WordNet
- an enzyme that catalyzes the conversion of a proenzyme to an active enzyme
- the basic unit of money in Papua New Guinea
UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
English Journal
- Gαq signalling: The new and the old.
- Sánchez-Fernández G1, Cabezudo S1, García-Hoz C1, Benincá C2, Aragay AM3, Mayor F Jr1, Ribas C4.Author information 1Departamento de Biología Molecular and Centro de Biologia Molecular "Severo Ochoa", CSIC-UAM, Universidad Autónoma de Madrid, Spain; Instituto de Investigación Sanitaria La Princesa, Madrid, Spain.2Department of Cardiovascular Development and Repair, CNIC, Spain.3Department of Cell Biology, Molecular Biology Institute of Barcelona, Spain.4Departamento de Biología Molecular and Centro de Biologia Molecular "Severo Ochoa", CSIC-UAM, Universidad Autónoma de Madrid, Spain; Instituto de Investigación Sanitaria La Princesa, Madrid, Spain. Electronic address: cribas@cbm.uam.es.AbstractIn the last few years the interactome of Gαq has expanded considerably, contributing to improve our understanding of the cellular and physiological events controlled by this G alpha subunit. The availability of high-resolution crystal structures has led the identification of an effector-binding region within the surface of Gαq that is able to recognise a variety of effector proteins. Consequently, it has been possible to ascribe different Gαq functions to specific cellular players and to identify important processes that are triggered independently of the canonical activation of phospholipase Cβ (PLCβ), the first identified Gαq effector. Novel effectors include p63RhoGEF, that provides a link between G protein-coupled receptors and RhoA activation, phosphatidylinositol 3-kinase (PI3K), implicated in the regulation of the Akt pathway, or the cold-activated TRPM8 channel, which is directly inhibited upon Gαq binding. Recently, the activation of ERK5 MAPK by Gq-coupled receptors has also been described as a novel PLCβ-independent signalling axis that relies upon the interaction between this G protein and two novel effectors (PKCζ and MEK5). Additionally, the association of Gαq with different regulatory proteins can modulate its effector coupling ability and, therefore, its signalling potential. Regulators include accessory proteins that facilitate effector activation or, alternatively, inhibitory proteins that downregulate effector binding or promote signal termination. Moreover, Gαq is known to interact with several components of the cytoskeleton as well as with important organisers of membrane microdomains, which suggests that efficient signalling complexes might be confined to specific subcellular environments. Overall, the complex interaction network of Gαq underlies an ever-expanding functional diversity that puts forward this G alpha subunit as a major player in the control of physiological functions and in the development of different pathological situations.
- Cellular signalling.Cell Signal.2014 May;26(5):833-848. doi: 10.1016/j.cellsig.2014.01.010. Epub 2014 Jan 17.
- In the last few years the interactome of Gαq has expanded considerably, contributing to improve our understanding of the cellular and physiological events controlled by this G alpha subunit. The availability of high-resolution crystal structures has led the identification of an effector-binding reg
- PMID 24440667
- Molecular targets for cancer therapy in the PI3K/AKT/mTOR pathway.
- Polivka J Jr1, Janku F2.Author information 1Department of Histology and Embryology and Biomedical Centre, Faculty of Medicine Plzen, Charles University Prague, Husova 3, 301 66 Plzen, Czech Republic; Department of Neurology, Faculty Hospital Plzen, Alej Svobody 80, 304 60 Plzen, Czech Republic.2Department of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA. Electronic address: fjanku@mdanderson.org.AbstractAberrations in various cellular signaling pathways are instrumental in regulating cellular metabolism, tumor development, growth, proliferation, metastasis and cytoskeletal reorganization. The fundamental cellular signaling cascade involved in these processes, the phosphatidylinositol 3-kinase/protein kinase-B/mammalian target of rapamycin (PI3K/AKT/mTOR), closely related to the mitogen-activated protein kinase (MAPK) pathway, is a crucial and intensively explored intracellular signaling pathway in tumorigenesis. Various activating mutations in oncogenes together with the inactivation of tumor suppressor genes are found in diverse malignancies across almost all members of the pathway. Substantial progress in uncovering PI3K/AKT/mTOR alterations and their roles in tumorigenesis has enabled the development of novel targeted molecules with potential for developing efficacious anticancer treatment. Two approved anticancer drugs, everolimus and temsirolimus, exemplify targeted inhibition of PI3K/AKT/mTOR in the clinic and many others are in preclinical development as well as being tested in early clinical trials for many different types of cancer. This review focuses on targeted PI3K/AKT/mTOR signaling from the perspective of novel molecular targets for cancer therapy found in key pathway members and their corresponding experimental therapeutic agents. Various aberrant prognostic and predictive biomarkers are also discussed and examples are given. Novel approaches to PI3K/AKT/mTOR pathway inhibition together with a better understanding of prognostic and predictive markers have the potential to significantly improve the future care of cancer patients in the current era of personalized cancer medicine.
- Pharmacology & therapeutics.Pharmacol Ther.2014 May;142(2):164-175. doi: 10.1016/j.pharmthera.2013.12.004. Epub 2013 Dec 9.
- Aberrations in various cellular signaling pathways are instrumental in regulating cellular metabolism, tumor development, growth, proliferation, metastasis and cytoskeletal reorganization. The fundamental cellular signaling cascade involved in these processes, the phosphatidylinositol 3-kinase/prote
- PMID 24333502
Japanese Journal
- Phosphatidylinositol 3-kinase class II α-isoform PI3K-C2α is required for transforming growth factor β-induced smad signaling in endothelial cells
- Aki Sho,Yoshioka Kazuaki,Okamoto Yasuo,Takuwa Noriko,Takuwa Yoh
- Journal of Biological Chemistry 290(10), 6086-6105, 2015-03-06
- … We have recently demonstrated that the PI3K class II-α isoform (PI3K-C2α), which generates phosphatidylinositol 3-phosphate and phosphatidylinositol 3,4-bisphosphates, plays crucial roles in angiogenesis, by analyzing PI3K-C2α knock-out mice. … TGFβ, which is also an essential angiogenic factor, signals via the serine/threonine kinase receptor complex to induce phosphorylation of Smad2 and Smad3 (Smad2/3). …
- NAID 120005593954
- 成熟B細胞腫瘍に対する経口PI3Kδ阻害薬とBTK阻害薬 : イデラリシブとイブルチニブ (特集 新規ターゲットおよび医薬品による血液がん治療の新たな展開)
Related Links
- The phosphatidylinositol 3-kinases (PI3Ks) are grouped into three classes (I – III) which differ in structure and function (Fruman et al. 1998; Vanhaesebroeck et al. 1997; Vanhaesebroeck and Waterfield 1999). Class I enzymes have ...
- Phosphatidylinositol 3-kinases (PI3Ks) are lipid kinases that regulate diverse cellular processes including proliferation, adhesion, survival, and motility. Dysregulated PI3K pathway signaling occurs in one-third of human ...
★リンクテーブル★
[★]
キナーゼ カイネース リン酸化酵素 phosphoenzyme phosphotransferase
[★]
ホスファチジルイノシトール