Sentences with phrase «kinase b»

Holten et al. [48] investigated a number of important biochemical muscle adaptations in both diabetic and non-diabetic individuals in response to 4 weeks of one - legged low - intensity strength training and reported possible mechanisms leading to a training effect including increased protein content of GLUT4, insulin receptor, glycogen synthase and protein - kinase B (PKB) without an increase in muscle mass.

IGF - I is perhaps the most important mediator of muscle growth and repair (49), possibly through the use of protein kinase B — mechanistic target of rapamycin — p70 ribosomal protein S6 kinase signaling.

Given this observation, we hope that the off - target effects on Aurora kinase B and ERBB2 (if any) will also be in a vastly different concentration range of 100 nM.

Many of these kinases are involved in growth - related pathways, tumorigenesis pathways, and cell cycle control, such as Aurora kinase B (Borisa and Bhatt, 2017).

In addition, caffeine may increase the activity of several signaling enzymes, including the calcium - dependent protein kinase and protein kinase B (also called Akt), which have roles in muscle glucose uptake during and after exercise.

In a discovery screen profiling 102 cell lines against 8,400 compounds, PRISM led the researchers to a specific novel compound, BRD - 7880; the specific action against cell lines in the panel rapidly led them to discover that this compound worked by inhibiting aurora kinase B, an enzyme involved in cell division that is abnormally regulated in several cancers.

Iva describes her award winning PhD thesis «Role of membrane binding in the activation of Protein Kinase B (PKB) and Protein Kinase C (PKC)»

The protein kinase B - RAF is mutated in approximately 8 % of human cancers.

A great example for a successful PhD is Iva Lučić from the group of Thomas Leonard at the Max F. Perutz Laboratories (MPFL) at the Vienna BioCenter (VBC), who won the VBC PhD Award 2017 with her thesis entitled «Role of membrane binding in the activation of Protein Kinase B (PKB) and Protein Kinase C (PKC)».

Here, we show that enhanced hiPS - HEP cells respond to insulin with phosphorylation of protein kinase B - α (Akt), even at low insulin concentrations (Figure 4, Panels E and F), and that the genes involved in glycogen metabolism, gluconeogenesis, and insulin signaling are expressed at similar levels as in hphep cells (Figure 4, Panels B, C, and D).

Abbreviations: AGL = glycogen debranching enzyme; GSK3A / B = glycogen synthase kinase 3 α / β; GYS2 = glycogen synthase 2; PYGL = glycogen phosphorylase, liver form; PCK1 / 2 = phosphoenolpyruvate carboxykinase 1/2; FBP1 / 2 = fructose -1,6-bisphosphatase 1/2; G6PC = glucose -6-phosphatase; G6PD = glucose -6-phosphate 1 - dehydrogenase; GLUT - 2 = glucose transporter 2; INSR = insulin receptor; IRS1 / 2 = insulin receptor substrate 1/2; PIK3CA / B / D = PI3 - kinase subunit α / β / δ; and AKT1 = protein kinase B - α.

The enhanced hiPS - HEP cells respond to insulin with phosphorylation of protein kinase B - α (Akt), even at low insulin concentrations, and the genes involved in glycogen metabolism, gluconeogenesis, and insulin signaling are expressed at similar levels as in hphep cells.

Aminoglycoside - induced degeneration of adult spiral ganglion neurons involves differential modulation of tyrosine kinase B and p75 neurotrophin receptor signaling.

Then, the research group examined the molecular mechanism behind the impaired synaptic functions and behaviors in ARHGAP33 KO mice and found that ARHGAP33 is localized to the Golgi apparatus to regulate intracellular protein trafficking of the Tropomyosin receptor kinase B (TrkB) receptor, a neurotrophin receptor, to synaptic sites.

With this new understanding of the enzyme, called Inositol trisphosphate 3 - kinase B (ItpkB), scientists are closer to improving therapies for diseases such as bone marrow failure syndrome, anemia, leukemia, lymphoma and immunodeficiencies.

Not exact matches

The target for ibrutinib, an enzyme called Bruton's tyrosine kinase (BTK), is a key component of B - cell receptor signaling.

The advent of therapies directed at tumors with mutations in epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and B - Raf proto - oncogene (BRAF) genes over the past decade have dramatically changed outcomes, he says.

In experiments using enzyme inhibitors, the possibility that cinnamtannin B - 1 enhanced mobilization through the use of activation of enzymes such as PI3 kinase near the cell membrane was shown.

They will know that compound X inhibits kinases A, B and C, but compound Z inhibits kinases D and E. With such a big data set people can easily find compounds of particular interest to them and know that the compounds are annotated with near full - kinome inhibition data.»

Wang, H, Gai, Q, Yang, X, Li, Z, Linders, B, Santoro, S, Zutter, M. Role of the a1 and a2 integrin cytoplasmic domains in cell morphology, motility and responsiveness to stimulation by the protein kinase C pathway.

Two proteins that serve as critical inhibitory regulators downstream of the TCR are diacylglycerol kinase ζ (DGKζ), a regulator of Ras and PKC - θ signaling, and Casitas b - lineage proto - oncogene b (Cbl - b), an E3 ubiquitin ligase that predominantly regulates PI (3) K signaling.

Revelli J.P, Smith D, Allen J, Jeter - Jones S, Shadoan M.K, Desai U, Schneider M, Sligtenhorst I, Kirkpatrick L, Platt K.A, Suwanichkul A, Savelieva K, Gerhardt B, Mitchell J, Syrewicz J, Zambrowicz B, Hamman B.D, Vogel P, Powell D.R. Profound obesity secondary to hyperphagia in mice lacking kinase suppressor of ras 2.

Cbl - b, a RING - type E3 ubiquitin ligase, targets phosphatidylinositol 3 - kinase for ubiquitination in T cells.

Histone H3 is specifically phosphorylated, presumably by the oncogenic kinase Aurora B, at serine 10 at the onset of mitosis.

MEK kinase 1 gene disruption alters cell migration and c - Jun NH2 - terminal kinase regulation but does not cause a measurable defect in NF - $ ąppa $ B activation.

DGKζ, a lipid kinase, phosphorylates the second messenger DAG, terminating DAG - mediated activation of RasGRP1 and PKC - θ, whereas Cbl - b, an E3 ubiquitin ligase, facilitates ubiquitination and subsequent degradation of the p85 subunit of PI (3) K. Previous studies have evaluated numerous aspects of T cell biology in the two models (16 — 18, 25, 38), but the signaling and functional effects of DKGζ deficiency and Cbl - b deficiency in T cells had not been directly compared.

Clathrin complexes with the inhibitor kappa B kinase signalosome: imaging the interactome.

Recently, interest has developed regarding the possibility of targeting intracellular inhibitory proteins to improve T cell activity against cancer, including diacylglycerol kinase ζ (DGKζ)(9, 10) and Casitas b - lineage proto - oncogene b (Cbl - b)(11), which attenuate signal transduction events downstream of the TCR and CD28.

The basal and B - RAF - stimulated kinase activities of a third variant are unaltered but its activation by RAS is significantly reduced, suggesting that it may act in a dominant - negative manner to modulate pathway signaling.

Kapoor P, Bao Y, Xiao J, Luo J, Shen J, Persinger J, Peng G, Ranish J, Bartholomew B, Shen X. (2015) Regulation of Mec1 kinase activity by the SWI / SNF chromatin remodeling complex.

Confocal images of P150 dystrophic retina transplanted with hNPCctx — GDNF and double stained with antibodies against human nuclear antigen (red) and either (A) recoverin, a photoreceptor and cone bipolar cell marker (green), or (B) protein kinase Cα (PKCα), a bipolar cell marker (green).

Moreover, these ATP - competitive inhibitors induce the formation of B - RAF and C - RAF dimers, leading to extracellular signal — regulated kinase (ERK) activation in diverse cancer cell types (23).

(A) Localization of 25 identified missense point mutations affecting 19 residues in the schematic structure of JAK1 with its functional domains and (B) in the three - dimensional modeled structure of kinase and pseudokinase domain published by Flex9.

This signal can effectively be inhibited using RIPK2 inhibitors 1 and 2 and regorafenib (a known RIPK2 kinase inhibitor) at 100 nM as determined using RIPK2 phospho - specific antibodies (Fig. 4, A and B).

Rao B, van Leeuwen IM, Higgins M, Campbel J, Thompson AM, Lane DP and Lain S. Evaluation of an Actinomycin D / VX -680 aurora kinase inhibitor combination in p53 - based cyclotherapy.

(C) RIPK2 in HCT116 cells were IP with an anti-RIPK2 antibody (A) and the supernatant after IP in (A) was IP in (B) with the same RIPK2 antibody, and in vitro kinase (IVK) assay was carried out on both samples.

Receptor - interacting protein kinase 2 (RIP2 or RICK, herein referred to as RIPK2) is linked to the pathogen pathway that activates nuclear factor κ - light - chain - enhancer of activated B cells (NFκB) and autophagic activation.

Among the 25 different mutations identified, 12 affect residues located in the pseudokinase domain and 13 in the kinase domain (Figure 1A and B).

Abbreviations: Aβ, amyloid β - peptide; AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; Ambra1, activating molecule in Beclin -1-regulated autophagy; AMPK, AMP - activated protein kinase; APP, amyloid precursor protein; AR, androgen receptor; Atg, autophagy - related; AV, autophagic vacuole; Bcl, B - cell lymphoma; BH3, Bcl - 2 homology 3; CaMKKβ, Ca2 + - dependent protein kinase kinase β; CHMP2B, charged multivesicular body protein 2B; CMA, chaperone - mediated autophagy; 2 ′ 5 ′ ddA, 2 ′, 5 ′ - dideoxyadenosine; deptor, DEP - domain containing mTOR - interacting protein; DRPLA, dentatorubral pallidoluysian atrophy; 4E - BP1, translation initiation factor 4E - binding protein - 1; Epac, exchange protein directly activated by cAMP; ER, endoplasmic reticulum; ERK1 / 2, extracellular - signal - regulated kinase 1/2; ESCRT, endosomal sorting complex required for transport; FAD, familial AD; FDA, U.S. Food and Drug Administration; FIP200, focal adhesion kinase family - interacting protein of 200 kDa; FoxO3, forkhead box O3; FTD, frontotemporal dementia; FTD3, FTD linked to chromosome 3; GAP, GTPase - activating protein; GR, guanidine retinoid; GSK3, glycogen synthase kinase 3; HD, Huntington's disease; hiPSC, human induced pluripotent stem cell; hVps, mammalian vacuolar protein sorting homologue; IKK, inhibitor of nuclear factor κB kinase; IMPase, inositol monophosphatase; IP3R, Ins (1,4,5) P3 receptor; I1R, imidazoline - 1 receptor; JNK1, c - Jun N - terminal kinase 1; LC3, light chain 3; LD, Lafora disease; L - NAME, NG - nitro - L - arginine methyl ester; LRRK2, leucine - rich repeat kinase 2; MIPS, myo - inositol -1-phosphate synthase; mLST8, mammalian lethal with SEC13 protein 8; MND, motor neuron disease; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; MVB, multivesicular body; NAC, N - acetylcysteine; NBR1, neighbour of BRCA1 gene 1; NOS, nitric oxide synthase; p70S6K, ribosomal protein S6 kinase - 1; PD, Parkinson's disease; PDK1, phosphoinositide - dependent kinase 1; PE, phosphatidylethanolamine; PI3K, phosphoinositide 3 - kinase; PI3KC1a, class Ia PI3K; PI3KC3, class III PI3K; PI3KK, PI3K - related protein kinase; PINK1, PTEN - induced kinase 1; PKA, protein kinase A; PLC, phospholipase C; polyQ, polyglutamine; PS, presenilin; PTEN, phosphatase and tensin homologue deleted from chromosome 10; Rag, Ras - related GTP - binding protein; raptor, regulatory - associated protein of mTOR; Rheb, Ras homologue enriched in brain; rictor, rapamycin - insensitive companion of mTOR; SBMA, spinobulbar muscular atrophy; SCA, spinocerebellar ataxia; SLC, solute carrier; SMER, small - molecule enhancer of rapamycin; SMIR, small - molecule inhibitor of rapamycin; SNARE, N - ethylmaleimide - sensitive factor - attachment protein receptor; SOD1, copper / zinc superoxide dismutase 1; TFEB, transcription factor EB; TOR, target of rapamycin; TSC, tuberous sclerosis complex; ULK1, UNC -51-like kinase 1; UVRAG, UV irradiation resistance - associated gene; VAMP, vesicle - associated membrane protein; v - ATPase, vacuolar H + - ATPase; Vps, vacuolar protein sorting

p38 kinase regulates nitric oxide - induced apoptosis of articular chondrocytes by accumulating p53 via NFkappa B - dependent transcription and stabilization by serine 15 phosphorylation.

Furthermore, we determined that RIPK2 inhibitor 1 effectively inhibited KHM2 cells at an approximate IC50 of 5 — 10 nM, and kinase activity was somewhat sensitive to detergent conditions (Fig. 4, B and C).

(B) Treatment of P19 cells with indicated nM concentrations of the p38 MAP kinase inhibitor SB202190 for 30 minutes, followed by western blotting.