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1. Full Text A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer
by Ng, King Pan and Hillmer, Axel M and Chuah, Charles T. H and Juan, Wen Chun and Ko, Tun Kiat and Teo, Audrey S. M and Ariyaratne, Pramila N and Takahashi, Naoto and Sawada, Kenichi and Fei, Yao and Soh, Sheila and Lee, Wah Heng and Huang, John W. J and Allen Jr, John C and Woo, Xing Yi and Nagarajan, Niranjan and Kumar, Vikrant and Thalamuthu, Anbupalam and Poh, Wan Ting and Ang, Ai Leen and Mya, Hae Tha and How, Gee Fung and Yang, Li Yi and Koh, Liang Piu and Chowbay, Balram and Chang, Chia-Tien and Nadarajan, Veera S and Chng, Wee Joo and Than, Hein and Lim, Lay Cheng and Goh, Yeow Tee and Zhang, Shenli and Poh, Dianne and Tan, Patrick and Seet, Ju-Ee and Ang, Mei-Kim and Chau, Noan-Minh and Ng, Quan-Sing and Tan, Daniel S. W and Soda, Manabu and Isobe, Kazutoshi and Nöthen, Markus M and Wong, Tien Y and Shahab, Atif and Ruan, Xiaoan and Cacheux-Rataboul, Valère and Sung, Wing-Kin and Tan, Eng Huat and Yatabe, Yasushi and Mano, Hiroyuki and Soo, Ross A and Chin, Tan Min and Lim, Wan-Teck and Ruan, Yijun and Ong, S Tiong
Nature Medicine, ISSN 1078-8956, 04/2012, Volume 18, Issue 4, pp. 521 - 528
Tyrosine kinase inhibitors (TKIs) elicit high response rates among individuals with kinase-driven malignancies, including chronic myeloid leukemia (CML) and... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | GEFITINIB | BIOCHEMISTRY & MOLECULAR BIOLOGY | EYE DISEASES | CHRONIC MYELOID-LEUKEMIA | CELL BIOLOGY | CELL LUNG-CANCER | FACTOR RECEPTOR EGFR | GROWTH | ACTIVATING MUTATIONS | MUTANT EGFR | Enzyme-Linked Immunosorbent Assay - methods | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Follow-Up Studies | Apoptosis - drug effects | Humans | Middle Aged | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Male | BH3 Interacting Domain Death Agonist Protein - genetics | Dose-Response Relationship, Drug | Protein Isoforms - metabolism | Transfection | Bcl-2-Like Protein 11 | Statistics, Nonparametric | Aged, 80 and over | Apoptosis Regulatory Proteins - genetics | Adult | Female | Gene Expression Regulation, Neoplastic - drug effects | Lung Neoplasms - genetics | Annexins - metabolism | Carcinoma, Non-Small-Cell Lung - genetics | Membrane Proteins - genetics | Gene Frequency | Exons - genetics | Genotype | Proto-Oncogene Proteins - genetics | International Cooperation | Drug Resistance, Neoplasm - genetics | Cell Line, Tumor | Polymorphism, Genetic - genetics | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Cohort Studies | Drug Resistance, Neoplasm - drug effects | Protein Isoforms - genetics | RNA, Small Interfering - metabolism | Sequence Deletion - genetics | Antimitotic agents | Physiological aspects | Protein tyrosine kinase | Dosage and administration | Genetic aspects | Research | Antineoplastic agents | Tumor proteins | Genetic polymorphisms | Inhibitor drugs | Mutation | Kinases | Gene expression | Apoptosis | Polymorphism
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2. Full Text Genetic Association of ARHGAP21 Gene Variant with Mandibular Prognathism
by Perillo, L and Monsurrò, A and Bonci, E and Torella, A and Mutarelli, M and Nigro, V
Journal of Dental Research, ISSN 0022-0345, 4/2015, Volume 94, Issue 4, pp. 569 - 576
Mandibular prognathism (MP) is a recognizable phenotype associated with dentoskeletal class III malocclusion. MP is a complex genetic trait, although familial... 
candidate gene | bone growth | genetic variant | next-generation sequencing | whole-exome sequencing | class III malocclusion | PROTEIN | ANNEXIN-II | FILAMIN | IDENTIFICATION | CHINESE POPULATION | BONE-RESORPTION | CLASS-III MALOCCLUSION | CLONING | DENTISTRY, ORAL SURGERY & MEDICINE | JAPANESE | LINKAGE | Humans | Middle Aged | Male | Malocclusion, Angle Class III - genetics | Mutation, Missense - genetics | Young Adult | Adult | Female | Filamins - genetics | Genetic Linkage - genetics | Child | Glycine - genetics | Genetic Association Studies | Serine - genetics | Genotype | Penetrance | Sequence Analysis, DNA | Homeodomain Proteins - genetics | Meiosis - genetics | Exome - genetics | Annexin A2 - genetics | Bone Morphogenetic Protein 3 - genetics | Pedigree | Adolescent | Aged | Genetic Variation - genetics | GTPase-Activating Proteins - genetics | Genes, Dominant - genetics | Prognathism - genetics
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3. Full Text Novel anti-apoptotic MicroRNAs 582-5p and 363 promote human glioblastoma stem cell survival via direct inhibition of Caspase 3, Caspase 9, and Bim
by Floyd, Desiree Hunt and Zhang, Ying and Dey, Bijan K and Kefas, Benjamin and Breit, Hannah and Marks, Kaitlyn and Dutta, Anindya and Herold-Mende, Christel and Synowitz, Michael and Glass, Rainer and Abounader, Roger and Purow, Benjamin W
PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, p. e96239
Glioblastoma is the most common and lethal primary brain tumor. Tumor initiation and recurrence are likely caused by a sub-population of glioblastoma stem... 
GLIOMA-CELLS | CANCER-CELLS | GROWTH-FACTOR RECEPTOR | NERVOUS-SYSTEM | IN-VITRO | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | AKT PATHWAY | SPHEROID CULTURES | PRECURSOR CELLS | BRAIN-TUMORS | Neoplastic Stem Cells - cytology | Caspase 9 - genetics | Caspase 9 - metabolism | Humans | Caspase 3 - metabolism | Gene Expression Regulation, Neoplastic | Glycoproteins - metabolism | Peptides - genetics | 3' Untranslated Regions - genetics | Cell Survival - genetics | MicroRNAs - metabolism | Antigens, CD - genetics | Antigens, CD - metabolism | Flow Cytometry | Peptides - metabolism | Bcl-2-Like Protein 11 | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | Caspase 3 - genetics | Apoptosis Regulatory Proteins - genetics | Glioblastoma - metabolism | Membrane Proteins - metabolism | Cell Survival - physiology | Glycoproteins - genetics | Proto-Oncogene Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | Proto-Oncogene Proteins - genetics | AC133 Antigen | Apoptosis Regulatory Proteins - metabolism | Cell Line, Tumor | MicroRNAs - genetics | DNA microarrays | MicroRNA | Analysis | Luciferase | Stem cells | Glioblastoma multiforme | Apoptosis | Brain | Flow cytometry | Brain tumors | Brain cancer | Glioblastoma | Fluorescence | Oncology | Biochemistry | Neurosurgery | Caspase-3 | Cancer therapies | Genetics | Cell survival | MiRNA | Caspase | siRNA | Ribonucleic acid--RNA | Survival | Neurology | Brain research | Mutagenesis | 3' Untranslated regions | Cell number | MicroRNAs | Cell lines | Caspase-9 | Neural stem cells | Annexin V | BIM protein | Cancer | Tumors | RNA | Ribonucleic acid
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4. Full Text A Network Model of a Cooperative Genetic Landscape in Brain Tumors
by Bredel, Markus and Scholtens, Denise M and Harsh, Griffith R and Bredel, Claudia and Chandler, James P and Renfrow, Jaclyn J and Yadav, Ajay K and Vogel, Hannes and Scheck, Adrienne C and Tibshirani, Robert and Sikic, Branimir I
JAMA, ISSN 0098-7484, 07/2009, Volume 302, Issue 3, pp. 261 - 275
CONTEXT: Gliomas, particularly glioblastomas, are among the deadliest of human tumors. Gliomas emerge through the accumulation of recurrent chromosomal... 
BREAST-CANCER | EXPRESSION PATTERNS | SURVIVAL | MOLECULAR CLASSIFICATION | CELLS | MEDICINE, GENERAL & INTERNAL | GLIOBLASTOMA | PROSTATE-CANCER | GROWTH | MALIGNANT GLIOMAS | GENOME | Metalloendopeptidases - genetics | RNA-Binding Proteins - genetics | Prognosis | Genes, Neoplasm | Humans | Middle Aged | Brain Neoplasms - pathology | Gene Expression Regulation, Neoplastic | Male | Risk | Cytochromes c - genetics | Genes, myc | Mitochondrial Proteins | Glioma - genetics | Glioma - pathology | Apoptosis Regulatory Proteins - genetics | Female | Brain Neoplasms - mortality | ATPases Associated with Diverse Cellular Activities | Genome-Wide Association Study | Glioma - mortality | Signal Transduction | Proportional Hazards Models | Brain Neoplasms - genetics | Gene Dosage | Annexin A7 - genetics | Hydroxyprostaglandin Dehydrogenases - genetics | Nuclear Proteins | Dosage Compensation, Genetic | Aldo-Keto Reductase Family 1 Member C3 | Epistasis, Genetic | Chromosome Aberrations | Survival Analysis | Models, Genetic | Mutation | 3-Hydroxysteroid Dehydrogenases - genetics | Gliomas | Genetic aspects | Diagnosis | Research | Identification and classification | Oncogenes | Cancer | Neurology | Genetics | Brain cancer | Tumors
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5. Full Text Relationship between the Inflammatory Molecular Profile of Breast Carcinomas and Distant Metastasis Development
by Eiró, Noemí and González, Lucía and González, Luis O and Fernandez-Garcia, Belen and Lamelas, Maria Luz and Marín, Laura and González-Reyes, Salomé and de Casar, José Manuell and Vizoso, Francisco J
PLoS ONE, ISSN 1932-6203, 11/2012, Volume 7, Issue 11, p. e49047
Inflammatory conditions may promote tumor progression and aggressiveness. In previous reports, we found a group of breast cancer tumors characterized by... 
MATRIX METALLOPROTEINASES | CELLS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | HUMAN PAPILLOMA-VIRUS | GROWTH-FACTOR | INHIBITORS | TUMOR-GROWTH | CANCER | EXPRESSION | PROMOTES ANGIOGENESIS | Inflammation - pathology | Interleukin-1 Receptor-Associated Kinases - metabolism | Leukocytes, Mononuclear - metabolism | Interleukin-1 Receptor-Associated Kinases - genetics | Follow-Up Studies | Humans | NF-kappa B - metabolism | Interleukins - metabolism | Breast Neoplasms - metabolism | Interleukins - genetics | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Inflammation - metabolism | Neoplasm Metastasis | Chemokine CCL3 - genetics | Claudin-3 - genetics | Interferon-beta - genetics | Chemokine CCL3 - metabolism | Claudin-3 - metabolism | Female | Carcinoma - pathology | Matrix Metalloproteinase 1 - genetics | Myeloid Differentiation Factor 88 - genetics | Matrix Metalloproteinase 11 - metabolism | Up-Regulation - genetics | Disease Progression | Leukocytes, Mononuclear - pathology | Tissue Inhibitor of Metalloproteinase-1 - genetics | ADAM Proteins - metabolism | Annexin A2 - genetics | Breast Neoplasms - genetics | Interferon-beta - metabolism | NF-kappa B - genetics | Breast Neoplasms - pathology | Matrix Metalloproteinase 11 - genetics | Inflammation - genetics | Carcinoma - genetics | Carcinoma - metabolism | ADAM Proteins - genetics | Matrix Metalloproteinase 1 - metabolism | Annexin A2 - metabolism | Myeloid Differentiation Factor 88 - metabolism | Breast cancer | Inflammation | Prognosis | B cells | Annexins | Analysis | Gene regulation | Metastasis | Matrix metalloproteinase | Tissue inhibitor of metalloproteinase 1 | Metastases | Interleukin 6 | Proteins | Ethics | Angiogenesis | Breast carcinoma | Interleukin 5 | Interleukin 1 | Metalloproteinase | Growth factors | Interstitial collagenase | IRAK protein | ADAMTS-1 protein | Cytokines | Gene expression | Interleukin 17 | Womens health | Medical prognosis | MyD88 protein | Breast | Chemokines | Tumors
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6. Full Text Lineage-specific splicing of a brain-enriched alternative exon promotes glioblastoma progression
by Ferrarese, Roberto and Harsh IV, Griffith R and Yadav, Ajay K and Bug, Eva and Maticzka, Daniel and Reichardt, Wilfried and Dombrowski, Stephen M and Miller, Tyler E and Masilamani, Anie P and Dai, Fangping and Kim, Hyunsoo and Hadler, Michael and Scholtens, Denise M and Yu, Irene L.Y and Beck, Jürgen and Srinivasasainagendra, Vinodh and Costa, Fabrizio and Baxan, Nicoleta and Pfeifer, Dietmar and Von Elverfeldt, Dominik and Backofen, Rolf and Weyerbrock, Astrid and Duarte, Christine W and He, Xiaolin and Prinz, Marco and Chandler, James P and Vogel, Hannes and Chakravarti, Arnab and Rich, Jeremy N and Carro, Maria S and Bredel, Markus
Journal of Clinical Investigation, ISSN 0021-9738, 07/2014, Volume 124, Issue 7, pp. 2861 - 2876
Tissue-specific alternative splicing is critical for the emergence of tissue identity during development, yet the role of this process in malignant... 
PROGENITOR CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | PROTEIN-INTERACTION NETWORKS | STEM-LIKE CELLS | INTEGRATED GENOMIC ANALYSIS | TUMOR-SUPPRESSOR GENE | EXPRESSION ARRAYS | TRACT-BINDING-PROTEIN | FACTOR RECEPTOR GENE | ENDOTHELIAL GROWTH-FACTOR | PRE-MESSENGER-RNA | Receptor, Epidermal Growth Factor - genetics | Alternative Splicing | Exons | Humans | Brain Neoplasms - pathology | MicroRNAs - metabolism | RNA, Messenger - metabolism | Polypyrimidine Tract-Binding Protein - antagonists & inhibitors | RNA, Neoplasm - metabolism | Brain Neoplasms - metabolism | Gene Knockdown Techniques | Receptor, Epidermal Growth Factor - metabolism | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | Cell Transformation, Neoplastic - genetics | Neoplastic Stem Cells - pathology | Glioblastoma - metabolism | Tumor Cells, Cultured | Cell Lineage - genetics | RNA, Messenger - genetics | Brain Neoplasms - genetics | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Heterogeneous-Nuclear Ribonucleoproteins - antagonists & inhibitors | Polypyrimidine Tract-Binding Protein - metabolism | Signal Transduction - genetics | Annexin A7 - genetics | Disease Progression | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Glioblastoma - pathology | RNA, Neoplasm - genetics | Neovascularization, Pathologic - genetics | MicroRNAs - genetics | Polypyrimidine Tract-Binding Protein - genetics | Exon (Molecular genetics) | Neoplastic processes | Tumor suppressor genes | Development and progression | Genetic aspects | Properties | Glioblastoma multiforme | Proteins | Senescence | Genes | Rodents | Brain cancer | Medical prognosis | Colleges & universities | Regulation | Tumorigenesis | Mutation | Tumors | Cancer
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7. Full Text Genetic variations in the p11/tPA/BDNF pathway are associated with post stroke depression
by Liang, Jinfeng and Yue, Yingying and Jiang, Haitang and Geng, Deqin and Wang, Jun and Lu, Jianxin and Li, Shenghua and Zhang, Kezhong and Wu, Aiqin and Yuan, Yonggui
Journal of Affective Disorders, ISSN 0165-0327, 01/2018, Volume 226, pp. 313 - 325
The effects of BDNF on post stroke depression (PSD) may be influenced by genetic variations in intracellular signal transduction pathways, such as the... 
Post stroke depression | Gene | BDNF | Pathway | PSYCHIATRY | NEUROTROPHIC FACTOR | SUSCEPTIBILITY | RISK | RELIABILITY | POSTSTROKE DEPRESSION | MAJOR DEPRESSION | CLINICAL NEUROLOGY | P11 S100A10 | ANNEXIN II TETRAMER | SCALE | Depressive Disorder - genetics | Haplotypes | Brain-Derived Neurotrophic Factor - genetics | Genetic Predisposition to Disease | Gene Frequency | Humans | Middle Aged | Asian Continental Ancestry Group - genetics | Genotype | Male | Receptor, trkB - genetics | Depressive Disorder - etiology | Tissue Plasminogen Activator - genetics | Stroke - genetics | Membrane Glycoproteins - genetics | S100 Proteins - genetics | Annexin A2 - genetics | Epistasis, Genetic | Aged, 80 and over | Adult | Female | Aged | Polymorphism, Single Nucleotide | Genetic research | Cellular signal transduction | Genetic aspects | Genetic polymorphisms | Stroke (Disease) | Depression, Mental
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8. Full Text Endothelial Cell Annexin A2 Regulates Polyubiquitination and Degradation of Its Binding Partner S100A10/p11
by Kai-Li He and Arunkumar B. Deora and Huabao Xiong and Qi Ling and Babette B. Weksler and Ruben Niesvizky and Katherine A. Hajjar
Journal of Biological Chemistry, ISSN 0021-9258, 07/2008, Volume 283, Issue 28, pp. 19192 - 19200
The annexin A2 (A2) heterotetramer, consisting of two copies of A2 and two copies of S100A10/p11, promotes fibrinolytic activity on the surface of vascular... 
COMPLEX | EPITHELIAL-CELLS | CHANNEL | PHOSPHORYLATION | FUNCTIONAL EXPRESSION | P11 PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | POSTTRANSLATIONAL MECHANISM | PLASMINOGEN | UBIQUITIN-PROTEASOME PATHWAY | Protein Binding - genetics | Oncogene Protein pp60(v-src) - metabolism | Tissue Plasminogen Activator - metabolism | Autoantibodies - blood | Humans | Fibrin - genetics | Ubiquitin - metabolism | Tissue Plasminogen Activator - genetics | S100 Proteins - genetics | Fibrinolysin - genetics | Hemorrhage - etiology | Antiphospholipid Syndrome - genetics | Thrombosis - blood | Antiphospholipid Syndrome - blood | Fibrinolysin - metabolism | Hemorrhage - genetics | Endothelial Cells - metabolism | Oncogene Protein pp60(v-src) - genetics | S100 Proteins - metabolism | Hemorrhage - blood | Ubiquitin - genetics | Leukemia, Promyelocytic, Acute - blood | Protein Transport - genetics | Mice, Knockout | Proteasome Endopeptidase Complex - genetics | Animals | Annexin A2 - genetics | Thrombosis - etiology | Fibrinolysis - genetics | Cell Line, Tumor | Leukemia, Promyelocytic, Acute - complications | Mice | Leukemia, Promyelocytic, Acute - genetics | Proteasome Endopeptidase Complex - metabolism | Fibrin - metabolism | Annexin A2 - metabolism | Ubiquitination - genetics
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9. Full Text The tick protein sialostatin L2 binds to annexin A2 and inhibits NLRC4-mediated inflammasome activation
by Wang, Xiaowei and Shaw, Dana K and Sakhon, Olivia S and Snyder, Greg A and Sundberg, Eric J and Santambrogio, Laura and Sutterwala, Fayyaz S and Stephen Dumler, J and Shirey, Kari Ann and Perkins, Darren J and Richard, Katharina and Chagas, Andrezza C and Calvo, Eric and Kopecký, Jan and Kotsyfakis, Michail and Pedra, Joao H.F
Infection and Immunity, ISSN 0019-9567, 06/2016, Volume 84, Issue 6, pp. 1796 - 1805
Tick saliva contains a number of effector molecules that inhibit host immunity and facilitate pathogen transmission. How tick proteins regulate immune... 
SYSTEM | INFECTIOUS DISEASES | NAIP/NLRC4 INFLAMMASOMES | RECOGNITION | BORNE PATHOGENS | DOCKING | SERVER | HUMAN GRANULOCYTIC ANAPLASMOSIS | BACTERIAL LIGANDS | NEEDLE PROTEIN | ANAPLASMA-PHAGOCYTOPHILUM INFECTION | IMMUNOLOGY | Interleukin-18 - immunology | Caspases - immunology | Humans | Ixodes - chemistry | Arachnid Vectors - genetics | Interleukin-1beta - genetics | Ixodes - genetics | Calcium-Binding Proteins - immunology | Protein Isoforms - chemistry | Macrophages - microbiology | Calcium-Binding Proteins - chemistry | Amino Acid Sequence | Apoptosis Regulatory Proteins - immunology | Signal Transduction | Apoptosis Regulatory Proteins - chemistry | Models, Molecular | Recombinant Proteins - chemistry | Arachnid Vectors - immunology | Cystatins - immunology | Annexin A2 - genetics | Immune Evasion | Cystatins - genetics | Escherichia coli - genetics | Cystatins - chemistry | Mice | Interleukin-18 - genetics | Ixodes - immunology | Calcium-Binding Proteins - genetics | Ehrlichiosis - pathology | Caspase 1 - immunology | Anaplasma phagocytophilum - genetics | Annexin A2 - chemistry | Escherichia coli - metabolism | Apoptosis Regulatory Proteins - genetics | Annexin A2 - immunology | Macrophages - immunology | Arachnid Vectors - chemistry | Ehrlichiosis - microbiology | Caspases - genetics | Gene Expression Regulation | Ehrlichiosis - immunology | Interleukin-1beta - immunology | Recombinant Proteins - genetics | Inflammasomes - genetics | Anaplasma phagocytophilum - immunology | Animals | Recombinant Proteins - immunology | Caspase 1 - genetics | Inflammasomes - immunology | Protein Binding | Protein Isoforms - immunology | Protein Isoforms - genetics
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10. Full Text Annexin-like alpha giardins: a new cytoskeletal gene family in Giardia lamblia
by Weiland, Malin E.-L and McArthur, Andrew G and Morrison, Hilary G and Sogin, Mitchell L and Svärd, Staffan G and Teknisk-naturvetenskapliga vetenskapsområdet and Biologiska sektionen and Uppsala universitet and Institutionen för cell- och molekylärbiologi and Mikrobiologi
International Journal for Parasitology, ISSN 0020-7519, 2005, Volume 35, Issue 6, pp. 617 - 626
Through a genome survey and phylogenetic analysis, we have identified and sequenced 14 new coding regions for alpha-giardins in . These proteins are related to... 
Parasite | Cytoskeleton | Giardia | Flagella | Annexin | EARLY-DIVERGING EUKARYOTE | PHYLOGENY | PROTEIN | cytoskeleton | INVITRO | EXCYSTATION | CYST WALL | IDENTIFICATION | GENOME | flagella | parasite | annexin | SEQUENCE | BAYESIAN-INFERENCE | PARASITOLOGY | RNA, Protozoan - genetics | Genes, Protozoan - genetics | Genome, Protozoan | Cytoskeletal Proteins - genetics | Gene Expression Regulation - genetics | RNA, Messenger - genetics | Cytoskeleton - genetics | Molecular Sequence Data | Phylogeny | Epitopes - genetics | Protozoan Proteins - genetics | Genetic Vectors - genetics | Animals | Base Sequence | Reverse Transcriptase Polymerase Chain Reaction - methods | Cloning, Molecular - methods | Giardia lamblia - genetics | Proteins | Messenger RNA | Water quality | Genetic research | Marine biology | Annexins | Marine laboratories | Antigenic determinants | RNA; Protozoan/genetics | Mikrobiologi, immunologi, infektionssjukdomar | Medical and Health Sciences | Reverse Transcriptase Polymerase Chain Reaction/methods | Medicin och hälsovetenskap | Mikrobiologi inom det medicinska området | MEDICINE | Cytoskeleton/genetics | Protozoan Proteins/genetics | Cloning; Molecular/methods | Epitopes/genetics | RNA; Messenger/genetics | Gene Expression Regulation/genetics | Basic Medicine | Cytoskeletal Proteins/genetics | Genome; Protozoan | Microbiology in the medical area | Microbiology, immunology, infectious diseases | MEDICIN | Medicinska och farmaceutiska grundvetenskaper | Genetic Vectors/genetics | Giardia lamblia/genetics | Genes; Protozoan/genetics
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11. Full Text MicroRNA-206 functions as a pleiotropic modulator of cell proliferation, invasion and lymphangiogenesis in pancreatic adenocarcinoma by targeting ANXA2 and KRAS genes
by Keklikoglou, I and Hosaka, K and Bender, C and Bott, A and Koerner, C and Mitra, D and Will, R and Woerner, A and Muenstermann, E and Wilhelm, H and Cao, Y and Wiemann, S and Avdelningen för kardiovaskulär medicin and Medicinska fakulteten and Institutionen för medicin och hälsa and Linköpings universitet
Oncogene, ISSN 0950-9232, 09/2015, Volume 34, Issue 37, pp. 4867 - 4878
Recent advances in cancer biology have emerged important roles for microRNAs (miRNAs) in regulating tumor responses. However, their function in mediating... 
SUPPRESSOR | DUCTAL ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR LYMPHANGIOGENESIS | HUMAN-ENDOTHELIAL-CELLS | CANCER | PROMOTES ANGIOGENESIS | CELL BIOLOGY | ONCOLOGY | GROWTH | GENETICS & HEREDITY | NF-KAPPA-B | TRANSCRIPTION FACTOR | EXPRESSION | Human Umbilical Vein Endothelial Cells | ras Proteins - genetics | Cell Proliferation - genetics | Proto-Oncogene Proteins p21(ras) | Adenocarcinoma - pathology | Neoplasm Invasiveness | Humans | Pancreatic Neoplasms - pathology | Cells, Cultured | Gene Expression Regulation, Neoplastic | Pancreatic Neoplasms - genetics | Proto-Oncogene Proteins - genetics | Mice, SCID | Carcinoma, Pancreatic Ductal - pathology | Carcinoma, Pancreatic Ductal - genetics | Animals | Annexin A2 - genetics | HEK293 Cells | Adenocarcinoma - genetics | Mice | MicroRNAs - genetics | MicroRNAs - physiology | Lymphangiogenesis - genetics | Molecular targeted therapy | MicroRNA | Pancreatic cancer | Innovations | Development and progression | Genetic aspects | Properties | Gene expression | Health aspects | Cancer therapies | MicroRNAs | Genes | Cells | Original | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper
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