Protein kinase C beta II (PKCβII) has been implicated in diabetic nephropathy (DN). Mesangial cell (MC) hypertrophy is a pathologic feature of DN. PKCβII...
The formation of N-desmethyl LY333531 in human liver microsomal samples exhibited Michaelis-Menten kinetics yielding apparent KM values ranging from 1 to 3 μM. Identification of the enzyme involved in the formation ofN-desmethyl LY333531 was initiated via correlating the rate of its formation following incubation with a concentration of LY333531 approximating the KM value (1 μM) to immunoquantified levels and/or form-selective catalytic activities of specific drug-metabolizing enzymes in a bank of 20 human liver microsomes. The only catalytic activity to significantly correlate with formation of N-desmethyl LY333531 was that associated with CYP3A. Further corroborating the role of CYP3A in this biotransformation, formation of N-desmethyl LY333531 was observed by both expressed CYP3A4 and CYP2D6 but to a much greater extent by CYP3A4 (57-fold greater formation rate with CYP3A4 versus CYP2D6). To help delineate the role that either CYP3A or CYP2D6 plays in the formation of N-desmethyl LY333531, ...
Institute of Human Nutrition, Columbia University, New York, New York 10032, USA. As F9 embryonal carcinoma cells differentiate into parietal endoderm-like cells, expression of conventional protein kinase C (PKC) changes. Undifferentiated stem cells express PKCbeta but not PKCalpha, whereas differentiated parietal endoderm cells express PKCalpha but not PKCbeta. To determine whether changes in PKCalpha and/or PKCbeta expression control retinoic acid (RA)- and dibutyryl cyclic AMP-induced F9 cell differentiation, we established cell lines stably expressing PKCalpha, PKCbeta, antisense PKCalpha, or antisense PKCbeta RNAs. Constitutive expression of PKCalpha or inhibition of PKCbeta expression in F9 stem cells enhanced RA induced differentiation, both by increasing total expression and accelerating RA-induced expression of laminins A, B1, B2, and type IV collagen. In addition, expressing PKCbeta in a parietal endoderm cell line caused these cells to retrodifferentiate into stem cells. Based on ...
Complete information for PRKCB gene (Protein Coding), Protein Kinase C Beta, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Microcrystals of protein kinase C beta 1 have been grown from solutions of poly(ethylene glycol). Image analysis of electron micrographs of the protein crystals, which diffracted to 5.0 nm, revealed p3 symmetry with a unit cell of about 10.3 nm x 10.3 nm. The electron stain-excluding densities showed a three-domain ring structure in projection, giving kidney bean-shaped molecules of about 7.0 nm x 4.5 nm diameter, packed as trimers. The implications of these observations for the function of the enzyme are discussed.. ...
Background: Diabetic cardiomyopathy (DCM) is increasingly recognized as contributing to the morbidity and mortality of diabetic patients. We have recently demonstrated that the (mRen-2)27 transgenic rat (Ren-2) develops the haemodynamic and structural changes of DCM when diabetes is induced with streptozotocin (STZ). While multifactorial in its pathogenesis, the β isoform of protein kinase C (PKC) has been recently implicated as a central mediator in the development of diabetic complications. Accordingly, we hypothesized that its inhibition with the orally active, selective inhibitor of PKC-beta, ruboxistaurin (RBX) would preserve cardiac function and reduce collagenous matrix deposition.. Methods: Six week-old homozygous Ren-2 (n=34) rats were randomized to receive STZ (diabetic) or vehicle (non-diabetic) and followed for 6 weeks. Two days post STZ injection, when diabetes was confirmed, rats were further randomized to vehicle or RBX at 20mg/kg daily. Insulin (2-4 units x3 per week) was used ...
These reference sequences exist independently of genome builds. Explain. These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above. ...
Subjects will be randomly assigned to receive one of the following: R-CHOP plus enzastaurin or R-CHOP plus placebo, during two treatment periods: induction and maintenance. Induction phase: all subjects will receive R-CHOP for up to six, 21-day cycles. Subjects in the enzastaurin arm will receive a 1125 mg loading dose on Day 2 followed by 500 mg daily. Subjects in the placebo arm will take an identical number of tablets.. After 4-,6 cycles of induction therapy treatment assignment will be unblinded. Subjects in the enzastaurin arm who have achieved a response will have the opportunity to continue in the single-agent, maintenance phase of the study, and will receive single-agent enzastaurin at 500 mg/day for up to 2 years. Eligible subjects must begin the maintenance phase of the study within 6 weeks of completing induction therapy. ...
Rabbit polyclonal PKC beta 1 + PKC beta 2 antibody validated for WB, ELISA, IHC and tested in Human. Immunogen corresponding to synthetic peptide
PKC beta 2兔单克隆抗体[Y125](ab32026)可与小鼠, 大鼠, 人样本反应并经WB, IP, IHC, Flow Cyt, ICC/IF实验严格验证,被8篇文献引用并得到2个独立的用户反馈。
GNAQ mutations at codon 209 have been recently identified in approximately 50% of uveal melanomas (UM) and are reported to be oncogenic through activating the MAPK/Erk1/2 pathway. Protein kinase C (PKC) is a component of signaling from GNAQ to Erk1/2. Inhibition of PKC might regulate GNAQ mutation-induced Erk1/2 activation, resulting in growth inhibition of UM cells carrying GNAQ mutations. UM cells carrying wild type or mutant GNAQ were treated with the PKC inhibitor enzastaurin. Effects on proliferation, apoptosis, and signaling events were evaluated. Enzastaurin downregulated the expression of several PKC isoforms including PKCβII PKCθ, PKCε and/or their phosphorylation in GNAQ mutated cells. Downregulation of these PKC isoforms in GNAQ mutated cells by shRNA resulted in reduced viability. Enzastaurin exhibited greater antiproliferative effect on GNAQ mutant cells than wild type cells through induction of G1 arrest and apoptosis. Enzastaurin-induced G1 arrest was associated with inhibition ...
The maintenance of mature peripheral B cells depends on at least two survival cues, tonic signaling from the B cell receptor (BCR) complex and the extracellular cytokine B cell activating factor of the TNF family (BAFF). In addition to enhancing viability, BAFF controls the functional efficiency of the peripheral B cell pool by regulating complex physiological processes including cell growth, metabolism, energy homeostasis and entry into the cell cycle. BAFF-mediated induction of two molecular mechanisms, namely activation of the Akt signal transduction pathway and upregulation of the oncogenic kinase Pim-2 results in the modification of effector proteins including transcription factors and regulators of protein synthesis which are capable of executing the observed cellular physiological changes. The classic protein kinase C beta is instrumental in BAFF-induced Akt-activation and PKC beta-deficient B cells and mice show signs of partial refractiveness to BAFF. The protein tyrosine kinase Syk ...
Monoklonale und polyklonale PKC beta Antikörper für viele Methoden. Ausgesuchte Qualitäts-Hersteller für PKC beta Antikörper. Hier bestellen.
Rabbit monoclonal antibody raised against a human PRKCB peptide using ARM Technology. A synthetic peptide of human PRKCB is used for rabbit immunization.Customer or Abnova will decide on the preferred peptide sequence. (H00005579-K) - Products - Abnova
Pharmacological agents that inhibit enzymes of the B-cell receptor (BCR) pathway are of increasing importance in the treatment of B-cell malignancies. These include inhibitors of Bruton tyrosine kinase (BTK), phosphatidylinositol 3-kinase (PI3K), splenic tyrosine kinase and protein kinase C beta. Two agents are already approved in the USA and Europe: ibrutinib, a BTK inhibitor, for the treatment of chronic lymphatic leukaemia (CLL), mantle cell lymphoma (MCL) and Waldenstroms macroglobulinemia;and idelalisib, a PI3K delta inhibitor, for the treatment of CLL and follicular lymphoma. In addition, the role of these drugs in diffuse large B-cell lymphoma and marginal zone lymphoma is under investigation, as single agents and in combination with chemotherapy. In CLL, both ibrutinib and idelalisib have an established role as first-line therapy in patients with del(17p), and in MCL, ibrutinib is a standard option for patients relapsing after chemoimmunotherapy. Unexpected toxicities have been ...
Protein phosphatase involved in regulation of Akt and PKC signaling. Mediates dephosphorylation in the C-terminal domain hydrophobic motif of members of the AGC Ser/Thr protein kinase family; specifically acts on Ser-473 of AKT2 and AKT3, Ser-660 of PRKCB and Ser-657 of PRKCA (PubMed:15808505, PubMed:17386267, PubMed:18162466). Isoform 2 seems to have a major role in regulating Akt signaling in hippocampal neurons (By similarity). Akt regulates the balance between cell survival and apoptosis through a cascade that primarily alters the function of transcription factors that regulate pro- and antiapoptotic genes. Dephosphorylation of Ser-473 of Akt triggers apoptosis and suppression of tumor growth. Dephosphorylation of PRKCA and PRKCB leads to their destabilization and degradation (PubMed:18162466). Dephosphorylates STK4 on Thr-387 leading to STK4 activation and apoptosis (PubMed:20513427). Dephosphorylates RPS6KB1 and is involved in regulation of cap-dependent translation ...
BioAssay record AID 1079124 submitted by ChEMBL: Inhibition of human full length PKC beta2 expressed in baculovirus assessed as substrate phosphorylation using fluorescence-labelled peptides as substrate at 420 uM after 90 mins by microfluidic peptide phosphorylation assay.
Retinal pharmacotherapeutics / Nguyen, Quan Dong (Hrsg.). - Basel : Karger, 2016. - (Developments in Ophthalmology ; 55). - S. 295-301. - ISBN 978-3-318-05565-8, ISBN 978-3-318-05564-1. - ISSN 0250-3751. - eISSN 1662- ...
Two peptides derived from the C1B domain of protein kinase Cγ (PKCγ) were shown to associate with classical PKC isozymes and modulate their activities. These C1B peptides are designated C1B1 (amino acid residues 101-112 ...
111713 - Comparación de la concentración de factores de crecimiento transformante beta I, mediante 2 métodos de obtención de sangre en perros clínicamente sanos - Comparison of the concentration of transforming growth factors beta I by 2 methods of | Veterinaria.org . La primera comunidad veterinaria de habla hispana con presencia en Espa a y Am rica del Sur.
Attached to the multimodal Paul S. Sarbanes Transit Center, this station is steps from the central arts district of Downtown Silver Spring. ...
Wiki-Pi: a web resource for human protein-protein interactions. It shows genes and PPIs with information about pathways, protein-protein interactions (PPIs), Gene Ontology (GO) annotations including cellular localization, molecular function and biological process, drugs, diseases, genome-wide association studies (GWAS), GO enrichments, PDB ID, Uniprot ID, HPRD ID, and word cloud from pubmed abstracts.
NOS isoform activation is related to liver failure during sepsis, but the mechanisms driving mitochondrial impairment remain unclear. We induced sepsis by
Compare & find the top performing anti-Mouse (Murine) PKC beta antibody for Immunofluorescence (Paraffin-embedded Sections) (IF (p)).
Athens, Greece (ots/PRNewswire) - - Approximately 40 percent of people with diabetes developnephropathy, the leading cause of kidney failure Eli Lilly and Company...
K04166 AGTR1; angiotensin II receptor type 1 K04634 GNAQ; guanine nucleotide-binding protein G(q) subunit alpha K04635 GNA11; guanine nucleotide-binding protein subunit alpha-11 K05858 PLCB; phosphatidylinositol phospholipase C, beta [EC:3.1.4.11] K05858 PLCB; phosphatidylinositol phospholipase C, beta [EC:3.1.4.11] K05858 PLCB; phosphatidylinositol phospholipase C, beta [EC:3.1.4.11] K05858 PLCB; phosphatidylinositol phospholipase C, beta [EC:3.1.4.11] K04958 ITPR1; inositol 1,4,5-triphosphate receptor type 1 K04959 ITPR2; inositol 1,4,5-triphosphate receptor type 2 K04960 ITPR3; inositol 1,4,5-triphosphate receptor type 3 K02677 PRKCA; classical protein kinase C alpha type [EC:2.7.11.13] K19662 PRKCB; classical protein kinase C beta type [EC:2.7.11.13] K19663 PRKCG; classical protein kinase C gamma type [EC:2.7.11.13] K18050 PRKCE; novel protein kinase C epsilon type [EC:2.7.11.13] K06070 PKD; protein kinase D [EC:2.7.11.13] K06070 PKD; protein kinase D [EC:2.7.11.13] K06070 PKD; protein ...
Catalytic domain of the Protein Serine/Threonine Kinase, Classical Protein Kinase C. Serine/Threonine Kinases (STKs), Classical (or Conventional) Protein Kinase C (cPKC) subfamily, catalytic (c) domain. STKs catalyze the transfer of the gamma-phosphoryl group from ATP to serine/threonine residues on protein substrates. The cPKC subfamily is part of a larger superfamily that includes the catalytic domains of other protein STKs, protein tyrosine kinases, RIO kinases, aminoglycoside phosphotransferase, choline kinase, and phosphoinositide 3-kinase (PI3K). PKCs are classified into three groups (classical, atypical, and novel) depending on their mode of activation and the structural characteristics of their regulatory domain. PKCs undergo three phosphorylations in order to take mature forms. In addition, cPKCs depend on calcium, DAG (1,2-diacylglycerol), and in most cases, phosphatidylserine (PS) for activation. cPKCs contain a calcium-binding C2 region in their regulatory domain. There are four cPKC ...
Receptor tyrosine kinase (RTK) c-Kit signalling is crucial for the proliferation, survival and differentiation of haematopoietic stem cells (HSCs). To further understand the mechanisms underlying these events we explored how the downstream mediators interact. The present study investigated the function of conventional protein kinase Cs (c-PKC) in c-Kit mediated signalling pathways in HSC-like cell lines. This analysis supported earlier findings, that steel factor (SF) activates c-PKC, extracellular signal-regulated kinase (Erk) and protein kinase B (PKB). The present results were consistent with an important role of c-PKC in the positive activation of Erk and for proliferation. Further, it was observed that c-PKC negatively regulated PKB activity upon SF stimulation, indicating that c-PKC acts as a suppressor of c-Kit signalling. Finally, these observations were extended to show that c-PKC mediated the phosphorylation of the endogenous c-Kit receptor on serine 746, resulting in decreased overall ...
Mounting evidence points to a key role of PKC signaling in the pathology of AD, a degenerative disease characterized by loss of synapses and plasticity mechanisms in the brain. The disease is associated with the appearance of extracellular amyloid plaques caused by the mis-cleavage of amyloid precursor protein (APP) and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein [83,84], two pathologies for which PKC involvement has been implicated over the years. But the critical importance of deregulated PKC signaling in AD was recently cemented by the results of an unbiased and comprehensive phosphoproteomic analysis of both human AD postmortem brains and brains from four AD mouse models [85]: PKC substrates accounted for over half of the core molecules that displayed increased phosphorylation in AD compared with control brains. The most robust increase in phosphorylation in AD compared with control brains occurred on MARCKS but also included PKC substrates such as ...
To characterize glucagon-like peptide (GLP)-1 signaling and its effect on renal endothelial dysfunction and glomerulopathy. We studied the expression and signaling of GLP-1 receptor (GLP-1R) on glomerular endothelial cells and the novel finding of protein kinase A-dependent phosphorylation of c-Raf at Ser259 and its inhibition of angiotensin II (Ang II) phospho-c-Raf(Ser338) and Erk1/2 phosphorylation. Mice overexpressing protein kinase C (PKC)β2 in endothelial cells (EC-PKCβ2Tg) were established. Ang II and GLP-1 actions in glomerular endothelial cells were analyzed with small interfering RNA of GLP-1R. PKCβ isoform activation induced by diabetes decreased GLP-1R expression and protective action on the renal endothelium by increasing its degradation via ubiquitination and enhancing phospho-c-Raf(Ser338) and Ang II activation of phospho-Erk1/2. EC-PKCβ2Tg mice exhibited decreased GLP-1R expression and increased phospho-c-Raf(Ser338), leading to enhanced effects of Ang II. Diabetic ...
BACKGROUND: Runx transcription factors play critical roles in the developmental control of cell fate and contribute variously as oncoproteins and tumor suppressors to leukemia and other cancers. To discover fundamental Runx functions in the cell biology of animal development, we have employed morpholino antisense-mediated knockdown of the sea urchin Runx protein SpRunt-1. Previously we showed that embryos depleted of SpRunt-1 arrest development at early gastrula stage and underexpress the conventional protein kinase C SpPKC1. RESULTS: We report here that SpRunt-1 deficiency leads to ectopic cell proliferation and extensive apoptosis. Suppression of the apoptosis by pharmacological inhibition of caspase-3 prevents the ectopic proliferation and rescues gastrulation, indicating that many of the overt defects obtained by knockdown of SpRunt-1 are secondary to the apoptosis. Inhibition or knockdown of SpPKC1 also causes apoptosis, while cell survival is rescued in SpRunt-1 morphant embryos coinjected with
Our previous studies demonstrate that PKC-β, but not PKC-α, is associated with the outer surface of melanosomes (Park et al., 1999), consistent with the known location of this cytoplasmic enzyme (Nishizuka, 1992). Brief trypsinization of melanosomes removed PKC-β (Park et al., 1999). However, the mechanism by which activated PKC-β associates with melanosomes and phosphorylates tyrosinase remained to be elucidated. Our present results demonstrate that RACK-I on melanosomes anchors activated PKC-β, allowing the kinase to phosphorylate tyrosinase. The localization of RACK-I to melanosomes is strongly suggested by its co-localization, as demonstrated by confocal microscopy, with tyrosinase, a transmembrane protein known to be detected at the melanosome surface (Jimbow and Fitzpatrick, 1973; Maul and Brumbaugh, 1971). However, further support for this localization is provided by the readily detectable level of RACK-I in the purified melanosome preparation, as demonstrated by immunoblotting. The ...
|p|GF 109203X is a potent and selective inhibitor of protein kinase C [1].|/p||p| Protein kinase C (PKC) is a family of protein kinase enzymes that are involved in controlling the function of other proteins through the phosphorylation of serine and threon
CHICAGO -- Women with advanced ovarian cancer gained no survival benefit when treated with the investigational agent enzastaurin in addition to chemotherapy, according to a study reported here.
Joint research proposal. We would be happy to offer With Our Compliments this 4 component Pyramid Energy Healing System along-with User Instructions to any researcher who is interested, willing, and able to test the same with instruments and / or in a live trial on any patient, and provide a detailed observation report of the experiment.. Mr. Kirti Betai. ...
New neurons are continuously generated from stem cells and built-into the adult hippocampal circuitry, adding to memory space function. formation, eradication, and relocation of synapses; modulating excitatory synaptic maturation; and taking part in practical synaptic plasticity. Significantly, microglia have the ability to feeling subtle changes within their environment and could use this info to in a different way modulate hippocampal wiring, impacting on memory space function ultimately. Deciphering the part of microglia in hippocampal circuitry constant rewiring will help to better understand the influence of microglia on memory function. induce neurite Enzastaurin enzyme inhibitor outgrowth (Nagata et al., 1993; Chamak et al., 1994, 1995). Second, several studies indicate that microglia induce neurite growth by releasing different factors after injury such Enzastaurin enzyme inhibitor as brain derived neurotrophic factor (BDNF) in the striatum, insulin growth factor-1 (IGF-1) in the ...
Background: Treatment of non-small cellular lung malignancy (NSCLC) remains a hard job in oncology. impaired by treatment with SU11274 and enzastaurin considerably, and their results had been synergistic in mixture (CI=0.32 and 0.09). Phosphorylation of MET, FAK, AKT, and GSK3? had been inhibited with both agencies in combination strongly. Conclusions: Concomitant inhibition of MET and PKC? improved cytotoxicity in vitro against NSCLC considerably, disrupting essential downstream 55576-66-4 manufacture signaling pathways. Additional evaluation in pet models can be warranted. and configurations.[21] Inhibition of PKC? with enzastaurin continues to be studied in thoracic malignancies. Our previous function has demonstrated the result of enzastaurin against malignant pleural mesothelioma,[41] and its own synergistic activity when coupled with cisplatin. In NSCLC, activity of enzastaurin and pemetrexed, a utilized antifolate substance typically, provides revealed synergistic activity against SW1573 ...
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Buy GSK-3 beta Inhibitors from Santa Cruz. These inhibit GSK-3 beta and may affect a variety of other cell signaling and Alzheimers disease related proteins.
Plasmid PKCalpha.K/N.FLAG from Dr. Alex Tokers lab contains the insert PKC alpha and is published in Adv Exp Med Biol. 2002 . 506(Pt A):237-41. This plasmid is available through Addgene.
购买Abcam DNA PKcs小鼠单克隆抗体[18-2](ab44815)可与大鼠, 人样本反应并经WB, IP, IHC, Inhib, ICC/IF实验严格验证并得到1个独立的用户反馈。所有产品均提供质保服务,中国75%以上现货。
I have started measuring in-situ Protein Kinase C activity in permeabilized cells grown in 96-well plates, based on a few references from the literature such as: Heasley L.E., J.Biol.Chem., 1989, 264, 8646. I always get high activity after stimulation with phorbol esters and very low activity after treatment with PKC inhibitors. The problem is that the activity in untreated cells is often almost as high as in stimulated cells. Any advice or protocol would be welcome. Thanks Bernard medbpl at emory.edu ...
In the paper he and his coauthors,among them Annarita Miluzio and Stefania Oliveto at INGM and Luciano Mutti, now at University of Salford, showed that mesothelioma lung cancer cells contain high levels of the active phosphorylated form of eIF6.. Based on what they knew about how eIF6 became activated, they decided to test whether a drug called Enzastaurin could deactivate it. Enzastaurin is currently in clinical trials for a range of other cancer types including prostate, lymphoma brain and bowel. Treating mesothelioma cells with Enzastaurin did indeed deactivate eIF6, by decreasing its phosphorylation.. This deactivation caused a reduction in the growth of the mesothelioma cells and also reduced cancer spread. Normally cancer cells metabolise food (glucose) very rapidly. This is essential to keep up with the high demand for energy required for the rapid multiplication of cancer cells within a tumour. The team deduced that this decrease in cell growth and reduction in cancer spread was caused ...
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TY - JOUR. T1 - Synthesis and protein kinase C binding activity of benzolactam-V7. AU - Ma, Dawei. AU - Wang, Guoqiang. AU - Wang, Shaomeng. AU - Kozikowski, Alan P.. AU - Lewin, Nancy E.. AU - Blumberg, Peter M.. PY - 1999/5/17. Y1 - 1999/5/17. N2 - Benzolactam-V7 (3a), a simplified analogues of (-)-indolactam-V with twist-form conformation, was synthesized and evaluated as a new protein kinase C modulator. Both 3a and its-7-substituted analogue 3c showed weak binding activity to displace PDBU binding from recombinant PKCα.. AB - Benzolactam-V7 (3a), a simplified analogues of (-)-indolactam-V with twist-form conformation, was synthesized and evaluated as a new protein kinase C modulator. Both 3a and its-7-substituted analogue 3c showed weak binding activity to displace PDBU binding from recombinant PKCα.. UR - http://www.scopus.com/inward/record.url?scp=0033577690&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0033577690&partnerID=8YFLogxK. U2 - ...
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Protein Kinase C Theta Type (nPKC Theta or PRKCQ or EC 2.7.11.13) - Pipeline Review, H1 2017 Size and Share Published in 2017-05-30 Available for US$ 3500 at Researchmoz.us