Results PDGF-directed invasion was completely inhibited by the pan PI3K inhibitor (1 uM). To define the role of the individual isoforms, we tested the effect of the isoform selective PI3K inhibitors. PI3Kdelta inhibition (INK007) significantly decreased the number of invading cells, with 60 ± 5% inhibition at 1 uM (p , 0.04). Similar results were observed with two other inhibitors with distinct chemical structures (CAL-101 and INK055). The PI3Kalpha inhibitor decreased invasion by 40 ± 5% while PI3Kbeta and PI3Kgamma inhibitors had no effect. Phalloidin staining was then used to visualise FLS actin rearrangement in response to PDGF with or without PI3K inhibitors. PI3Kdelta inhibition by INK007, CAL-101 and IPI-145 decreased lamellipodia formation by 50 ± 6% (p , 0.05). Similar inhibition was seen with the pan PI3K inhibitor, while the selective inhibitors of PI3Kalpha, PI3Kbeta or PI3Kgamma had no effect. We then hypothesised that PI3Kdelta might modulate activation of Rho GTPases in ...

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Type IB phosphoinositide 3OH-kinase (PI3K) is activated by G-protein βγ subunits (Gβγs). The enzyme is soluble and largely cytosolic in vivo. Its substrate, PtdIns(4,5)P2, and the Gβγs are localized at the plasma membrane. We have addressed the mechanism by which Gβγs regulate the PI3K using an in vitro approach. We used sedimentation assays and surface plasmon resonance to determine association of type IB PI3K with lipid monolayers and vesicles of varying compositions, some of which had Gβγs incorporated. Association and dissociation rate constants were determined. Our results indicated that in an assay situation in vitro the majority of PI3K will be associated with lipid vesicles, irrespective of the presence or absence of Gβγs. In line with this, a constitutively active membrane-targeted PI3K construct could still be activated substantially by Gβγs in vitro. We conclude that Gβγs activate type IB PI3K by a mechanism other than translocation to the plasma membrane.. ...

Sigma-Aldrich offers abstracts and full-text articles by [Michael Hannigan, Lijun Zhan, Zhong Li, Youxi Ai, Dianqing Wu, Chi-Kuang Huang].

The phosphatidylinositol 3 -kinase(PI3K)-Akt signaling pathway is activated by many types of cellular stimuli or toxic insults and regulates fundamental cellular functions such as transcription, translation, proliferation, growth, and survival. The binding of growth factors to their receptor tyrosine kinase (RTK) or G protein-coupled receptors (GPCR) stimulates class Ia and Ib PI3K isoforms, respectively. PI3K catalyzes the production of phosphatidylinositol-3,4,5-triphosphate (PIP3) at the cell membrane. PIP3 in turn serves as a second messenger that helps to activate Akt. Once active, Akt can control key cellular processes by phosphorylating substrates involved in apoptosis, protein synthesis, metabolism, and cell cycle ...

The phosphatidylinositol 3 -kinase(PI3K)-Akt signaling pathway is activated by many types of cellular stimuli or toxic insults and regulates fundamental cellular functions such as transcription, translation, proliferation, growth, and survival. The binding of growth factors to their receptor tyrosine kinase (RTK) or G protein-coupled receptors (GPCR) stimulates class Ia and Ib PI3K isoforms, respectively. PI3K catalyzes the production of phosphatidylinositol-3,4,5-triphosphate (PIP3) at the cell membrane. PIP3 in turn serves as a second messenger that helps to activate Akt. Once active, Akt can control key cellular processes by phosphorylating substrates involved in apoptosis, protein synthesis, metabolism, and cell cycle ...

The phosphatidylinositol 3 -kinase(PI3K)-Akt signaling pathway is activated by many types of cellular stimuli or toxic insults and regulates fundamental cellular functions such as transcription, translation, proliferation, growth, and survival. The binding of growth factors to their receptor tyrosine kinase (RTK) or G protein-coupled receptors (GPCR) stimulates class Ia and Ib PI3K isoforms, respectively. PI3K catalyzes the production of phosphatidylinositol-3,4,5-triphosphate (PIP3) at the cell membrane. PIP3 in turn serves as a second messenger that helps to activate Akt. Once active, Akt can control key cellular processes by phosphorylating substrates involved in apoptosis, protein synthesis, metabolism, and cell cycle ...

https://inspirehep.net/literature/892684 Inspire Record 892684 DOI 10.17182/hepdata.62222 https://doi.org/10.17182/hepdata.62222 We study the processes e+e- --, K+ K- pi+pi-gamma, K+ K- pi0pi0gamma, and K+ K- K+ K-gamma, where the photon is radiated from the initial state. About 84000, 8000, and 4200 fully reconstructed events, respectively, are selected from 454 fb-1 of BaBar data. The invariant mass of the hadronic final state defines the \epem center-of-mass energy, so that the K+ K- pi+pi- data can be compared with direct measurements of the e+e- --, K+ K- pi+pi- reaction. No direct measurements exist for the e+e- --, K+ K-pi0pi0 or e+e- --, K+ K-K+ K- reactions, and we present an update of our previous result with doubled statistics. Studying the structure of these events, we find contributions from a number of intermediate states, and extract their cross sections. In particular, we perform a more detailed study of the e+e- --, phi(1020)pipigamma reaction, and confirm the presence of the ...

PPP1CC overexpression lysate, 0.1 mg. Transient overexpression lysate of protein phosphatase 1, catalytic subunit, gamma isoform (PPP1CC)

pep:known chromosome:VEGA66:5:122158356:122175273:1 gene:OTTMUSG00000016349 transcript:OTTMUST00000039309 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Ppp1cc description:protein phosphatase 1, catalytic subunit, gamma isoform ...

TY - JOUR. T1 - PI3K7-deficient mice have reduced levels of allergen-induced eosinophilic inflammation and airway remodeling. AU - Lim, Dae Hyun. AU - Cho, Jae Youn. AU - Song, Dae Jin. AU - Lee, Sang Yeub. AU - Miller, Marina. AU - Broide, David H.. PY - 2009/2/1. Y1 - 2009/2/1. N2 - In this study, we have examined the role of phosphoinositide 3 kinase γ (PDKγ), a class Ib PI3K, in contributing to airway remodeling utilizing PI3Kγ-deficient mice exposed to chronic allergen challenge. Wild-type (WT) mice sensitized to ovalbumin (OVA) and chronically challenged with OVA for 1 mo developed significantly increased levels of eosinophilic inflammation and airway remodeling. In contrast, PI3Kγ-deficient mice challenged with OVA had significantly reduced numbers of bronchoalveolar lavage and peribronchial eosinophils compared with WT mice. There was no significant difference in the number of bone marrow or circulating peripheral blood eosinophils when comparing WT mice and PI3Kγ-deficient mice, ...

The present invention provides compounds of formula (I) which inhibit the activity of PI 3-kinase gamma isoform, which are useful for the treatment of diseases mediated by the activation of PI 3-kinase gamma isoform.

P48736: Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform; PI3-kinase subunit gamma; PI3K-gamma; PI3Kgamma; PtdIns-3-kinase subunit gamma; 2.7.1.153; Phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit gamma; PtdIns-3-kinase subunit p110-gamma; p110gamma; Phosphoinositide-3-kinase catalytic gamma polypeptide; Serine/threonine protein kinase PIK3CG; 2.7.11.1; p120- ...

FUNCTION: Phosphoinositide 3-kinase gamma is a lipid kinase that produces the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate. The kinase is composed of a catalytic subunit and one of several regulatory subunits, and is chiefly activated by G protein-coupled receptors. This gene encodes a regulatory subunit, and is distantly related to the phosphoinositide-3-kinase, regulatory subunit 5 gene which is located adjacent to this gene on chromosome 11. The protein binds to both the catalytic subunit and to G beta-gamma, and mediates activation of the kinase subunit downstream of G protein-coupled receptors. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2014 ...

Caffeine is a naturally occurring methylxanthine that acts as a non-selective adenosine receptor antagonist. Epidemiological studies demonstrated habitual coffee drinking to be significantly associated with liver cancer survival. We aimed to investigate the effects of caffeine and its analog CGS 15943 on hepatocellular carcinoma (HCC) and pancreatic cancer adenocarcinoma (PDAC). We demonstrate that caffeine and CGS 15943 block proliferation in HCC and PDAC cell lines by inhibiting the PI3K/Akt pathway. Importantly a kinase profiling assay reveals that CGS 15943 targets specifically the catalytic subunit of the class IB PI3K isoform (p110ƴ). These data give mechanistic insight into the action of caffeine and its analogs and they identify these compounds as promising lead compounds to develop drugs that can specifically target this PI3K isoform whose key role in cancer progression is emerging.. ...

Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, Smith HO, Yandell M, Evans CA, Holt RA, Gocayne JD, Amanatides P, Ballew RM, Huson DH, Wortman JR, Zhang Q, Kodira CD, Zheng XH, Chen L, Skupski M, Subramanian G, Thomas PD, Zhang J, Gabor Miklos GL, Nelson C, Broder S, Clark AG, Nadeau J, McKusick VA, Zinder N, Levine AJ, Roberts RJ, Simon M, Slayman C, Hunkapiller M, Bolanos R, Delcher A, Dew I, Fasulo D, Flanigan M, Florea L, Halpern A, Hannenhalli S, Kravitz S, Levy S, Mobarry C, Reinert K, Remington K, Abu-Threideh J, Beasley E, Biddick K, Bonazzi V, Brandon R, Cargill M, Chandramouliswaran I, Charlab R, Chaturvedi K, Deng Z, Di Francesco V, Dunn P, Eilbeck K, Evangelista C, Gabrielian AE, Gan W, Ge W, Gong F, Gu Z, Guan P, Heiman TJ, Higgins ME, Ji RR, Ke Z, Ketchum KA, Lai Z, Lei Y, Li Z, Li J, Liang Y, Lin X, Lu F, Merkulov GV, Milshina N, Moore HM, Naik AK, Narayan VA, Neelam B, Nusskern D, Rusch DB, Salzberg S, Shao W, Shue B, Sun J, Wang Z, Wang A, Wang X, Wang J, Wei M, Wides ...

Calcium-dependent, calmodulin-stimulated protein phosphatase which plays an essential role in the transduction of intracellular Ca(2+)-mediated signals. Dephosphorylates and activates transcription factor NFATC1. Dephosphorylates and inactivates transcription factor ELK1. Dephosphorylates DARPP32.

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TITLE Cerebellum Granule Cell Model COMMENT CaHVA channel Author: E.DAngelo, T.Nieus, A. Fontana Last revised: 8.5.2000 ENDCOMMENT NEURON { SUFFIX GRC_CA USEION ca READ eca WRITE ica RANGE gcabar, ica, g, alpha_s, beta_s, alpha_u, beta_u RANGE Aalpha_s, Kalpha_s, V0alpha_s RANGE Abeta_s, Kbeta_s, V0beta_s RANGE Aalpha_u, Kalpha_u, V0alpha_u RANGE Abeta_u, Kbeta_u, V0beta_u RANGE s_inf, tau_s, u_inf, tau_u } UNITS { (mA) = (milliamp) (mV) = (millivolt) } PARAMETER { :Kalpha_s = 0.063 (/mV) Checked! :Kbeta_s = -0.039 (/mV) Checked! :Kalpha_u = -0.055 (/mV) Checked! :Kbeta_u = 0.012 (/mV) Checked! Aalpha_s = 0.04944 (/ms) Kalpha_s = 15.87301587302 (mV) V0alpha_s = -29.06 (mV) Abeta_s = 0.08298 (/ms) Kbeta_s = -25.641 (mV) V0beta_s = -18.66 (mV) Aalpha_u = 0.0013 (/ms) Kalpha_u = -18.183 (mV) V0alpha_u = -48 (mV) Abeta_u = 0.0013 (/ms) Kbeta_u = 83.33 (mV) V0beta_u = -48 (mV) v (mV) gcabar= 0.00046 (mho/cm2) eca = 129.33 (mV) celsius = 30 (degC) } STATE { s u } ASSIGNED { ica (mA/cm2) s_inf u_inf ...

TITLE Cerebellum Granule Cell Model COMMENT CaHVA channel Author: E.DAngelo, T.Nieus, A. Fontana Last revised: 8.5.2000 ENDCOMMENT NEURON { SUFFIX GRC_CA USEION ca READ eca WRITE ica RANGE gcabar, ica, g, alpha_s, beta_s, alpha_u, beta_u RANGE Aalpha_s, Kalpha_s, V0alpha_s RANGE Abeta_s, Kbeta_s, V0beta_s RANGE Aalpha_u, Kalpha_u, V0alpha_u RANGE Abeta_u, Kbeta_u, V0beta_u RANGE s_inf, tau_s, u_inf, tau_u } UNITS { (mA) = (milliamp) (mV) = (millivolt) } PARAMETER { :Kalpha_s = 0.063 (/mV) Checked! :Kbeta_s = -0.039 (/mV) Checked! :Kalpha_u = -0.055 (/mV) Checked! :Kbeta_u = 0.012 (/mV) Checked! Aalpha_s = 0.04944 (/ms) Kalpha_s = 15.87301587302 (mV) V0alpha_s = -29.06 (mV) Abeta_s = 0.08298 (/ms) Kbeta_s = -25.641 (mV) V0beta_s = -18.66 (mV) Aalpha_u = 0.0013 (/ms) Kalpha_u = -18.183 (mV) V0alpha_u = -48 (mV) Abeta_u = 0.0013 (/ms) Kbeta_u = 83.33 (mV) V0beta_u = -48 (mV) v (mV) gcabar= 0.00046 (mho/cm2) eca = 129.33 (mV) celsius = 30 (degC) } STATE { s u } ASSIGNED { ica (mA/cm2) s_inf u_inf ...

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ID PK3CG_HUMAN Reviewed; 1102 AA. AC P48736; A4D0Q6; Q8IV23; Q9BZC8; DT 01-FEB-1996, integrated into UniProtKB/Swiss-Prot. DT 04-APR-2006, sequence version 3. DT 22-NOV-2017, entry version 184. DE RecName: Full=Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform; DE Short=PI3-kinase subunit gamma; DE Short=PI3K-gamma; DE Short=PI3Kgamma; DE Short=PtdIns-3-kinase subunit gamma; DE EC=2.7.1.153; DE AltName: Full=Phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit gamma; DE Short=PtdIns-3-kinase subunit p110-gamma; DE Short=p110gamma; DE AltName: Full=Phosphoinositide-3-kinase catalytic gamma polypeptide; DE AltName: Full=Serine/threonine protein kinase PIK3CG; DE EC=2.7.11.1; DE AltName: Full=p120-PI3K; GN Name=PIK3CG; OS Homo sapiens (Human). OC Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; OC Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; OC Catarrhini; Hominidae; Homo. OX NCBI_TaxID=9606; RN [1] RP NUCLEOTIDE ...

Activation of phosphoinositide 3-kinase p110alpha isoform (PI3Kalpha) is cardioprotective in several cardiac pathologies. Marked impairment of left ventricular (LV) function characterizes the diabetic heart. The efficacy of PI3Kalpha cardioprotection has however not been sought in the diabetic heart. We tested the hypothesis that PI3Kalpha activation is protective against diabetes-induced LV dysfunction and remodeling in the mouse heart in vivo. Male cardiac-specific, constitutively-active PI3Kalpha transgenic (caPI3Kalpha; increases PI3Kalpha activity), dominant-negative PI3Kalpha transgenic (dnPI3Kalpha; decreases PI3Kalpha activity) and non-transgenic (Ntg) 6-wk old mice received streptozotocin (STZ, 55 mg/kg i.p./day for 5 days) or vehicle, and were followed for 12 weeks. Increases in blood glucose and glycated hemoglobin (GHB) with STZ were comparable among genotypes (see table). LV diastolic dysfunction was evident in Ntg diabetic mice, based on each of echocardiography-derived A wave ...

Ikbkg - Ikbkg (Myc-DDK-tagged ORF) - Rat inhibitor of kappaB kinase gamma (Ikbkg), (10 ug) available for purchase from OriGene - Your Gene Company.

Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gammaisoform (EC 2.7.1.153) (PI3-kinase p110 subunit gamma) (PtdIns-3-kinase subunit p110) (PI3K) (PI3Kgamma) (p120-PI3K ...

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As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.

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Hypertensive cardiac hypertrophy (HCH) is a common cause of heart failure (HF), a major public health problem worldwide. However, the molecular bases of HCH have not been completely elucidated. Neuron-derived orphan receptor-1 (NOR-1) is a nuclear receptor whose role in cardiac remodelling is poorly understood. The aim of the present study was to generate a transgenic mouse over-expressing NOR-1 in the heart (TgNOR-1) and assess the impact of this gain-of-function on HCH. The CAG promoter-driven transgenesis led to viable animals that over-expressed NOR-1 in the heart, mainly in cardiomyocytes and also in cardiofibroblasts. Cardiomyocytes from TgNOR-1 exhibited an enhanced cell surface area and myosin heavy chain 7 (Myh7)/Myh6 expression ratio, and increased cell shortening elicited by electric field stimulation. TgNOR-1 cardiofibroblasts expressed higher levels of myofibroblast markers than wild-type (WT) cells (α 1 skeletal muscle actin (Acta1), transgelin (Sm22α)) and were more prone to ...

Familial incontinentia pigmenti (IP; MIM 308310) is a genodermatosis that segregates as an X-linked dominant disorder and is usually lethal prenatally in males. In affected females it causes highly variable abnormalities of the skin, hair, nails, teeth, eyes and central nervous system. The prominent skin signs occur in four classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation and dermal scarring. Cells expressing the mutated X chromosome are eliminated selectively around the time of birth, so females with IP exhibit extremely skewed X-inactivation. The reasons for cell death in females and in utero lethality in males are unknown. The locus for IP has been linked genetically to the factor VIII gene in Xq28 (ref. 3). The gene for NEMO (NF-kappaB essential modulator)/IKKgamma (IkappaB kinase-gamma) has been mapped to a position 200 kilobases proximal to the factor VIII locus. NEMO is required for the activation of the transcription ...

Harris RA, McQuilkin SJ, Paylor R, Abeliovich A, Tonegawa S, Wehner JM. Mutant mice lacking the gamma isoform of protein kinase C show decreased behavioral actions of ethanol and altered function of gamma-aminobutyrate type A receptors. Proc Natl Acad Sci USA 1995 Apr 25;92(9):3658-3662 ...

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Catalytic subunit of the phosphorylase b kinase (PHK), which mediates the neural and hormonal regulation of glycogen breakdown (glycogenolysis) by phosphorylating and thereby activating glycogen phosphorylase. In vitro, phosphorylates PYGM, TNNI3, MAPT/TAU, GAP43 and NRGN/RC3 (By similarity).

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