Signaling
Cellular signaling involves a cascade of activities that begin with a physical or chemical signal received at the cell's surface.
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0 Guide-Glossary
Signaling
Signal transduction from receptor to cellular activation
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intracellular signaling
While a large number of cell-surface receptors are employed in receiving environmental signals, fine-tuning of signaling relies upon a larger number of intracellular receptors.
Labels: cell-surface receptors, environmental signals, intracellular receptors
| 0 Guide-Glossaryreceptors
Receptor proteins are located in the cytoplasm, cell membrane, or nuclear membrane. Receptors responsible for intercellular signaling are located on the cell surface, while intracellular activities are mediated by cytoplasmic and nuclear receptors.
Biologically active molecules (ligands) exert their physiological effect by activating or inducing 3D conformational changes in receptor proteins, which participate in signal transduction, cellular signaling, gene regulation, cellular proliferation and differentiation, or regulation of cellular metabolic processes.
Cellular signal transduction involves the conversion of one signal or stimulus (mechanical or chemical) to another. The transduction process is usually performed by enzymes in association with second messengers.
Biologically active molecules (ligands) exert their physiological effect by activating or inducing 3D conformational changes in receptor proteins, which participate in signal transduction, cellular signaling, gene regulation, cellular proliferation and differentiation, or regulation of cellular metabolic processes.
Cellular signal transduction involves the conversion of one signal or stimulus (mechanical or chemical) to another. The transduction process is usually performed by enzymes in association with second messengers.
Labels: cell membrane, cytoplasm, differentiation, enzymes, ligands, nuclear membrane, proliferation, receptor protein, regulation, second messengers, signal transduction
| 0 Guide-Glossarysignaling in neoplasia
Eukaryotic cells coordinate cell growth with the availability of nutrients in their environment. Mutation of molecules involved in cell-growth signaling can result in the uncontrolled cellular proliferation that is characteristic of neoplasia. Signal transduction in cancer cells is a sophisticated process that involves receptor tyrosine kinases (RTKs) that eventually trigger multiple cytoplasmic kinases, which are often serine/threonine kinases.
A number of tumor models have identified several key cellular signaling pathways that work independently, in parallel, and/or through interconnections to promote cancer development. Three major signaling pathways that have been identified as playing important roles in cancer include the phosphatidyl inositol-3-kinase (PI3K)/AKT, protein kinase C (PKC) family, and mitogen-activated protein kinase (MAPK)/Ras signaling cascades.[↓]
ATM : ATR : DNA-PK : FRAP1 : kinases : MAPK : mTOR : Paks : PI-3-K : PIKK : PKC : Ras : receptor tyrosine kinases : serine/threonine kinases :
The mTOR protein kinase receives stimulatory signals from nutrients as well as Ras and phosphatidylinositol-3-OH kinase (PI(3)K) downstream from growth factors. Functioning as a critical growth-control node, mTOR is the 'mammalian target of rapamycin', a fungal derivative that halts protein synthesis by complexing with immunophilin FK-506 binding protein FKBP12 peptide prolyl cis/trans isomerase.
Officially termed FRAP1 for FK506 binding protein 12-rapamycin associated protein 1, mTOR is a serine/threonine kinase that regulates regulates translation and cell division. FRAP1 (mTOR) is an evolutionarily conserved member of the phosphoinositol kinase-related kinase (PIKK) family that includes DNA-PK, ATM, ATR and several other proteins. mTOR participates in the regulation of cell growth through initiation of gene translation in response to nutrients by integratating input from multiple upstream pathways, including growth factors, mitogens, leucine, insulin, and nutrients. mTOR initiates translation by activating the ribosomal p70S6k protein kinase (S6K1) and by inhibiting the eIF4E inhibitor 4E-BP1. FRAP1 is considered to be involved in numerous additional cellular functions including actin organization, membrane trafficking, secretion, protein degradation, protein kinase C signaling, ribosome biogenesis and tRNA synthesis. mTOR may contribute to the regulation of two pathways, referred to as TORC1 and TORC2 (for TOR Complex 1 and 2).
Components of the Ras and PI(3)K signalling pathways are mutated in most human cancers. The high frequency of mutations in these pathways suggests that the loss of growth-control checkpoints and the promotion of cell survival in nutrient-limited conditions may be an obligate event in carcinogenesis.[r]
p21-activated kinases (Paks) are serine/threonine kinases that function as downstream nodes oncogenic signalling pathways. Paks are well-known regulators of cytoskeletal remodelling and cell motility that promote cell proliferation, regulate apoptosis and accelerate mitosic abnormalities, resulting in tumorigenesis and cell invasiveness. Alterations in Pak expression have been detected in human tumours
Signal transduction in cancer cells is a sophisticated process that involves receptor tyrosine kinases (RTKs) that eventually trigger multiple cytoplasmic kinases, which are often serine/threonine kinases. A number of tumor models have identified several key cellular signaling pathways that work independently, in parallel, and/or through interconnections to promote cancer development. Three major signaling pathways that have been identified as playing important roles in cancer include the phosphatidyl inositol-3-kinase (PI3K)/AKT, protein kinase C (PKC) family, and mitogen-activated protein kinase (MAPK)/Ras signaling cascades. Faivre S, Djelloul S, Raymond E. New paradigms in anticancer therapy: targeting multiple signaling pathways with kinase inhibitors. Semin Oncol. 2006 Aug;33(4):407-20.
~ activator ~ cadherins ¤ Cancer ¤ carcinogenesis ~ cyclin-dependent kinases ~ cytokines ~ gene regulation ¤ genetic predispositon~ growth factors ¤ oncogenes ¤ malignant transformation ¤ mitogens ¤ mutagens ¤ neoplasia ¤ non-mutagenic carcinogens ¤ p53 ¤ proliferation ¤ proto-oncogenes ~ promoters ¤ Ras ¤ Rb ~ receptor tyrosine kinases ~ regulatory proteins ~ replication ~ repressor ~ response elements ~ retrotransposons ~ restriction enzmes ~ reverse transcriptase ~ Rho GTPase ~ ribosomes ~ serine/threonine kinases ¤ signaling molecules ~ silencers ¤ T-antigens ¤ TP53 ~ transcription ~ transcription factors ~ translation ¤ tumor antigens ¤ tumor suppressors ¤ tumorigenic viruses ¤ viral carcinogens ¤
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A number of tumor models have identified several key cellular signaling pathways that work independently, in parallel, and/or through interconnections to promote cancer development. Three major signaling pathways that have been identified as playing important roles in cancer include the phosphatidyl inositol-3-kinase (PI3K)/AKT, protein kinase C (PKC) family, and mitogen-activated protein kinase (MAPK)/Ras signaling cascades.[↓]
ATM : ATR : DNA-PK : FRAP1 : kinases : MAPK : mTOR : Paks : PI-3-K : PIKK : PKC : Ras : receptor tyrosine kinases : serine/threonine kinases :
The mTOR protein kinase receives stimulatory signals from nutrients as well as Ras and phosphatidylinositol-3-OH kinase (PI(3)K) downstream from growth factors. Functioning as a critical growth-control node, mTOR is the 'mammalian target of rapamycin', a fungal derivative that halts protein synthesis by complexing with immunophilin FK-506 binding protein FKBP12 peptide prolyl cis/trans isomerase.
Officially termed FRAP1 for FK506 binding protein 12-rapamycin associated protein 1, mTOR is a serine/threonine kinase that regulates regulates translation and cell division. FRAP1 (mTOR) is an evolutionarily conserved member of the phosphoinositol kinase-related kinase (PIKK) family that includes DNA-PK, ATM, ATR and several other proteins. mTOR participates in the regulation of cell growth through initiation of gene translation in response to nutrients by integratating input from multiple upstream pathways, including growth factors, mitogens, leucine, insulin, and nutrients. mTOR initiates translation by activating the ribosomal p70S6k protein kinase (S6K1) and by inhibiting the eIF4E inhibitor 4E-BP1. FRAP1 is considered to be involved in numerous additional cellular functions including actin organization, membrane trafficking, secretion, protein degradation, protein kinase C signaling, ribosome biogenesis and tRNA synthesis. mTOR may contribute to the regulation of two pathways, referred to as TORC1 and TORC2 (for TOR Complex 1 and 2).
Components of the Ras and PI(3)K signalling pathways are mutated in most human cancers. The high frequency of mutations in these pathways suggests that the loss of growth-control checkpoints and the promotion of cell survival in nutrient-limited conditions may be an obligate event in carcinogenesis.[r]
p21-activated kinases (Paks) are serine/threonine kinases that function as downstream nodes oncogenic signalling pathways. Paks are well-known regulators of cytoskeletal remodelling and cell motility that promote cell proliferation, regulate apoptosis and accelerate mitosic abnormalities, resulting in tumorigenesis and cell invasiveness. Alterations in Pak expression have been detected in human tumours
Signal transduction in cancer cells is a sophisticated process that involves receptor tyrosine kinases (RTKs) that eventually trigger multiple cytoplasmic kinases, which are often serine/threonine kinases. A number of tumor models have identified several key cellular signaling pathways that work independently, in parallel, and/or through interconnections to promote cancer development. Three major signaling pathways that have been identified as playing important roles in cancer include the phosphatidyl inositol-3-kinase (PI3K)/AKT, protein kinase C (PKC) family, and mitogen-activated protein kinase (MAPK)/Ras signaling cascades. Faivre S, Djelloul S, Raymond E. New paradigms in anticancer therapy: targeting multiple signaling pathways with kinase inhibitors. Semin Oncol. 2006 Aug;33(4):407-20.
~ activator ~ cadherins ¤ Cancer ¤ carcinogenesis ~ cyclin-dependent kinases ~ cytokines ~ gene regulation ¤ genetic predispositon~ growth factors ¤ oncogenes ¤ malignant transformation ¤ mitogens ¤ mutagens ¤ neoplasia ¤ non-mutagenic carcinogens ¤ p53 ¤ proliferation ¤ proto-oncogenes ~ promoters ¤ Ras ¤ Rb ~ receptor tyrosine kinases ~ regulatory proteins ~ replication ~ repressor ~ response elements ~ retrotransposons ~ restriction enzmes ~ reverse transcriptase ~ Rho GTPase ~ ribosomes ~ serine/threonine kinases ¤ signaling molecules ~ silencers ¤ T-antigens ¤ TP53 ~ transcription ~ transcription factors ~ translation ¤ tumor antigens ¤ tumor suppressors ¤ tumorigenic viruses ¤ viral carcinogens ¤
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Labels: cell-growth signaling, FRAP1, MAPK/Ras, mTOR, PI3K/AKT, PIKK, PKC, RTK, serine/threonine kinases, signal transduction
associated
Associated science sites • Abiogenesis and Evolution • Algorithms of Evolution • Archea Eubacteria • Cancer • Cell Biology • Complex Systems • Cyanobacteria • Diagrams Tables • Endosymbiosis • Enzymes • Evo Devo • Evolution in Action • Fat • Geology • Glossary • Immunology • Life Chemistry • Medical Science • Mechanisms of Evolution • Molecule • Molecular Biology • Molecular Paths • Neurosciences • Organics • Origin of Life • Paleogeology • Pathways • Photosynthesis • Protein • Receptor • Rocks & Minerals • SET • Signaling • Sleep • Stem & Progenitor Cells • Stromatolites • Taxonomy Phylogeny • Tissue • Virus •
And some philosophy/general interest sites: Avidity : Eine Kleine Nattermusing : eMusings : Galaria : Godspell Follies : Harper's Folly : Mimble Wimble : Sintheist : Tabula Flexuosa :
And some philosophy/general interest sites: Avidity : Eine Kleine Nattermusing : eMusings : Galaria : Godspell Follies : Harper's Folly : Mimble Wimble : Sintheist : Tabula Flexuosa :
Labels: abiogenesis, biochemistry, biological evolution, biomedical science, biopoiesis, cell biology, evo devo, geology, refuting creationist nonsense, serial endosymbiosis, taxonomy
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• Abiogenesis and Evolution • Algorithms of Evolution • Archea Eubacteria • Cancer • Cell Biology • Complex Systems • Cyanobacteria • Diagrams Tables • Endosymbiosis • Enzymes • Evo Devo • Evolution in Action • Fat • Geology • Galaria • Glossary • Godspell Follies • Harper's Folly • Immunology • Life Chemistry • Medical Science • Mechanisms of Evolution • Mimble Wimble • Molecule • Molecular Biology • Molecular Paths • Organics • Origin of Life • Paleogeology • Pathways • Photosynthesis • Protein • Receptor • Rocks & Minerals • SET • Signaling • Sleep • Stem & Progenitor Cells • Stromatolites • Tabula Flexuosa • Taxonomy Phylogeny • Tissue • Virus •
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site map
Labels: Signaling Site Map
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