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Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, deletion and activation of results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and... 
CELLCYCLE | SIGNALING | EPITHELIAL-MESENCHYMAL TRANSITION | ONCOGENIC K-RAS | CANCER-CELLS | SUPPRESSOR | GENE | ONCOLOGY | SRC | KINASE INHIBITOR | EXPRESSION PROFILES | MUTATIONS | TUMORIGENESIS | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer | Index Medicus
Journal Article
by Burk, Robert D and Chen, Zigui and Saller, Charles and Tarvin, Katherine and Carvalho, Andre L and Scapulatempo-Neto, Cristovam and Silveira, Henrique C and Fregnani, José H and Creighton, Chad J and Anderson, Matthew L and Castro, Patricia and Wang, Sophia S and Yau, Christina and Benz, Christopher and Gordon Robertson, A and Mungall, Karen and Lim, Lynette and Bowlby, Reanne and Sadeghi, Sara and Brooks, Denise and Sipahimalani, Payal and Mar, Richard and Ally, Adrian and Clarke, Amanda and Mungall, Andrew J and Tam, Angela and Lee, Darlene and Chuah, Eric and Schein, Jacqueline E and Tse, Kane and Kasaian, Katayoon and Ma, Yussanne and Marra, Marco A and Mayo, Michael and Balasundaram, Miruna and Thiessen, Nina and Dhalla, Noreen and Carlsen, Rebecca and Moore, Richard A and Holt, Robert A and Jones, Steven J. M and Wong, Tina and Pantazi, Angeliki and Parfenov, Michael and Kucherlapati, Raju and Hadjipanayis, Angela and Seidman, Jonathan and Kucherlapati, Melanie and Ren, Xiaojia and Xu, Andrew W and Yang, Lixing and Park, Peter J and Lee, Semin and Rabeno, Brenda and Huelsenbeck-Dill, Lori and Borowsky, Mark and Cadungog, Mark and Iacocca, Mary and Petrelli, Nicholas and Swanson, Patricia and Ojesina, Akinyemi I and Ojesina, Akinyemi I and Ojesina, Akinyemi I and Le, Xuan and Sandusky, George and Adebamowo, Sally N and Akeredolu, Teniola and Adebamowo, Clement and Reynolds, Sheila M and Shmulevich, Ilya and Shelton, Candace and Crain, Daniel and Mallery, David and Curley, Erin and Gardner, Johanna and Penny, Robert and Morris, Scott and Shelton, Troy and Liu, Jia and Lolla, Laxmi and Chudamani, Sudha and Wu, Ye and Birrer, Michael and McLellan, Michael D and Bailey, Matthew H and Miller, Christopher A and Wyczalkowski, Matthew A and Fulton, Robert S and Fronick, Catrina C and Lu, Charles and Mardis, Elaine R and Appelbaum, Elizabeth L and Schmidt, Heather K and Fulton, Lucinda A and Cordes, Matthew G and Li, Tiandao and Ding, Li and Wilson, Richard K and Rader, Janet S and Behmaram, Behnaz and ... and Canc Genome Atlas Res Network and Eli &Edythe L. Broad Institute of Massachusetts Institute of Technology &Harvard University and Research Institute at Nationwide Children's Hospital and University of Alabama at Birmingham and McDonnell Genome Institute at Washington University and Washington University in St Louis and University of Wisconsin School of Medicine &Public Health and National Hospital, Abuja, Nigeria and Baylor College of Medicine and Barretos Cancer Hospital and Indiana University School of Medicine and Ontario Tumour Bank, The Ottawa Hospital and Massachusetts General Hospital and University of New Mexico Health Sciences Center and National Institute on Deafness &Other Communication Disorders and University of North Carolina at Chapel Hill and Buck Institute for Research on Aging and Cancer Genome Atlas Research Network and Medical College of Wisconsin and University of Abuja Teaching Hospital and University of Oklahoma Health Sciences Center and Institute of Human Virology and St Joseph's Candler Health System and University of Pittsburgh and University of Texas MD Anderson Cancer Center and National Cancer Institute and Montefiore Medical Center and University of Southern California and Institute for Systems Biology and University of Washington and Analytical Biological Services and Harvard Medical School and National Human Genome Research Institute and Memorial Sloan Kettering Cancer Center and Medical University of South Carolina and Ontario Tumour Bank, London Health Sciences Centre and SRA International and University of Kansas Medical Center and University of Lausanne and ILSbio, LLC and University of Bergen and University of California, Irvine and Canada's Michael Smith Genome Sciences Centre and International Genomics Consortium and Oregon Health &Science University and NantOmics and Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University and University of São Paulo, Ribeir ão Preto Medical School and HudsonAlpha Institute for Biotechnology and Albert Einstein College of Medicine and Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center and National Institute of Environmental Health Sciences and Van Andel Research Institute and Ontario Tumour Bank, Ontario Institute for Cancer Research and University of California Santa Cruz and Beckman Research Institute of City of Hope and Leidos Biomedical and Helen F. Graham Cancer Center &Research Institute at Christiana Care Health Services and The Cancer Genome Atlas Research Network
Nature, ISSN 0028-0836, 03/2017, Volume 543, Issue 7645, pp. 378 - 384
Cervical cancer remains one of the leading causes of cancer-related deaths worldwide. Here we report the extensive molecular characterization of 228 primary... 
TRANSCRIPTION FACTORS | BREAST-CANCER | TO-MESENCHYMAL TRANSITION | ACCURATE | DNA METHYLATION | RNA-SEQ | MULTIDISCIPLINARY SCIENCES | 14-3-3-SIGMA | RESISTANCE | EXPRESSION | SIGNATURE | Receptors, Transforming Growth Factor beta - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Carcinoma, Squamous Cell - genetics | Genomics | Humans | APOBEC-1 Deaminase - genetics | Phosphatidylinositol 3-Kinases - metabolism | Molecular Targeted Therapy | Caspase 8 - genetics | Mitogen-Activated Protein Kinase Kinases - metabolism | Human papillomavirus 16 - isolation & purification | Female | Adenocarcinoma - genetics | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | PTEN Phosphohydrolase - genetics | Signal Transduction | Programmed Cell Death 1 Ligand 2 Protein - genetics | Protein-Serine-Threonine Kinases - genetics | Uterine Cervical Neoplasms - drug therapy | RNA, Long Noncoding - genetics | Receptor, ErbB-3 - genetics | Transcription Factors - genetics | Uterine Cervical Neoplasms - genetics | Virus Integration | B7-H1 Antigen - genetics | Receptors, Transforming Growth Factor beta - metabolism | HLA-A Antigens - genetics | Proteomics | Mutation | Keratins - genetics | Human papillomavirus 16 - genetics | Uterine Cervical Neoplasms - classification | Causes of | Care and treatment | Genetic aspects | Gene mutations | Health aspects | Cervical cancer | Human papillomavirus | Gynecology | Molecular biology | Cancer therapies | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 02/2012, Volume 482, Issue 7385, pp. 419 - 422
Journal Article
Nature Genetics, ISSN 1061-4036, 02/2015, Volume 47, Issue 3, pp. 250 - 256
Resistance to RAF-and MEK-targeted therapy is a major clinical challenge(1-4). RAF and MEK inhibitors are initially but only transiently effective in some but... 
COLON-CANCER | SURVIVAL | LUNG | ACTIVATION | INHIBITION | MELANOMA | SIGNALING PATHWAY | TRANSCRIPTION | GENETICS & HEREDITY | BRAF | KRAS | Humans | Molecular Targeted Therapy | Phosphoproteins - metabolism | Gene Knockdown Techniques | Heterografts | MAP Kinase Signaling System - genetics | HEK293 Cells | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins B-raf - metabolism | MAP Kinase Kinase Kinases - genetics | Protein-Serine-Threonine Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Phosphoproteins - genetics | Mice, SCID | HT29 Cells | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Genes, ras | Antimitotic agents | Gene mutations | Genetic aspects | Research | Antineoplastic agents | Drug resistance | Health aspects | Thyroid cancer | Lung cancer | Colorectal cancer | Melanoma | Kinases | Charitable foundations | Cancer therapies | Design of experiments | Tumors | Index Medicus
Journal Article
BMC Genomics, ISSN 1471-2164, 05/2015, Volume 16, Issue 1, pp. 386 - 386
Background: The mitogen-activated protein kinase (MAPK) cascade consists of three types of reversibly phosphorylated kinases, namely, MAPK, MAPK kinase... 
MAPKKK | Abiotic stress | MAPKK | Biotic stress | Cucumis sativus | MAPK | Plant hormones | PROTEIN-KINASE GENE | ARABIDOPSIS-THALIANA | SATIVUS | CASCADE | PLANT-RESISTANCE | SIGNALING PATHWAY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | SEQUENCE | GENETICS & HEREDITY | BRASSICA-NAPUS L | EXPRESSION | RICE | Gene Duplication | Mitogen-Activated Protein Kinase Kinases - genetics | Genomics | Molecular Sequence Data | Cucumis sativus - genetics | Gene Expression Profiling | Cucumis sativus - physiology | Phylogeny | Promoter Regions, Genetic - genetics | Mitogen-Activated Protein Kinases - chemistry | MAP Kinase Kinase Kinases - chemistry | Mitogen-Activated Protein Kinase Kinases - metabolism | MAP Kinase Signaling System - genetics | Conserved Sequence | Transcription, Genetic | Protein-Serine-Threonine Kinases - metabolism | Multigene Family - genetics | Protein Structure, Tertiary | Amino Acid Sequence | Genome, Plant - genetics | MAP Kinase Kinase Kinases - genetics | Stress, Physiological - genetics | Protein-Serine-Threonine Kinases - genetics | Chromosome Mapping | MAP Kinase Kinase Kinases - metabolism | Cucumis sativus - growth & development | Amino Acid Motifs | Mitogen-Activated Protein Kinase Kinases - chemistry | Sequence Alignment | MAP Kinase Signaling System - drug effects | Cucumis sativus - cytology | Mitogen-Activated Protein Kinases - genetics | Protein-Serine-Threonine Kinases - chemistry | Plant Growth Regulators - pharmacology | Evolution, Molecular | Mitogen-Activated Protein Kinases - metabolism | Hardiness | Genetic aspects | Plants | Properties | Protein kinases | Identification and classification | Cucumbers | Amino acids | Mitogens | Index Medicus
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 129, Issue 7, pp. 1415 - 1426
Protein kinases control cellular decision processes by phosphorylating specific substrates. Thousands of in vivo phosphorylation sites have been identified,... 
CELLBIO | ACTIVATION | DNA-DAMAGE RESPONSE | 53BP1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | SPECTROMETRY-BASED PROTEOMICS | ATM | EUKARYOTIC PROTEINS | PROTEIN-PHOSPHORYLATION | MASS-SPECTROMETRY | SIGNALING NETWORKS | CELL BIOLOGY | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | DNA Repair Enzymes - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | CDC2 Protein Kinase - metabolism | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Cell Cycle Proteins - genetics | DNA Damage - genetics | Proteomics - methods | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | CDC2 Protein Kinase - genetics | Computational Biology - methods | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Repressor Proteins - genetics | Ataxia Telangiectasia Mutated Proteins | Binding Sites - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Glycogen Synthase Kinase 3 - genetics | Signal Transduction - physiology | Software | Tumor Suppressor p53-Binding Protein 1 | Index Medicus
Journal Article
The Plant Cell, ISSN 1040-4651, 6/2011, Volume 23, Issue 6, pp. 2440 - 2455
Recognition of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern recognition receptors (PRRs) constitutes an important layer of... 
Leaves | Receptors | Phenotypes | Cell death | Antibodies | Innate immunity | Ligands | Plants | Seedlings | Plant cells | BACTERIAL ELICITOR FLAGELLIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | QUALITY-CONTROL | CELL-DEATH | PROTEIN COMPLEX | PLANT SCIENCES | CELL BIOLOGY | PERONOSPORA-PARASITICA | MOLECULAR-PATTERNS | PERCEPTION | PLANT IMMUNITY | BAK1 | PATTERN-RECOGNITION RECEPTORS | Protein Kinases - metabolism | Protein Kinases - genetics | Arabidopsis - enzymology | Plant Diseases - immunology | Peptides - genetics | Arabidopsis - immunology | Molecular Sequence Data | Multienzyme Complexes - metabolism | Recombinant Fusion Proteins - metabolism | Pseudomonas syringae - pathogenicity | Arabidopsis Proteins - metabolism | Peptides - metabolism | Amino Acid Sequence | Arabidopsis Proteins - genetics | Signal Transduction | Protein-Serine-Threonine Kinases - genetics | Pseudomonas syringae - immunology | Multienzyme Complexes - genetics | Arabidopsis Proteins - immunology | Immunity, Innate | Arabidopsis - genetics | Oomycetes - pathogenicity | Arabidopsis - microbiology | Oomycetes - immunology | Protein-Serine-Threonine Kinases - immunology | Arabidopsis thaliana | Plant physiology | Peptides | Plant immunology | Physiological aspects | Research | Phosphotransferases | Index Medicus | s | peronospora-parasitica | cell-death | quality-control | pattern-recognition receptors | bacterial elicitor flagellin | bak1 | protein complex | plant immunity | molecular-patterns | perception
Journal Article