同: GRK

WordNet

any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
a unit of force equal to the force exerted by gravity; used to indicate the force to which a body is subjected when it is accelerated (同)gee, g-force
an enzyme that catalyzes the conversion of a proenzyme to an active enzyme
the 7th letter of the Roman alphabet (同)g

PrepTutorEJDIC

蛋白(たんばく)質
=sense organ / 受信装置

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1. ペプチドホルモンのシグナル伝達および調節peptide hormone signal transduction and regulation [show details]
…termination of receptor activation by receptor phosphorylation, which is initiated by specific G protein-coupled receptor kinases (GRKs) or second messenger-dependent kinases (eg, protein kinase A and protein …
2. β-2アドレナリン受容体機能不全および喘息の多型性beta 2 adrenergic receptor dysfunction and polymorphism in asthma [show details]
…the receptor by an agonist. Phosphorylation of the receptor, either by PKA-dependent pathways or by activation of one of a family of G-protein receptor kinases termed beta-adrenergic receptor kinase (beta-ARKs) …
3. 血小板生物学platelet biology [show details]
… the G-proteins are inactive. Agonist-stimulated receptors promote the replacement of GDP with GTP, switching on the G protein. G protein-coupled receptors typically have… serine/threonine kinases such as PKC, platelets contain a large number of tyrosine kinases, some of which become active during platelet activation. Human platelets contain tyrosine kinases that are receptors for extracellular…
4. 腎不全患者に生じる抗がん剤の腎毒性と用量変更：分子標的薬および免疫療法chemotherapy nephrotoxicity and dose modification in patients with kidney impairment molecularly targeted agents and immunotherapies [show details]
…tyrosine kinase that is the constitutively activated protein gene product of the Philadelphia chromosome in chronic myelogenous leukemia (CML); some also inhibit the tyrosine kinase receptor KIT (CD117) …
5. 分子標的薬である血管新生阻害剤の毒性：心血管系以外への影響toxicity of molecularly targeted antiangiogenic agents non cardiovascular effects [show details]
…prolongation. Some of these side effects may reflect the promiscuity of kinase inhibitors, which inhibit multiple other receptors in addition to VEGFRs (referred to as off-target activity). Some toxicities …

English Journal

Angiotensin II Activation of TRPC6 Channels in Rat Podocytes Requires Generation of Reactive Oxygen Species.

Anderson M, Roshanravan H, Khine J, Dryer SE.Author information Department of Biology and Biochemistry, University of Houston, Houston, Texas.AbstractAngiotensin II (AII) plays a major role in the progression of chronic kidney diseases. Podocytes are essential components of the ultrafiltration apparatus, and are targets for AII signaling. AII has been shown to increase generation of reactive oxygen species (ROS) in podocytes. Canonical transient receptor potential-6 (TRPC6) channels stimulate Ca(2+) influx in podocytes, and have been implicated in glomerular disease. We observed that AII increased cationic currents in rat podocytes in an isolated glomerulus preparation in which podocytes are still attached to the underlying capillary. This effect was completely blocked by SKF-96365, by micromolar La(3+) , and by siRNA knockdown of TRPC6, indicating that TRPC6 is the primary source of Ca(2+) influx mobilized by endogenously expressed angiotensin II receptors in these cells. These responses were also blocked by the AT1R antagonist losartan, the phospholipase C inhibitor D-609, and by inhibition of G protein signaling. The pan-protein kinase C inhibitor chelerythrine had no effect. Importantly, pretreating podocytes with the ROS quencher manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP) eliminated AII activation of TRPC6. Significant reductions of AII effects on podocyte TRPC6 were also observed after pretreatment with NADPH oxidase inhibitors apocynin or diphenylene iodonium (DPI). These data suggest that ROS production permits activation of TRPC6 channels by G protein and PLC-dependent cascades initiated by AII acting on AT1Rs in podocytes. This pathway also provides a basis whereby two forms of cellular stress-oxidative stress and Ca(2+) overload-converge on common pathways relevant to disease. J. Cell. Physiol. 229: 434-442, 2014. © 2013 Wiley Periodicals, Inc.
Journal of cellular physiology.J Cell Physiol.2014 Apr;229(4):434-42. doi: 10.1002/jcp.24461.
Angiotensin II (AII) plays a major role in the progression of chronic kidney diseases. Podocytes are essential components of the ultrafiltration apparatus, and are targets for AII signaling. AII has been shown to increase generation of reactive oxygen species (ROS) in podocytes. Canonical transient
PMID 24037962

A-kinase anchoring protein-Lbc promotes pro-fibrotic signaling in cardiac fibroblasts.

Cavin S1, Maric D1, Diviani D2.Author information 1Department of Pharmacology and Toxicology, Faculté de Biologie et Médecine, University of Lausanne, 1005, Switzerland.2Department of Pharmacology and Toxicology, Faculté de Biologie et Médecine, University of Lausanne, 1005, Switzerland. Electronic address: Dario.diviani@unil.ch.AbstractIn response to stress or injury the heart undergoes an adverse remodeling process associated with cardiomyocyte hypertrophy and fibrosis. Transformation of cardiac fibroblasts to myofibroblasts is a crucial event initiating the fibrotic process. Cardiac myofibroblasts invade the myocardium and secrete excess amounts of extracellular matrix proteins, which cause myocardial stiffening, cardiac dysfunctions and progression to heart failure. While several studies indicate that the small GTPase RhoA can promote profibrotic responses, the exchange factors that modulate its activity in cardiac fibroblasts are yet to be identified. In the present study, we show that AKAP-Lbc, an A-kinase anchoring protein (AKAP) with an intrinsic Rho-specific guanine nucleotide exchange factor (GEF) activity, is critical for activating RhoA and transducing profibrotic signals downstream of type I angiotensin II receptors (AT1Rs) in cardiac fibroblasts. In particular, our results indicate that suppression of AKAP-Lbc expression by infecting adult rat ventricular fibroblasts with lentiviruses encoding AKAP-Lbc specific short hairpin (sh) RNAs strongly reduces the ability of angiotensin II to promote RhoA activation, differentiation of cardiac fibroblasts to myofibroblasts, collagen deposition as well as myofibroblast migration. Interestingly, AT1Rs promote AKAP-Lbc activation via a pathway that requires the α subunit of the heterotrimeric G protein G12. These findings identify AKAP-Lbc as a key Rho-guanine nucleotide exchange factor modulating profibrotic responses in cardiac fibroblasts.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Feb;1843(2):335-45. doi: 10.1016/j.bbamcr.2013.11.008. Epub 2013 Nov 22.
In response to stress or injury the heart undergoes an adverse remodeling process associated with cardiomyocyte hypertrophy and fibrosis. Transformation of cardiac fibroblasts to myofibroblasts is a crucial event initiating the fibrotic process. Cardiac myofibroblasts invade the myocardium and secre
PMID 24269843

Isoforms of protein kinase C involved in phorbol ester-induced sphingosine 1-phosphate receptor 1 phosphorylation and desensitization.

Morquecho-León MA1, Bazúa-Valenti S1, Romero-Ávila MT1, García-Sáinz JA2.Author information 1Departamento de Biología Celular y Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apartado Postal 70-248, México D.F. 04510, Mexico.2Departamento de Biología Celular y Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apartado Postal 70-248, México D.F. 04510, Mexico. Electronic address: agarcia@ifc.unam.mx.AbstractThe role of protein kinase C (PKC) isozymes in phorbol myristate acetate (PMA)-induced sphingosine 1-phosphate (S1P) receptor 1 (S1P1) phosphorylation was studied. Activation of S1P1 receptors induced an immediate increase in intracellular calcium, which was blocked by preincubation with PMA. Both S1P and PMA were able to increase S1P1 phosphorylation in a concentration- and time-dependent fashion. Down-regulation of PKC (overnight incubation with PMA) blocked the subsequent effect of the phorbol ester on S1P1 phosphorylation, without decreasing that of the natural agonist. Pharmacological inhibition of PKC α prevented the effects of PMA on S1P-triggered intracellular calcium increase and on S1P1 phosphorylation; no such effect was observed on the effects of the sphingolipid agonist. The presence of PKC α and β isoforms in S1P1 immunoprecipitates was evidenced by Western blotting. Additionally, expression of dominant-negative mutants of PKC α or β and knockdown of these isozymes using short hairpin RNA, markedly attenuated PMA-induced S1P1 phosphorylation. Our results indicate that the classical isoforms, mainly PKC α, mediate PMA-induced phosphorylation and desensitization of S1P1.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Feb;1843(2):327-34. doi: 10.1016/j.bbamcr.2013.11.002. Epub 2013 Nov 13.
The role of protein kinase C (PKC) isozymes in phorbol myristate acetate (PMA)-induced sphingosine 1-phosphate (S1P) receptor 1 (S1P1) phosphorylation was studied. Activation of S1P1 receptors induced an immediate increase in intracellular calcium, which was blocked by preincubation with PMA. Both S
PMID 24239722

Japanese Journal

Irciniastatin A Induces Potent and Sustained Activation of Extracellular Signal-Regulated Kinase and Thereby Promotes Ectodomain Shedding of Tumor Necrosis Factor Receptor 1 in Human Lung Carcinoma A549 Cells

Quach Hue Tu,Hirano Seiya,Fukuhara Sayuri [他]
Biological & pharmaceutical bulletin 38(6), 941-946, 2015-06
NAID 40020471602

Bone Morphogenetic Proteins Are Mediators of Luteolysis in the Human Corpus Luteum

Nio-Kobayashi Junko,Trendell Jennifer,Giakoumelou Sevasti,Boswell Lyndsey,Nicol Linda,Kudo Masataka,Sakuragi Noriaki,Iwanaga Toshihiko,Duncan William Colin
Endocrinology 156(4), 1494-1503, 2015-04
… H89, a protein kinase A inhibitor, increased the expression of both BMP2 (P<.05) and BMP4 (P<.05) while decreasing BMP6 (P<.01). … PMA, a protein kinase C activator, decreased both BMP4 and BMP6 expression (P<.0001) while enhancing the mRNA abundance of BMP2 (P<.01). … BMPs significantly down-regulated transcripts for LH/choriogonadotropin receptor (LHCGR; …
NAID 120005611263

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
… The PI3K-C2α actions are mediated at least in part through its participation in the internalization of VEGF receptor-2 and sphingosine-1-phosphate receptor S1P1 and thereby their signaling on endosomes. … 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