | Carcinoma, Squamous Cell - surgery | Mouth Neoplasms - metabolism | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Muscle Proteins - metabolism | G1 Phase Cell Cycle Checkpoints | Female | Cyclin-Dependent Kinase 6 - genetics | Transcription Factors - antagonists & inhibitors | Phosphoproteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Adaptor Proteins, Signal Transducing - genetics | Mouth Neoplasms - pathology | Aged | Cyclin E - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Immunohistochemistry | Medical colleges | Embryonic development | Squamous cell carcinoma | Growth | Analysis | DNA polymerases | Genetic transcription | Health aspects | Development and progression | TRANSCRIPTION FACTORS | CHAIN REACTIONS | BIOLOGICAL MARKERS | CELL PROLIFERATION | CELL CYCLE | INTERACTIONS | 60 APPLIED LIFE SCIENCES | PLANT GROWTH
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3. Full Text Epigenetic Silencing Mediates Mitochondria Stress-Induced Longevity
by Schroeder, Elizabeth A and Raimundo, Nuno and Shadel, Gerald S
Cell Metabolism, ISSN 1550-4131, 06/2013, Volume 17, Issue 6, pp. 954 - 964
Reactive oxygen species (ROS) play complex roles in aging, having both damaging effects and signaling functions. Transiently elevating mitochondrial stress,... 
YEAST | INCREASING OXIDATIVE STRESS | CHRONOLOGICAL LIFE-SPAN | DNA-DAMAGE CHECKPOINT | HISTONE H3 | TRANSCRIPTION | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | SACCHAROMYCES-CEREVISIAE | RAD53 KINASE | TELOMERES | CELL BIOLOGY | Reactive Oxygen Species - metabolism | Saccharomyces cerevisiae - genetics | Intracellular Signaling Peptides and Proteins - metabolism | DNA Repair - genetics | Checkpoint Kinase 2 - metabolism | Saccharomyces cerevisiae - metabolism | Checkpoint Kinase 2 - genetics | Mitochondria - genetics | Cell Cycle Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | Epigenomics | Silent Information Regulator Proteins, Saccharomyces cerevisiae - metabolism | Cell Cycle Proteins - metabolism | Gene Silencing | Protein-Serine-Threonine Kinases - genetics | Mitochondria - metabolism | Signal Transduction - genetics | Longevity - genetics | Saccharomyces cerevisiae Proteins - genetics | Histone Demethylases - metabolism | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | DNA Damage | Longevity - physiology | Automated teller machines | Mitochondrial DNA | Phosphotransferases | Genes | Protein binding
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4. Full Text Prognostic Mutations in Myelodysplastic Syndrome after Stem-Cell Transplantation
by Lindsley, R. Coleman and Saber, Wael and Mar, Brenton G and Redd, Robert and Wang, Tao and Haagenson, Michael D and Grauman, Peter V and Hu, Zhen-Huan and Spellman, Stephen R and Lee, Stephanie J and Verneris, Michael R and Hsu, Katharine and Fleischhauer, Katharina and Cutler, Corey and Antin, Joseph H and Neuberg, Donna and Ebert, Benjamin L
The New England Journal of Medicine, ISSN 0028-4793, 02/2017, Volume 376, Issue 6, pp. 536 - 547
Prognostic systems for myelodysplasia rely on clinical factors, but particular genetic lesions can influence relapse rate, overall survival, and... 
MEDICINE, GENERAL & INTERNAL | PREDISPOSITION | CLONAL HEMATOPOIESIS | CLASSIFICATION | CHECKPOINT | ACUTE MYELOID-LEUKEMIA | SHWACHMAN-DIAMOND-SYNDROME | TP53 | SOMATIC MUTATIONS | OVARIAN-CARCINOMA | BLOOD | ras Proteins - genetics | Prognosis | Humans | Middle Aged | Janus Kinase 2 - genetics | Hematopoietic Stem Cell Transplantation | Transplantation, Homologous | Proteins - genetics | Young Adult | Genes, p53 | Myelodysplastic Syndromes - therapy | DNA Mutational Analysis | Adolescent | Survival Analysis | Adult | Myelodysplastic Syndromes - genetics | Mutation | Protein Phosphatase 2C - genetics | Transplantation Conditioning | Child | Complications and side effects | Gene mutations | Patient outcomes | Stem cells | Transplantation | Diagnosis | Research | Myelodysplastic syndromes | Phenotypes | Transplants & implants | Pathogenesis | p53 Protein | Janus kinase 2 | Stem cell transplantation | Bone marrow | Patients | Myelodysplastic syndrome | Hemopoiesis
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5. Full Text Evolution of neoantigen landscape during immune checkpoint blockade in non-small cell lung cancer
by Anagnostou, Valsamo and Smith, Kellie N and Forde, Patrick M and Niknafs, Noushin and Bhattacharya, Rohit and White, James and Zhang, Theresa and Adleff, Vilmos and Phallen, Jillian and Wali, Neha and Hruban, Carolyn and Guthrie, Violeta B and Rodgers, Kristen and Naidoo, Jarushka and Kang, Hyunseok and Sharfman, William and Georgiades, Christos and Verde, Franco and Illei, Peter and Li, Qing Kay and Gabrielson, Edward and Brock, Malcolm V and Zahnow, Cynthia A and Baylin, Stephen B and Scharpf, Robert B and Brahmer, Julie R and Karchin, Rachel and Pardoll, Drew M and Velculescu, Victor E
Cancer Discovery, ISSN 2159-8274, 03/2017, Volume 7, Issue 3, pp. 264 - 276
Immune checkpoint inhibitors have shown significant therapeutic responses against tumors containing increased mutation-associated neoantigen load. We have... 
METASTATIC MELANOMA | CTLA-4 BLOCKADE | ONCOLOGY | PD-1 BLOCKADE | COLORECTAL-CANCER | PANCREATIC-CANCER | COPY NUMBER | RESISTANCE | MUTATIONS | SEQUENCING DATA | TUMOR PURITY | Humans | Middle Aged | Antibodies, Monoclonal - therapeutic use | Lung Neoplasms - pathology | Male | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Ipilimumab - pharmacology | Immunotherapy | Ipilimumab - therapeutic use | Janus Kinase 1 - genetics | Adult | Female | Receptors, Antigen, T-Cell - immunology | Cell Cycle Checkpoints - immunology | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Receptors, Antigen, T-Cell - metabolism | Antigens, Neoplasm - immunology | Carcinoma, Non-Small-Cell Lung - genetics | Antibodies, Monoclonal - pharmacology | Janus Kinase 2 - genetics | CTLA-4 Antigen - genetics | Drug Resistance, Neoplasm - immunology | Lung Neoplasms - therapy | CTLA-4 Antigen - immunology | Antineoplastic Agents, Immunological - pharmacology | Carcinoma, Non-Small-Cell Lung - immunology | Carcinoma, Non-Small-Cell Lung - therapy | Drug Resistance, Neoplasm - genetics | Lung Neoplasms - immunology | Antineoplastic Agents, Immunological - therapeutic use | Cell Cycle Checkpoints - drug effects | Receptors, Antigen, T-Cell - genetics | Mutation | Programmed Cell Death 1 Receptor - immunology | Programmed Cell Death 1 Receptor - genetics | Cohort Studies
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6. Full Text A study of over 35,000 women with breast cancer tested with a 25‐gene panel of hereditary cancer genes
by Buys, Saundra S and Sandbach, John F and Gammon, Amanda and Patel, Gayle and Kidd, John and Brown, Krystal L and Sharma, Lavania and Saam, Jennifer and Lancaster, Johnathan and Daly, Mary B
Cancer, ISSN 0008-543X, 05/2017, Volume 123, Issue 10, pp. 1721 - 1730
BACKGROUND As panel testing becomes more common in clinical practice, it is important to understand the prevalence and trends associated with the pathogenic... 
breast cancer type 1 (BRCA1) | panel testing | hereditary breast and ovarian cancer | BRCA2 | triple‐negative breast cancer | triple-negative breast cancer | POPULATION | BRCA2 MUTATIONS | METAANALYSIS | VARIANTS | RISK | PREVALENCE | FAMILY-HISTORY | SUSCEPTIBILITY GENES | COWDEN-SYNDROME | ONCOLOGY | DIFFUSE GASTRIC-CANCER | Genetic Testing | Age Factors | Humans | Middle Aged | Young Adult | Checkpoint Kinase 2 - genetics | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Genes, BRCA2 | Adult | Female | RNA Helicases - genetics | Lynch Syndrome II - genetics | Neoplastic Syndromes, Hereditary - genetics | Genes, BRCA1 | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Hereditary Breast and Ovarian Cancer Syndrome - genetics | DNA-Binding Proteins - genetics | Fanconi Anemia Complementation Group Proteins | Breast Neoplasms - genetics | Triple Negative Breast Neoplasms - genetics | Aged | Ataxia Telangiectasia Mutated Proteins - genetics | Ubiquitin-Protein Ligases - genetics | Women | Breast cancer | Genetic aspects | Diagnosis | Research | Health aspects | Oncogenes | BRCA2 protein | CHK2 protein | Threonine | BRCA1 protein | Genes | Health risks | Protein C | Genetic screening | DNA helicase | Men | Breast | Ataxia | Ataxia telangiectasia mutated protein | Protein-serine/threonine kinase | Mutation | Health risk assessment | Age | Cancer
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7. Full Text Cancer susceptibility gene mutations in individuals with colorectal cancer
by Yurgelun, Matthew B and Kulke, Matthew H and Fuchs, Charles S and Allen, Brian A and Uno, Hajime and Hornick, Jason L and Ukaegbu, Chinedu I and Brais, Lauren K and McNamara, Philip G and Mayer, Robert J and Schrag, Deborah and Meyerhardt, Jeffrey A and Ng, Kimmie and Kidd, John and Singh, Nanda and Hartman, Anne-Renee and Wenstrup, Richard J and Syngal, Sapna
Journal of Clinical Oncology, ISSN 0732-183X, 04/2017, Volume 35, Issue 10, pp. 1086 - 1095
Purpose Hereditary factors play an important role in colorectal cancer (CRC) risk, yet the prevalence of germline cancer susceptibility gene mutations in... 
BREAST-CANCER | STATEMENT | LYNCH-SYNDROME | BRCA2 MUTATIONS | TASK-FORCE | ONCOLOGY | FREQUENCY | RISK | MUTYH-ASSOCIATED POLYPOSIS | FOUNDER MUTATIONS | AMERICAN SOCIETY | Colorectal Neoplasms - genetics | Humans | Middle Aged | Colorectal Neoplasms - chemistry | DNA-Binding Proteins - analysis | Male | Tumor Suppressor Protein p53 - genetics | Young Adult | Checkpoint Kinase 2 - genetics | DNA Mutational Analysis | Tumor Suppressor Proteins - genetics | Epithelial Cell Adhesion Molecule - genetics | Aged, 80 and over | Genes, BRCA2 | Germ-Line Mutation | Adult | Female | Genes, BRCA1 | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Adenomatous Polyposis Coli Protein - genetics | Genetic Predisposition to Disease | Colorectal Neoplasms, Hereditary Nonpolyposis - genetics | Mismatch Repair Endonuclease PMS2 - analysis | DNA Glycosylases - genetics | Penetrance | MutS Homolog 2 Protein - genetics | DNA-Binding Proteins - genetics | Genes, p16 | MutL Protein Homolog 1 - analysis | MutL Protein Homolog 1 - genetics | Aged | MutS Homolog 2 Protein - analysis | Mismatch Repair Endonuclease PMS2 - genetics | Epithelial Cell Adhesion Molecule - analysis | Genetic epidemiology | Epidemiology | Hereditary Cancers & Genetic Predisposition | ORIGINAL REPORTS
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8. Full Text HDAC1 and HDAC2 integrate checkpoint kinase phosphorylation and cell fate through the phosphatase-2A subunit PR130
by Göder, Anja and Emmerich, Claudia and Nikolova, Teodora and Kiweler, Nicole and Schreiber, Maria and Kühl, Toni and Imhof, Diana and Christmann, Markus and Heinzel, Thorsten and Schneider, Günter and Krämer, Oliver H
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 764 - 17
Checkpoint kinases sense replicative stress to prevent DNA damage. Here we show that the histone deacetylases HDAC1/HDAC2 sustain the phosphorylation of the... 
CANCER-CELLS | RIBONUCLEOTIDE REDUCTASE | CHK1 | TUMOR SUPPRESSION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | GENOME INTEGRITY | DOUBLE-STRAND BREAKS | HISTONE DEACETYLASE INHIBITORS | REPLICATION FORK COLLAPSE | ATR | Phosphorylation | Ataxia Telangiectasia Mutated Proteins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Tumor Suppressor Protein p53 - genetics | CDC2 Protein Kinase - metabolism | Checkpoint Kinase 2 - metabolism | Checkpoint Kinase 2 - genetics | Protein-Tyrosine Kinases - genetics | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Histone Deacetylase 1 - genetics | Histone Deacetylase 2 - genetics | CDC2 Protein Kinase - genetics | Cell Cycle Proteins - metabolism | Gene Expression Regulation | Protein Phosphatase 2 - genetics | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Checkpoint Kinase 1 - metabolism | Cell Cycle | Protein Phosphatase 2 - metabolism | Histone Deacetylase 2 - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Checkpoint Kinase 1 - genetics | Histone Deacetylase 1 - metabolism | Histone deacetylase | p53 Protein | DNA damage | Serine | Homologous recombination | Homology | Dephosphorylation | Kinases | Phosphatase | Damage prevention | Cell fate | Cell cycle | Inhibition | HDAC2 protein | Null cells | Deoxyribonucleic acid--DNA | Stresses | CHK2 protein | Threonine | Phase transformations | CHK1 protein | Protein-serine/threonine phosphatase | Replication protein A | Protein A | Ablation | Stress | DNA biosynthesis | S phase | Replication | Threonine phosphatase | Phase transition | Tumors | Apoptosis
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9. Full Text CDK4 T172 Phosphorylation Is Central in a CDK7-Dependent Bidirectional CDK4/CDK2 Interplay Mediated by p21 Phosphorylation at the Restriction Point
by Bisteau, Xavier and Paternot, Sabine and Colleoni, Bianca and Ecker, Karin and Coulonval, Katia and de Groote, Philippe and Declercq, Wim and Hengst, Ludger and Roger, Pierre P
PLoS Genetics, ISSN 1553-7390, 05/2013, Volume 9, Issue 5, p. e1003546
Cell cycle progression, including genome duplication, is orchestrated by cyclin-dependent kinases (CDKs). CDK activation depends on phosphorylation of their... 
CYCLIN-DEPENDENT KINASES | MAMMALIAN TARGET | THYROID EPITHELIAL-CELLS | ACTIVATING KINASE | CHEMICAL GENETICS | GENETICS & HEREDITY | SUBCELLULAR-LOCALIZATION | T-LOOP | 2-DIMENSIONAL GEL-ELECTROPHORESIS | PHARMACOLOGICAL INHIBITION | MURINE FIBROBLASTS | Cyclin-Dependent Kinase 2 - metabolism | Phosphorylation | Cyclin-Dependent Kinases - metabolism | p21-Activated Kinases - genetics | Cyclin-Dependent Kinase 4 - genetics | HCT116 Cells | Humans | Cyclin-Dependent Kinase 2 - genetics | Cyclin-Dependent Kinase 4 - metabolism | p21-Activated Kinases - metabolism | G1 Phase Cell Cycle Checkpoints - genetics | Protein Binding | Cell Cycle Checkpoints - genetics | Mutation | cdc25 Phosphatases - metabolism | Cyclin-Dependent Kinases - genetics | Physiological aspects | Research | Phosphotransferases | Cell cycle | Medical research | Text editing | Cyclin-dependent kinases | Cell division | Kinases | Cancer
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10. Full Text Cyclin K regulates prereplicative complex assembly to promote mammalian cell proliferation
by Lei, Tingjun and Zhang, Peixuan and Zhang, Xudong and Xiao, Xue and Zhang, Jingli and Qiu, Tong and Dai, Qian and Zhang, Yujun and Min, Ling and Lei, Qian and Yin, Rutie and Ding, Ping and Li, Ni and Qu, Yi and Mu, Dezhi and Qin, Jun and Zhu, Xiaofeng and Xiao, Zhi-Xiong and Li, Qintong
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 1876 - 15
The assembly of prereplicative complex (pre-RC) during G1 phase must be tightly controlled to sustain cell proliferation and maintain genomic stability.... 
REPLICATION | INSTABILITY | TERMINAL DOMAIN | RNA | PHOSPHORYLATION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | KINASE | CDK12 | EXPRESSION | CANCER | Genomic Instability | NIH 3T3 Cells | Oncogene Proteins - genetics | RNA, Small Interfering - genetics | Cell Proliferation | Cyclin-Dependent Kinases - metabolism | Humans | Cyclins - genetics | Carcinogenesis - metabolism | Cyclin E - genetics | S Phase Cell Cycle Checkpoints - genetics | Breast Neoplasms - metabolism | Cyclins - metabolism | Female | Cyclin-Dependent Kinases - genetics | Fibroblasts - metabolism | Cyclin-Dependent Kinase 2 - metabolism | Cyclins - antagonists & inhibitors | HCT116 Cells | Mice, Inbred C57BL | Carcinogenesis - genetics | Oncogene Proteins - metabolism | Cyclin-Dependent Kinase 2 - genetics | G1 Phase Cell Cycle Checkpoints - genetics | Carcinogenesis - pathology | G2 Phase Cell Cycle Checkpoints - genetics | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Fibroblasts - cytology | Mice | Cyclin E - metabolism | Primary Cell Culture | RNA, Small Interfering - metabolism | Cyclin-dependent kinase 2 | Cell proliferation | Phosphorylation | Cell growth | Cyclin-dependent kinases | Tumorigenesis | Control stability | Kinases | Assembly | G1 phase
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11. Full Text A Mortalin/HSPA9-Mediated Switch in Tumor-Suppressive Signaling of Raf/MEK/Extracellular Signal-Regulated Kinase
by Pui-Kei Wu and Seung-Keun Hong and Sudhakar Veeranki and Mansi Karkhanis and Dmytro Starenki and Jose A. Plaza and Jong-In Park
Molecular and Cellular Biology, ISSN 0270-7306, 10/2013, Volume 33, Issue 20, pp. 4051 - 4067
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
CANCER-CELLS | BCL-X-L | ACTIVATED PROTEIN-KINASE | MORTALIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | GENE-EXPRESSION | CELL SENESCENCE | ONCOGENE-INDUCED SENESCENCE | P53 | FAMILY | CELL BIOLOGY | Humans | Gene Expression Regulation, Neoplastic | Tumor Suppressor Protein p53 - metabolism | HSP70 Heat-Shock Proteins - genetics | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase 2 - metabolism | Signal Transduction - genetics | Tumor Suppressor Protein p53 - genetics | HSP70 Heat-Shock Proteins - metabolism | MAP Kinase Kinase 1 - genetics | Cell Cycle Checkpoints | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Luciferases | Proto-Oncogene Proteins B-raf - genetics | Cell Death | Cell Line, Tumor | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | MAP Kinase Kinase 2 - genetics | Genes, Reporter | Proto-Oncogene Proteins B-raf - metabolism | Index Medicus
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