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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 | Index Medicus
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2. Full Text miR-375 Is Down-Regulated in Squamous Cervical Cancer and Inhibits Cell Migration and Invasion via Targeting Transcription Factor SP1
by Wang, Fenfen|Li, Yang|Zhou, Jiansong|Xu, Junfen|Peng, Chanjuan|Ye, Feng|Shen, Yuanming|Lu, Weiguo|Wan, Xiaoyun|Xie, Xing
American Journal of Pathology, The, ISSN 0002-9440, 2011, Volume 179, Issue 5, pp. 2580 - 2588
Pelvic lymph node metastases are regarded as the most important risk factor and a predictor of poor prognosis for patients with cervical cancer. Exploration of... 
Pathology | BREAST-CANCER | SURVIVAL | DNA-BINDING | LYMPH-NODE METASTASIS | STAGE | CARCINOMAS | RECEPTOR | PATHOLOGY | IDENTIFICATION | MICRORNA EXPRESSION | HUMAN GASTRIC-CANCER | Gene Expression | Cell Proliferation | G1 Phase Cell Cycle Checkpoints - physiology | Carcinoma, Squamous Cell - metabolism | Down-Regulation | Humans | Middle Aged | MicroRNAs - metabolism | Sp1 Transcription Factor - metabolism | Lymphatic Metastasis | RNA, Neoplasm - metabolism | Cell Movement - genetics | Gene Knockdown Techniques | Uterine Cervical Neoplasms - metabolism | Biomarkers, Tumor - metabolism | Adult | Female | Aged | Tumor Cells, Cultured | Neoplasm Invasiveness - genetics | Index Medicus | Abridged Index Medicus | Regular
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3. Full Text SP1-induced upregulation of the long noncoding RNA TINCR regulates cell proliferation and apoptosis by affecting KLF2 mRNA stability in gastric cancer
by Xu, T.-P and Liu, X.-X and Xia, R and Yin, L and Kong, R and Chen, W.-M and Huang, M.-D and Shu, Y.-Q
Oncogene, ISSN 0950-9232, 03/2015, Volume 34, Issue 45, pp. 5648 - 5661
The long noncoding RNA TINCR shows aberrant expression in human squamous carcinomas. However, its expression and function in gastric cancer remain unclear. We... 
SURVIVAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION FACTOR SP1 | CELL BIOLOGY | NCRNAS | REPRESSION | ONCOLOGY | POOR-PROGNOSIS | GENETICS & HEREDITY | CARCINOMAS | KRUPPEL-LIKE FACTOR-2 | INHIBITORS | HALLMARKS | DECREASED EXPRESSION | RNA-Binding Proteins - genetics | Cell Proliferation | Cytoskeletal Proteins - genetics | Humans | Stomach Neoplasms - metabolism | Sp1 Transcription Factor - metabolism | Stomach Neoplasms - pathology | RNA, Messenger - metabolism | RNA, Neoplasm - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | RNA, Long Noncoding - biosynthesis | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cytoskeletal Proteins - metabolism | Stomach Neoplasms - genetics | Kruppel-Like Transcription Factors - biosynthesis | RNA, Messenger - genetics | RNA, Long Noncoding - genetics | RNA Stability | Sp1 Transcription Factor - genetics | Cell Line, Tumor | RNA, Neoplasm - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Kruppel-Like Transcription Factors - genetics | RNA-Binding Proteins - metabolism | Apoptosis | Cell proliferation | Complications and side effects | Care and treatment | Analysis | Development and progression | Stomach cancer | Proteins | Ribonucleic acid--RNA | Kinases | Gene expression | Cancer therapies | Index Medicus
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4. Full Text MiR-145, miR-133a and miR-133b inhibit proliferation, migration, invasion and cell cycle progression via targeting transcription factor Sp1 in gastric cancer
by Qiu, Tianzhu and Zhou, Xin and Wang, Jian and Du, Yiping and Xu, Jun and Huang, Zebo and Zhu, Wei and Shu, Yongqian and Liu, Ping
FEBS Letters, ISSN 0014-5793, 04/2014, Volume 588, Issue 7, pp. 1168 - 1177
MicroRNAs have recently emerged as key regulators of gastric cancers. Here we found that miR-145, miR-133a and miR-133b were down-regulated in gastric cancer... 
Cell cycle progression | miR-133b | Sp1 | Migration | miR-145 | miR-133a | Proliferation | Gastric cancer | Invasion | SURVIVAL | METASTASIS | MECHANISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | HUMAN GLIOMA | CELL BIOLOGY | BIOPHYSICS | PATHWAY | COLORECTAL-CANCER | GROWTH | EXPRESSION | CARCINOMA | MICRORNA | Stomach Neoplasms - genetics | Cell Proliferation | Neoplasm Invasiveness | Down-Regulation | Humans | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | Sp1 Transcription Factor - metabolism | Stomach Neoplasms - pathology | Cell Cycle Checkpoints | RNA Interference | Sp1 Transcription Factor - genetics | Cell Line, Tumor | MicroRNAs - genetics | 3' Untranslated Regions | Binding Sites | Cell Movement | Development and progression | Stomach cancer | Cell cycle | Cancer | Index Medicus
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5. Full Text Hydrogen Sulfide-Linked Sulfhydration of NF-κB Mediates Its Antiapoptotic Actions
by Sen, Tanusree and Sen, Nilkantha and Paul, Bindu D and Gadalla, Moataz M and Mustafa, Asif K and Xu, Risheng and Kim, Seyun and Snyder, Solomon H
Molecular Cell, ISSN 1097-2765, 01/2012, Volume 45, Issue 1, pp. 13 - 24
Nuclear factor κB (NF-κB) is an antiapoptotic transcription factor. We show that the antiapoptotic actions of NF-κB are mediated by hydrogen sulfide (H S)... 
OXIDATION | APOPTOSIS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | REACTIVITY | CYSTATHIONINE GAMMA-LYASE | DEATH | CYSTEINES | PROTEIN S-NITROSYLATION | SUBUNIT | CELL BIOLOGY | Hydrogen Sulfide - chemistry | Gene Expression Regulation | Cystathionine gamma-Lyase - metabolism | Sp1 Transcription Factor - metabolism | Cystathionine gamma-Lyase - physiology | NF-kappa B - chemistry | Animals | Transcription Factor RelA - metabolism | NF-kappa B - physiology | Transcription Factor RelA - chemistry | Tumor Necrosis Factor-alpha - physiology | Mice | Apoptosis - physiology | Cystathionine gamma-Lyase - genetics | Index Medicus
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6. 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, pp. e48208 - 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 | Index Medicus
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7. Full Text miR‐124, ‐128, and ‐137 Orchestrate Neural Differentiation by Acting on Overlapping Gene Sets Containing a Highly Connected Transcription Factor Network
by Santos, Márcia C. T and Tegge, Allison N and Correa, Bruna R and Mahesula, Swetha and Kohnke, Luana Q and Qiao, Mei and Ferreira, Marco A. R and Kokovay, Erzsebet and Penalva, Luiz O. F
STEM CELLS, ISSN 1066-5099, 01/2016, Volume 34, Issue 1, pp. 220 - 232
The ventricular‐subventricular zone harbors neural stem cells (NSCs) that can differentiate into neurons, astrocytes, and oligodendrocytes. This process... 
miR‐137 | Transcription factors | Sp1 | miR‐128 | mir‐124 | Neural stem cell | miRNA | Differentiation | Neurogenesis | miR-137 | mir-124 | miR-128 | STEM-CELLS | MICRORNA REGULATION | ADULT NEUROGENESIS | PANCREATIC-CANCER | NEURONAL DIFFERENTIATION | FACTOR EXPRESSION | SUBVENTRICULAR ZONE | CELL & TISSUE ENGINEERING | CELL BIOLOGY | MESSENGER-RNA | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | REGULATORY NETWORKS | HEMATOLOGY | HUNTINGTONS-DISEASE | Cell Proliferation | Humans | Gene Expression Regulation | Oligonucleotides, Antisense - metabolism | MicroRNAs - metabolism | Neurons - cytology | Sp1 Transcription Factor - metabolism | Gene Regulatory Networks | Neural Stem Cells - cytology | Cell Differentiation - genetics | Cell Self Renewal | Animals | Sequence Analysis, RNA | Transfection | Mice | MicroRNAs - genetics | Neurons - metabolism | Genome | RNA | Analysis | Genes | Stem cells | Genetic research | Genetic aspects | Cell differentiation | Index Medicus
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8. Full Text Orphan nuclear receptor NR4A1 regulates transforming growth factor-beta signaling and fibrosis
by Palumbo-Zerr, K and Zerr, P and Distler, A and Fliehr, J and Mancuso, R and Huang, JG and Mielenz, D and Tomcik, M and Furnrohr, BG and Scholtysek, C and Dees, C and Beyer, C and Kronke, G and Metzger, D and Distler, O and Schettl, G and Distler, JHW
NATURE MEDICINE, ISSN 1078-8956, 02/2015, Volume 21, Issue 2, pp. 150 - 158
Mesenchymal responses are an essential aspect of tissue repair. Failure to terminate this repair process correctly, however, results in fibrosis and organ... 
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | MECHANISMS | MODEL | MURINE | CELL BIOLOGY | RESPONSES | REPAIR | DIFFERENTIATION | EXPRESSION | Liver - pathology | Skin - cytology | Skin - metabolism | Humans | Middle Aged | Scleroderma, Systemic - pathology | Co-Repressor Proteins - metabolism | Male | Sp1 Transcription Factor - metabolism | Wound Healing | Case-Control Studies | Idiopathic Pulmonary Fibrosis - metabolism | Young Adult | Adult | Female | Lung - metabolism | Repressor Proteins - metabolism | Skin - pathology | Fibroblasts - metabolism | Lung - pathology | Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics | Signal Transduction | Liver Cirrhosis, Alcoholic - pathology | Liver - metabolism | Scleroderma, Systemic - metabolism | Cells, Cultured | Mice, Knockout | Histone Demethylases - metabolism | Animals | Adolescent | Fibrosis | Idiopathic Pulmonary Fibrosis - pathology | Nuclear Receptor Subfamily 4, Group A, Member 1 - metabolism | Aged | Mice | Nuclear Receptor Subfamily 4, Group A, Member 1 - physiology | Liver Cirrhosis, Alcoholic - metabolism | Transforming Growth Factor beta - metabolism | Histone Deacetylase 1 - metabolism | Index Medicus
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9. Full Text Involvement of p300/CBP and epigenetic histone acetylation in TGF-β1-mediated gene transcription in mesangial cells
by Yuan, Hang and Reddy, Marpadga A and Sun, Guangdong and Lanting, Linda and Wang, Mei and Kato, Mitsuo and Natarajan, Rama
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 2013, Volume 304, Issue 5, pp. F601 - F613
Transforming growth factor-β1 (TGF-β1)-induced expression of plasminogen activator inhibitor-1 (PAI-1) and p21 in renal mesangial cells (MCs) plays a major... 
p300/CBP | Diabetic nephropathy | TGF-β1 | Histone acetylation | Mesangial cell | Promoter Regions, Genetic | Diabetic Nephropathies - metabolism | Epigenesis, Genetic | Kidney Glomerulus - drug effects | Rats | Diabetic Nephropathies - genetics | Smad Proteins - genetics | Sp1 Transcription Factor - metabolism | Mesangial Cells - metabolism | Mesangial Cells - drug effects | p300-CBP Transcription Factors - metabolism | Animals | Histones - genetics | Plasminogen Activator Inhibitor 1 - metabolism | Sp1 Transcription Factor - genetics | p300-CBP Transcription Factors - genetics | Kidney Glomerulus - metabolism | Transcription, Genetic | Mice | Acetylation | Histones - metabolism | Plasminogen Activator Inhibitor 1 - genetics | Smad Proteins - metabolism | Transforming Growth Factor beta1 - pharmacology | Index Medicus | p300 | CBP | mesangial cell | diabetic nephropathy | histone acetylation
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10. Full Text STAT3 interacts with Skp2/p27/p21 pathway to regulate the motility and invasion of gastric cancer cells
by Wei, Zheng and Jiang, Xian and Jiang, Hongchi and Qiao, Haiquan and Zhai, Bo and Zhang, Lianfeng and Zhang, Qiang and Wu, Yuanhong and Sun, Xueying
Cellular Signalling, ISSN 0898-6568, 04/2013, Volume 25, Issue 4, pp. 931 - 938
The interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway mediates cell proliferation and migration.... 
Cytoskeleton | p27 | Gastric cancer | Migration | Invasion | Signal transducer and activator of transcription 3 | P27 | ACTIVATION | E-CADHERIN | BETA-CATENIN | INTERLEUKIN-6 | IL-6 | CELL BIOLOGY | OVEREXPRESSION | SIGNALING PATHWAY | SKP2 | CARCINOMA | CYCLE | Up-Regulation | Cell Proliferation | Cadherins - metabolism | Humans | Stomach Neoplasms - metabolism | Sp1 Transcription Factor - metabolism | Stomach Neoplasms - pathology | rhoA GTP-Binding Protein - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Matrix Metalloproteinase 9 - metabolism | Microtubules - metabolism | RNA Interference | Janus Kinase 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Focal Adhesion Kinase 1 - metabolism | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Signal Transduction | Matrix Metalloproteinase 2 - metabolism | Down-Regulation | S-Phase Kinase-Associated Proteins - metabolism | Cell Adhesion | GPI-Linked Proteins - metabolism | Cell Line, Tumor | STAT3 Transcription Factor - antagonists & inhibitors | Stathmin - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - genetics | RNA, Small Interfering - metabolism | Phosphates | Enzymes | Cysteine | Analysis | Fluorescein | Cancer cells | Tubulins | Stomach cancer | Enzyme-linked immunosorbent assay | Cancer | Index Medicus
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11. Full Text Myocardin-related transcription factor-A complexes activate type I collagen expression in lung fibroblasts
by Luchsinger, Larry L and Patenaude, Cassandra A and Smith, Barbara D and Layne, Matthew D
Journal of Biological Chemistry, ISSN 0021-9258, 12/2011, Volume 286, Issue 51, pp. 44116 - 44125
Pulmonary fibrosis is characterized by the excessive deposition of a collagen-rich extracellular matrix. The accumulation of collagen within the lung... 
COL1A2 TRANSCRIPTION | POSTTRANSCRIPTIONAL REGULATION | GROWTH-FACTOR-BETA | IDIOPATHIC PULMONARY FIBROSIS | EXTRACELLULAR-MATRIX SYNTHESIS | DEPENDENT TRANSCRIPTION | MECHANICAL-STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | MUSCLE ALPHA-ACTIN | SERUM-RESPONSE FACTOR | Cell Line | Oncogene Proteins, Fusion - metabolism | Collagen Type I - metabolism | Serum Response Factor - metabolism | Humans | Gene Expression Regulation | Rats | Sp1 Transcription Factor - metabolism | DNA-Binding Proteins - metabolism | Transcription Factors - metabolism | Animals | Trans-Activators - metabolism | Cell Differentiation | Lung - metabolism | Mice | Fibroblasts - metabolism | Index Medicus | Gene Regulation | MRTF-A | Co-regulator Transcription | Sp1 | Collagen | Myofibroblast | Fibrosis | Serum-response Factor (SRF)
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12. Full Text HTERT promotes tumor angiogenesis by activating VEGF via interactions with the Sp1 transcription factor
by Liu, Ning and Ding, Deqiang and Hao, Wanyu and Yang, Fan and Wu, Xiaoying and Wang, Miao and Xu, Xiaoling and Ju, Zhenyu and Liu, Jun-Ping and Song, Zhangfa and Shay, Jerry W and Guo, Yunliang and Cong, Yu-Sheng
Nucleic Acids Research, ISSN 0305-1048, 10/2016, Volume 44, Issue 18, pp. 8693 - 8703
Angiogenesis is recognized as an important hallmark of cancer. Although telomerase is thought to be involved in tumor angiogenesis, the evidence and underlying... 
GLIOBLASTOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | B-DEPENDENT TRANSCRIPTION | PROLIFERATION | HALLMARKS | TELOMERASE REVERSE-TRANSCRIPTASE | EXPRESSION | CELL | HUMAN CANCER | ENDOTHELIAL GROWTH-FACTOR | Stomach Neoplasms - genetics | Promoter Regions, Genetic | Protein Binding - genetics | Cell Proliferation | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Mice, Inbred C57BL | Gene Expression Regulation, Neoplastic | Sp1 Transcription Factor - metabolism | Up-Regulation - genetics | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Carcinogenesis - metabolism | Stomach Neoplasms - blood supply | Carcinogenesis - pathology | Animals | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Telomerase - metabolism | Transcription, Genetic | Neovascularization, Pathologic - metabolism | HeLa Cells | Neovascularization, Physiologic | Index Medicus | Gene regulation, Chromatin and Epigenetics
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13. Full Text Triptolide-induced cell death in Pancreatic cancer is mediated by O-GlcNAc modification of transcription factor Sp1
by Banerjee, Sulagna and Sangwan, Veena and McGinn, Olivia and Chugh, Rohit and Dudeja, Vikas and Vickers, Selwyn M and Saluja, Ashok K
Journal of Biological Chemistry, ISSN 0021-9258, 11/2013, Volume 288, Issue 47, pp. 33927 - 33938
Pancreatic cancer, the fourth most prevalent cancer-related cause of death in the United States, is a disease with a dismal survival rate of 5% 5 years after... 
PATHWAYS | APOPTOSIS | ACTIVATION | ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | Pancreatic Cancer | KAPPA-B | O-GlcNAc | N-ACETYLGLUCOSAMINE TRANSFERASE | Heat Shock Protein | Minnelide | IN-VITRO | INHIBITION | Sp1 | Triptolide | Pancreas | TUMOR-GROWTH | EXPRESSION | Pancreatic Neoplasms - metabolism | Humans | Cell Survival - genetics | N-Acetylglucosaminyltransferases - genetics | Antineoplastic Agents, Alkylating - pharmacology | NF-kappa B - metabolism | Sp1 Transcription Factor - metabolism | Glycosylation - drug effects | Neoplasm Proteins - metabolism | Acetylglucosamine - metabolism | Heat Shock Transcription Factors | DNA-Binding Proteins - metabolism | Pancreatic Neoplasms - drug therapy | Cell Nucleus - metabolism | Epoxy Compounds - pharmacology | Cell Death - genetics | Cell Nucleus - pathology | Cell Death - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Neoplasm Proteins - genetics | Active Transport, Cell Nucleus - genetics | Gene Expression Regulation, Neoplastic - genetics | HSP70 Heat-Shock Proteins - biosynthesis | Diterpenes - pharmacology | Cell Survival - drug effects | Pancreatic Neoplasms - pathology | HSP70 Heat-Shock Proteins - genetics | Pancreatic Neoplasms - genetics | Signal Transduction - genetics | Transcription Factors - genetics | Acetylglucosamine - genetics | DNA-Binding Proteins - genetics | Down-Regulation - drug effects | Down-Regulation - genetics | N-Acetylglucosaminyltransferases - metabolism | Transcription Factors - metabolism | Phenanthrenes - pharmacology | Cell Nucleus - genetics | NF-kappa B - genetics | Signal Transduction - drug effects | Sp1 Transcription Factor - genetics | Active Transport, Cell Nucleus - drug effects | Cell Line, Tumor | N-Acetylglucosaminyltransferases - antagonists & inhibitors | Index Medicus | Molecular Bases of Disease
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