El fosfatidilinositol 3,5-bifosfato (PI(3,5)P2) es uno de los componentes fosfolipídicos de la membrana celular así como de la membrana de orgánulos. Los fosfoinosítidos más importantes son los del grupo fosfatidilinositol bifosfato. Cuando determinados ligandos se unen a receptores de la membrana. Fosfatidilinositol 3,4-bifosfato. Quite the same Wikipedia. Just better.
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Universidad Industrial de Santander, Bucaramanga, Colombia. The signaling pathway of phosphatidylinositol 3-kinase PI3K is critical in many aspects of growth and cell survival. The path of PI3K is stimulated physiologically as a result of many growth factors and regulatory factors.
Several genetic alterations such as amplification, mutation and chromosomal arrangements may compromise the PI3K pathway, generating permanent activation in different cancer types have found evidence of these deleterious genetic modifications. Abnormal activation of the PI3K pathway results in alteration of the control mechanisms of growth and cell survival, which favors the competitive growth, and frequently metastatic capacity, greater resistance to treatment.
IRS; sustrato receptor de insulina. PIP2; fosfatidil inositol 3,4 difosfato. PIP3; fosfatidil inositol 3,4,5 trifosfato. PKC; protein kinasa C. Vol 4, ; Existen tres tipos de PI3K. Akt tiene tres isoformas conocidas, derivadas de distintos genes: Se han identificado diferentes PDK2 potenciales. Estas mutaciones ocurren con mayor frecuencia en canceres HER2-amplificados y en positivos para receptor hormonal Funciones asociados a las diferentes isoformas de p de PI3K.
CP realizo el primer manuscrito. Todos los autores leyeron y aprobaron el manuscrito final. Identification and characterization of a new oncogene derived from the regulatory subunit of phosphoinositide 3-kinase.
The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease. J Mol Cell Cardiol. Specificity and mechanism of action of some commonly used protein kinase inhibitors.
Role of phosphatidylinositol 3-kinase pathway (PI3K/Akt) in humans
Pawson T, Nash P. Protein-protein interactions define specificity in signal transduction. Proliferative defect and embryonic lethality in mice homozygous for a deletion in the palpha subunit of phosphoinositide 3-kinase. Phosphoinositide 3-kinase catalytic subunit deletion and regulatory subunit deletion have opposite effects fosfatidilinpsitol insulin sensitivity in mice. Impaired B and T cell antigen receptor signaling fosfatiidilinositol pdelta PI 3-kinase mutant mice.
Upregulated function of phosphatidylinositolkinase in genetically hypertensive rats: Clin Exp Pharmacol Physiol. Essential role for the pdelta isoform in phosphoinositide 3-kinase activation and cell proliferation in acute myeloid leukemia.
Over-expression of the pbeta but not palpha isoform of PI 3-kinase inhibits motility in breast cancer cells.
Phosphatidylinositide 3-kinase gamma regulates key pathologic responses to cholecystokinin in pancreatic acinar cells.
Class I phosphoinositide 3-kinase pbeta is required for apoptotic cell and Fcgamma receptor-mediated phagocytosis by macrophages. Glucose-potentiated chemotaxis in human vascular gifosfato muscle is dependent on cross-talk between the PI3K and MAPK signaling pathways. Targeted inhibition of beta-adrenergic receptor kinaseassociated phosphoinositide-3 kinase activity preserves beta-adrenergic receptor signaling and prolongs survival in heart failure induced by calsequestrin overexpression.
J Am Coll Cardiol. Molecular cloning and characterisation of a novel putative protein-serine kinase related to the cAMP-dependent and protein kinase C families. Mechanism of activation of protein kinase B by insulin and IGF A retroviral oncogene, akt, encoding a serine-threonine kinase containing an SH2-like region. Blume-Jensen P, Hunter T. Integrin-linked kinase regulates phosphorylation of serine of protein kinase B by an indirect mechanism.
Protein kinase C betaII regulates Akt phosphorylation on Ser in fosfatdiilinositol cell type- and stimulus-specific fashion.
Testa JR, Bellacosa A. AKT plays a central role in tumorigenesis. Dwarfism, impaired skin development, skeletal muscle atrophy, delayed bone development, and impeded adipogenesis in mice lacking Akt1 and Akt2. Vivanco I, Sawyers CL. The phosphatidylinositol 3-Kinase AKT pathway in human cancer. Targeting the PI3K-Akt pathway in human cancer: Centrosome hyperamplification in human cancer: MDM2 in Breast Cancer.
Curr Opin Genet Dev. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Phosphatidylinositol 3-kinase signaling inhibits DAF DNA binding and function via dependent and independent pathways. Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy. Schmelzle T, Hall MN.
TOR, a central controller of cell growth. Translational control of the antiapoptotic function of Ras. Akt regulates growth by directly phosphorylating Tsc2.
Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin mTOR -mediated downstream signaling. Tuberous sclerosis genes regulate cellular protein gosfatidilinositol.
Biochem Biophys Res Commun.
Activation of Akt and eIF4E survival pathways by rapamycin-mediated mammalian target of rapamycin inhibition. The Akt-mTOR tango and its relevance to cancer. Management of cellular energy by the AMP-activated protein kinase system. The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stress.
Phosphorylation of p27Kip1 at threonine by p90 fosfatidilinsoitol protein S6 kinases promotes its binding fosfatidilinnositol and cytoplasmic localization. Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization. Role of VHL gene mutation in human cancer. Zhang D, Brodt P. Induction of hTERT expression and phosphorylation by estrogen via Akt cascade in human ovarian cancer cell lines.
Mechanisms of tamoxifen resistance: J Natl Cancer Inst. Targeting mammalian bifoosfato of rapamycin synergistically enhances chemotherapy-induced cytotoxicity in breast cancer cells. Radiation sensitization of human cancer cells in vivo by inhibiting the activity of PI3K using LY Estrogen receptor alpha forms estrogen-dependent multimolecular complexes with insulin-like growth factor receptor and phosphatidylinositol 3-kinase in the adult rat brain.
Brain Res Mol Brain Res. Hanahan D, Weinberg RA. The hallmarks of cancer. Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic. PIK3CA is implicated as an oncogene in ovarian cancer. Genomic gain of PIK3CA and increased expression of palpha are associated with progression of dysplasia into invasive squamous cell carcinoma.
PIK3CA as an oncogene in cervical cancer. Genetic alterations of phosphoinositide 3-kinase subunit genes in human glioblastomas. Amplification and overexpression of the AKT2 oncogene in a subset of human pancreatic ductal adenocarcinomas.
Molecular alterations of the AKT2 oncogene in ovarian and breast carcinomas. Loss of heterozygosity on 10q PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer.
Allelic loss of the PTEN region 10q23 in breast carcinomas of poor pathophenotype. Fosfstidilinositol Cancer Res Treat. PTEN promoter is methylated in a proportion of invasive breast cancers.
Frequent inactivation of PTEN by promoter hypermethylation bifoefato microsatellite instability-high sporadic colorectal cancers. A screen of the complete protein kinase gene family identifies diverse patterns of somatic mutations fosvatidilinositol human breast cancer. Somatic mutations of the protein kinase gene family in human lung cancer.
Mutational analysis of the tyrosine phosphatome in colorectal cancers. Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras. Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes.
Detection of K-ras gene mutations in non-neoplastic lung tissue and lung cancers. Mutations of fosfaidilinositol BRAF gene in human cancer. Int J Gynecol Pathol. Combined trastuzumab and paclitaxel treatment better inhibits ErbBmediated angiogenesis in breast carcinoma through a more effective inhibition of Akt than either treatment alone.