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humans (596) 596
sp1 transcription factor - metabolism (531) 531
animals (476) 476
sp3 transcription factor (421) 421
promoter regions, genetic (407) 407
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dna-binding proteins - metabolism (363) 363
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gene expression regulation, enzymologic (43) 43
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1. Full Text Betulinic acid inhibits prostate cancer growth through inhibition of specificity protein transcription factors
by Chintharlapalli, Sudhakar and Papineni, Sabitha and Ramaiah, Shashi K and Safe, Stephen
Cancer Research, ISSN 0008-5472, 03/2007, Volume 67, Issue 6, pp. 2816 - 2823
Betulinic acid is a pentacyclic triterpene natural product initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal... 
PROXIMAL PROMOTER | NITRIC-OXIDE PRODUCTION | ONCOLOGY | NATURAL-PRODUCTS | PANCREATIC-CANCER | DRUG DISCOVERY | HUMAN-MELANOMA CELLS | DOWN-REGULATION | FACTOR EXPRESSION | 2-CYANO-3,12-DIOXOOLEAN-1,9-DIEN-28-OIC ACID | SYNTHETIC OLEANANE | Prostatic Neoplasms - metabolism | Sp3 Transcription Factor - antagonists & inhibitors | Triterpenes - pharmacology | Microtubule-Associated Proteins - genetics | Apoptosis - drug effects | Microtubule-Associated Proteins - metabolism | Humans | Male | Sp1 Transcription Factor - metabolism | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Neoplasm Proteins - metabolism | Promoter Regions, Genetic - drug effects | Sp1 Transcription Factor - antagonists & inhibitors | Liver - drug effects | Neoplasm Proteins - genetics | Prostatic Neoplasms - drug therapy | Sp3 Transcription Factor - metabolism | Prostatic Neoplasms - blood supply | Prostatic Neoplasms - pathology | Inhibitor of Apoptosis Proteins | Cell Growth Processes - drug effects | Liver - metabolism | Sp3 Transcription Factor - genetics | Sp Transcription Factors - antagonists & inhibitors | Angiogenesis Inhibitors - pharmacology | Sp Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Sp4 Transcription Factor - metabolism | Animals | Mice, Nude | Neovascularization, Pathologic - drug therapy | Cell Line, Tumor | Mice | Proteasome Endopeptidase Complex - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Sp4 Transcription Factor - antagonists & inhibitors | Sp4 Transcription Factor - genetics
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2. Full Text Sp1 transcription factor: A long-standing target in cancer chemotherapy
by Vizcaíno, Carolina and Mansilla, Sylvia and Portugal, José
Pharmacology and Therapeutics, ISSN 0163-7258, 08/2015, Volume 152, pp. 111 - 124
Sp1 (specificity protein 1) is a well-known member of a family of transcription factors that also includes Sp2, Sp3 and Sp4, which are implicated in an ample... 
Anticancer drugs | Transcription factors | Prognosis | Sp1 | Targeted therapy | Sp3 | PANCREATIC-CANCER | DOWN-REGULATION | FACTOR EXPRESSION | DNA-BINDING ACTIVITY | BREAST-CANCER | PHARMACOLOGY & PHARMACY | TOLFENAMIC ACID | NF-KAPPA-B | TUMOR-GROWTH | ENDOTHELIAL GROWTH-FACTOR | GENE-TRANSCRIPTION | Neoplasms - metabolism | Gene Targeting - methods | Promoter Regions, Genetic | Humans | Gene Expression Regulation, Neoplastic | Sp1 Transcription Factor - metabolism | Antineoplastic Agents - administration & dosage | Neoplasms - therapy | Animals | Neoplasms - genetics | Sp1 Transcription Factor - genetics | Binding Sites - physiology | Drug Delivery Systems - methods | Index Medicus
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3. Full Text Aspirin Inhibits Colon Cancer Cell and Tumor Growth and Downregulates Specificity Protein (Sp) Transcription Factors
by Pathi, Satya and Jutooru, Indira and Chadalapaka, Gayathri and Nair, Vijayalekshmi and Lee, Syng-Ook and Safe, Stephen
PLoS ONE, ISSN 1932-6203, 10/2012, Volume 7, Issue 10, p. e48208
Acetylsalicylic acid (aspirin) is highly effective for treating colon cancer patients postdiagnosis; however, the mechanisms of action of aspirin in colon... 
SURVIVAL | ANGIOGENESIS | INDUCED APOPTOSIS | ACETYL SALICYLIC-ACID | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | IN-VIVO | FACTOR EXPRESSION | DEGRADATION | NF-KAPPA-B | ANTIINFLAMMATORY DRUGS | Colonic Neoplasms - genetics | Colonic Neoplasms - drug therapy | Humans | Sp3 Transcription Factor - genetics | Sp Transcription Factors - metabolism | Sp1 Transcription Factor - metabolism | Colonic Neoplasms - metabolism | Xenograft Model Antitumor Assays | Sp4 Transcription Factor - metabolism | Animals | Sp1 Transcription Factor - genetics | Mice, Nude | Female | Aspirin - therapeutic use | Cell Proliferation - drug effects | Mice | Sp Transcription Factors - genetics | Aspirin - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Gene Expression Regulation, Neoplastic - genetics | Sp3 Transcription Factor - metabolism | Sp4 Transcription Factor - genetics | Care and treatment | Aspirin | RNA | Growth | B cells | DNA binding proteins | Prevention | Colon cancer | Genetic research | Salicylates | Vascular endothelial growth factor | Apoptosis | Cancer | Tumors | Salts | Transcription factors | Bcl-2 protein | Genes | Colorectal cancer | Acetylsalicylic acid | Cyclin D1 | Anticancer properties | Proteins | β-catenin | Cell growth | Xenografts | Physiology | Inhibition | Colon | Salicylic acid | Immunoglobulins | RNA-mediated interference | Caspase | Pharmacology | Survivin | Gene expression | Metabolism | Sp1 protein | Zinc | Studies | Sodium salicylate | Acids | Ribonucleic acids | Sodium | Phenols | Antitumor activity | Sulfate | Zinc sulfate
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4. Full Text The role of Sp1 and Sp3 in normal and cancer cell biology
by Li, Lin and Davie, James R
Annals of Anatomy, ISSN 0940-9602, 2010, Volume 192, Issue 5, pp. 275 - 283
Sp1 and Sp3 are transcription factors expressed in all mammalian cells. These factors are involved in regulating the transcriptional activity of genes... 
Sp1 | Sp3 and chromatin remodeling | DIHYDROPYRIMIDINE DEHYDROGENASE | ANATOMY & MORPHOLOGY | TRANSCRIPTION FACTOR SP1 | DOWN-REGULATION | HUMAN GASTRIC-CANCER | ELEMENT HALF-SITE | FACTOR-BINDING | ESTROGEN-RECEPTOR-ALPHA | GENE-EXPRESSION | HISTONE DEACETYLASE INHIBITORS | GROWTH-FACTOR EXPRESSION | Sp3 Transcription Factor - physiology | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Chromatin Assembly and Disassembly | Sp1 Transcription Factor - chemistry | Sp1 Transcription Factor - metabolism | Sp3 Transcription Factor - chemistry | DNA-Binding Proteins - chemistry | DNA-Binding Proteins - metabolism | Transcription, Genetic | Sp1 Transcription Factor - physiology | Sp3 Transcription Factor - metabolism
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5. Full Text Sp1: Emerging roles—Beyond constitutive activation of TATA-less housekeeping genes
by Wierstra, Inken
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 2008, Volume 372, Issue 1, pp. 1 - 13
Cell proliferation | Sp1 | SREBP-1 | Mediator | Smad | Tumorigenesis | Transcription factor | TAF4 | Synergism | p53 | RNA-POLYMERASE-II | transcription factor | DNA-BINDING DOMAIN | HISTONE DEACETYLASE INHIBITOR | cell proliferation | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION FACTOR SP1 | ACCELERATES TUMOR-FORMATION | COFACTOR COMPLEX CRSP | PROTEASOME-DEPENDENT DEGRADATION | BIOPHYSICS | synergism | tumorigenesis | mediator | C-MYC PROMOTER | NF-KAPPA-B | ENDOTHELIAL GROWTH-FACTOR | Cell Proliferation | Humans | Sp3 Transcription Factor - genetics | Transcriptional Activation | Sp1 Transcription Factor - metabolism | Animals | Sp1 Transcription Factor - genetics | Cell Transformation, Neoplastic - genetics | TATA Box | Burkitt Lymphoma - genetics | Huntington Disease - genetics | Mice | Protein Processing, Post-Translational | Sp1 Transcription Factor - physiology | Sp3 Transcription Factor - metabolism
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6. Full Text Sp1/Sp3 transcription factors regulate hallmarks of megakaryocyte maturation and platelet formation and function
by Meinders, Marjolein and Kulu, Divine I and van de Werken, Harmen J. G and Hoogenboezem, Mark and Janssen, Hans and Brouwer, Rutger W. W and van Ijcken, Wilfred F. J and Rijkers, Erik-Jan and Demmers, Jeroen A. A and Krüger, Imme and van den Berg, Timo K and Suske, Guntram and Gutiérrez, Laura and Philipsen, Sjaak
Blood, ISSN 0006-4971, 2015, Volume 125, Issue 12, pp. 1957 - 1967
Sp1 and Sp3 belong to the specificity proteins (Sp)/Kruppel-like transcription factor family. They are closely related, ubiquitously expressed, and recognize... 
LIGHT-CHAIN KINASE | INHERITED THROMBOCYTOPENIAS | FACTOR SP3 | MUTATION | MICE | HEMATOLOGY | PROPLATELET FORMATION | GATA1 | AGGREGATION | GPIB-IX-V | RUNX1 | Naphthalenes - chemistry | Signal Transduction | Sp3 Transcription Factor - genetics | Proteome | Sp1 Transcription Factor - metabolism | Thrombocytopenia - metabolism | Mice, Knockout | Platelet Aggregation | Transcription Factors - metabolism | Lectins, C-Type - metabolism | Animals | Flow Cytometry | Azepines - chemistry | Sp1 Transcription Factor - genetics | Spleen - metabolism | Blood Platelets - cytology | Blood Platelets - metabolism | Bone Marrow - metabolism | Platelet Membrane Glycoproteins - metabolism | Mice | Megakaryocytes - cytology | Sp3 Transcription Factor - metabolism
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7. Full Text High Glucose Increases Angiopoietin-2 Transcription in Microvascular Endothelial Cells through Methylglyoxal Modification of mSin3A
by Dachun Yao and Tetsuya Taguchi and Takeshi Matsumura and Richard Pestell and Diane Edelstein and Ida Giardino and Guntram Suske and Naila Rabbani and Paul J. Thornalley and Vijay P. Sarthy and Hans-Peter Hammes and Michael Brownlee
Journal of Biological Chemistry, ISSN 0021-9258, 10/2007, Volume 282, Issue 42, pp. 31038 - 31045
Methylglyoxal is a highly reactive dicarbonyl degradation product formed from triose phosphates during glycolysis. Methylglyoxal forms stable adducts primarily... 
DIABETIC-RETINOPATHY | ACTIVATION | ADVANCED GLYCATION | SP1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | O-GLYCOSYLATION | MICE | 3 MAJOR PATHWAYS | EXPRESSION | HYPERGLYCEMIC DAMAGE | GLYOXALASE-I | Tumor Necrosis Factor-alpha - metabolism | Transcription, Genetic - drug effects | Kidney - pathology | Sweetening Agents - metabolism | Angiopoietin-2 - genetics | Protein Processing, Post-Translational - genetics | Diabetes Mellitus, Experimental - genetics | N-Acetylglucosaminyltransferases - genetics | Glycolysis - drug effects | Acetylglucosamine - metabolism | Glycolysis - genetics | Pyruvaldehyde - metabolism | Kidney - metabolism | Diabetic Angiopathies - pathology | Protein Processing, Post-Translational - drug effects | Arginine - genetics | Intercellular Adhesion Molecule-1 - biosynthesis | Vascular Cell Adhesion Molecule-1 - genetics | Response Elements - genetics | Diabetes Mellitus, Experimental - metabolism | Diabetic Angiopathies - genetics | Repressor Proteins - metabolism | Sp3 Transcription Factor - metabolism | Diabetic Angiopathies - metabolism | Sweetening Agents - pharmacology | Endothelial Cells - metabolism | Gene Expression Regulation - genetics | Sp3 Transcription Factor - genetics | Angiopoietin-2 - biosynthesis | Repressor Proteins - genetics | Glucose - pharmacology | Acetylglucosamine - genetics | N-Acetylglucosaminyltransferases - metabolism | Gene Expression Regulation - drug effects | Tumor Necrosis Factor-alpha - pharmacology | Animals | Intercellular Adhesion Molecule-1 - genetics | Diabetes Mellitus, Experimental - pathology | Glucose - metabolism | Vascular Cell Adhesion Molecule-1 - biosynthesis | Mice | Endothelial Cells - pathology | Arginine - metabolism | Cell Line, Transformed
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8. Full Text Histone deacetylase inhibitors inhibit rhabdomyosarcoma by reactive oxygen species-dependent targeting of specificity protein transcription factors
by Hedrick, Erik and Crose, Lisa and Linardic, Corinne M and Safe, Stephen
Molecular Cancer Therapeutics, ISSN 1535-7163, 09/2015, Volume 14, Issue 9, pp. 2143 - 2153
The two major types of rhabdomyosarcoma (RMS) are predominantly diagnosed in children, namely embryonal (ERMS) and alveolar (ARMS) RMS, and patients are... 
SURVIVAL | INVASION | CANCER CELL | INTERGROUP RHABDOMYOSARCOMA | ONCOLOGY | CURCUMIN | DOWN-REGULATION | MICRORNAS | FACTOR SP1 EXPRESSION | TUMOR-GROWTH | CHILDREN | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Down-Regulation | Humans | Rhabdomyosarcoma - metabolism | Sp1 Transcription Factor - metabolism | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Sp4 Transcription Factor - metabolism | Animals | Cell Line, Tumor | Histone Deacetylase Inhibitors - pharmacology | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Sp3 Transcription Factor - metabolism | Disease Models, Animal | HDAC inhibitors | cMyc | Sp transcription factors | ZBTBs | ROS
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9. Full Text The p65 subunit of NF-κB inhibits COL1A1 gene transcription in human dermal and scleroderma fibroblasts through its recruitment on promoter by protein interaction with transcriptional activators (c-Krox, Sp1, and Sp3)
by Beauchef, Gallic and Bigot, Nicolas and Kypriotou, Magdalini and Renard, Emmanuelle and Porée, Benoît and Widom, Russell and Dompmartin-Blanchere, Anne and Oddos, Thierry and Maquart, François-Xavier and Demoor, Magali and Boumediene, Karim and Galera, Philippe
Journal of Biological Chemistry, ISSN 0021-9258, 01/2012, Volume 287, Issue 5, pp. 3462 - 3478
Transcriptional mechanisms regulating type I collagen genes expression in physiopathological situations are not completely known. In this study, we have... 
HEPATIC STELLATE CELLS | TGF-BETA | PROCOLLAGEN MESSENGER-RNA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH-FACTOR BETA | BINDING SITES | NECROSIS-FACTOR-ALPHA | I COLLAGEN GENE | TNF-ALPHA | DEPENDENT MECHANISM | REPRESSES TRANSCRIPTION | Scleroderma, Localized - metabolism | Humans | Child, Preschool | Male | Sp1 Transcription Factor - metabolism | Transcription Factor RelA - genetics | DNA-Binding Proteins - metabolism | Collagen Type I - genetics | Adult | Transcription, Genetic | Child | Sp3 Transcription Factor - metabolism | Fibroblasts - metabolism | Dermis - metabolism | Response Elements | Gene Expression Regulation - genetics | Sp3 Transcription Factor - genetics | Scleroderma, Localized - pathology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Fibroblasts - pathology | Transcription Factors - metabolism | Collagen Type I - biosynthesis | Sp1 Transcription Factor - genetics | Transcription Factor RelA - metabolism | Dermis - pathology | Gene Regulation | Gene Transcription | Transcription Factors, Sp3, c-Krox | Sp1 | Collagen | Fibrosis | Type I Collagen | Skin | Scleroderma | Fibroblast | Nuclear Factor-κB
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10. Full Text The Transcription Factor Sp3 Cooperates with HDAC2 to Regulate Synaptic Function and Plasticity in Neurons
by Yamakawa, Satoko and Yamakawa, Hidekuni and Cheng, Jemmie and Penney, Jay and Gao, Fan and Rueda, Richard and Wang, Jun and Kritskiy, Oleg and Gjoneska, Elizabeta and Tsai, Li-Huei
Cell Reports, ISSN 2211-1247, 08/2017, Volume 20, Issue 6, pp. 1319 - 1334
The histone deacetylase HDAC2, which negatively regulates synaptic gene expression and neuronal plasticity, is upregulated in Alzheimer’s disease (AD) patients... 
memory | synaptic plasticity | Alzheimer’s disease | epigenetic | histone acetylation | Alzheimer's disease | HISTONE DEACETYLASE 2 | HIPPOCAMPUS | MEMORY | CHROMATIN | ALZHEIMERS-DISEASE | IN-VIVO | GENE-EXPRESSION | INHIBITORS | P25/CDK5 | PROMOTER | CELL BIOLOGY | Epigenesis, Genetic | Memory | Sp3 Transcription Factor - genetics | Male | Animals | Histones - genetics | Neuronal Plasticity | Alzheimer Disease - metabolism | Neurons - physiology | Female | Histone Code | Mice | Neurons - metabolism | Histone Deacetylase 2 - metabolism | Histones - metabolism | Sp3 Transcription Factor - metabolism
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11. Full Text p53-Dependent Nestin Regulation Links Tumor Suppression to Cellular Plasticity in Liver Cancer
by Tschaharganeh, Darjus F and Xue, Wen and Calvisi, Diego F and Evert, Matthias and Michurina, Tatyana V and Dow, Lukas E and Banito, Ana and Katz, Sarah F and Kastenhuber, Edward R and Weissmueller, Susann and Huang, Chun-Hao and Lechel, Andre and Andersen, Jesper B and Capper, David and Zender, Lars and Longerich, Thomas and Enikolopov, Grigori and Lowe, Scott W
Cell, ISSN 0092-8674, 07/2014, Volume 158, Issue 3, pp. 579 - 592
The p53 tumor suppressor coordinates a series of antiproliferative responses that restrict the expansion of malignant cells, and as a consequence, is lost or... 
INTERMEDIATE-FILAMENT NESTIN | STEM-CELLS | INTRAHEPATIC CHOLANGIOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | GROWTH | DEDIFFERENTIATION | MICE | DIFFERENTIATION | EXPRESSION | P53 | CELL BIOLOGY | Prognosis | Humans | Tumor Suppressor Protein p53 - metabolism | Sp1 Transcription Factor - metabolism | Hepatocytes - metabolism | Nestin - metabolism | Animals | Cell Transformation, Neoplastic | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Liver Neoplasms - pathology | Transcription, Genetic | Mice | Sp3 Transcription Factor - metabolism | Carcinoma, Hepatocellular - metabolism | Medical colleges | Liver cancer | Tumor proteins | Intermediate filament proteins
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