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Validated All-in-One™ qPCR Primer for PIK3CG(NM_001282426.2) Search again
Product ID:
HQP158708
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IMD97, PI3CG, PI3K, PI3Kgamma, PIK3, p110gamma, p120-PI3K
Gene Description:
phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma
Target Gene Accession:
NM_001282426.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a protein that belongs to the pi3/pi4-kinase family of proteins. The gene product is an enzyme that phosphorylates phosphoinositides on the 3-hydroxyl group of the inositol ring. It is an important modulator of extracellular signals, including those elicited by E-cadherin-mediated cell-cell adhesion, which plays an important role in maintenance of the structural and functional integrity of epithelia. In addition to its role in promoting assembly of adherens junctions, the protein is thought to play a pivotal role in the regulation of cytotoxicity in NK cells. The gene is located in a commonly deleted segment of chromosome 7 previously identified in myeloid leukemias. [provided by RefSeq].
Gene References into function
- PI3K promotes assembly of adherens junctions, which, in turn, control p38 MAPK activation and enterocyte differentiation.
- activates phosphatidylinositol 3 (PI3) kinase and requires PI3 kinase to regulate the cell cycle [TEL/platelet-derived growth factor receptor beta]
- PI3K inhibits HIV-1 transcription by targeting the viral protein Tat activation complex.
- data indicated that the v-Crk-induced activation of PI3K/AKT pathway was cooperatively achieved by two distinct interactions
- CB(1)-induced ERK activation was mediated by PI3K(IB) and this effect may have important consequences in the control of cell death/survival decision.
- Bordetella pertussis infection of human monocytes resulted in a marked recruitment of cellular PI3-K to the sites of B. pertussis contact
- Down-regulation of PIK3CG by CpG hypermethylation is associated with progression of colorectal cancer
- higher protein levels of the PI3K subunit p110 in neutrophils from MDS patients
- These results indicate that PI3k/Akt pathway is involved in the signaling cascade of glioma cells required to induce cell migration.
- regulates human immunodeficiency virus type 1 replication following viral entry in primary CD4+ T lymphocytes and macrophages
- PI3-K activation is signaled by rapid feedback amplification that involves P2Y(12) receptor-mediated activation of Syk.
- migrating glioma cells activate the PI3-K survival pathway, protecting migrating cells from apoptosis
- 1) the PI3K-Akt pathway plays an important role in preventing Fas-mediated apoptosis; and 2) a PI3 K inhibitor, such as LY294002, might be a useful anti-tumoral agent for gastric carcinoma
- Vanadyl sulfate treatment also prolonged the insulin-stimulated activation of phosphatidylinositol 3-kinase (PI3-K).
- Activation of hexosamine pathway affects glucose-induced phosphorylation of IRS-1. Impairs coupling of IRS-1 and PI 3-kinase and activativates Akt/mammalian target of rapamycin/phosphorylated heat- and acid-stable protein-1/p70S6 kinase pathway.
- Thus, our results identified a functional region in the IL-1R AcP required for the recruitment and activation of PI 3-kinase.
- PI3Kgamma appears to negatively control cardiac contractility through different signalling mechanisms [review]
- In Goto-Kakizaki rat soleus muscle, chronic administration of antioxidant alpha -lipoic-acid partly ameliorated the diabetes-related deficit in glucose metabolism including the enzymes Akt/PKB and PI-3 kinase.
- stromal cell-mediated apoptotic protection in B-lineage ALL is mediated by PI3K/mTOR and MEK via a synergistic mechanism
- PI 3-kinase-initiated signaling pathway is one of the most frequently altered in head and neck squamous cell carcinoma.
- Amiloride enhances TRAIL-induced cytotoxicity by inhibiting phosphorylation of the PI 3-Kinase-Akt pathway-associated kinases and phosphatases.
- there is a previously unknown, p101-related regulatory subunit for PI3Kgamma
- activation of the PI3K/Akt pathway identified as an anti-inflammatory signal that may contribute to the establishment of Salmonella typhimurium in the intestine.
- IL-4 > PI3K/Akt > NF-(kappa)B signaling pathways, which activate androgen receptor signaling, play an important role during the development of androgen independent prostate cancer cells.
- PI3-K promotes the expression of TFF3 and MUC2 and that the PI3-K pathway may play a pivotal role in intestinal goblet cell differentiation.
- p110gamma and p85alpha class Ia phosphoinositide 3-kinase (PI3K) subunits play roles in generating the antiapoptotic and chemoresistant phenotype associated with accelerated local tumor recurrence
- Acanthamoeba castellani-mediated brain microvascular endothelial cell death is dependent on phosphatidylinositol 3-kinase
- Stimulation of TNF-alpha-primed human neutrophils with fMLP results in biphasic activation of PI3K; the first phase is largely dependent on PI3Kgamma; the second phase is largely dependent on PI3Kdelta and regulates parallel activation of ROS production
- the PI3-kinase/p38(MAPK)/CREB pathway contributes to the EGF activation of NF-IL6beta gene expression
- the nSH2 domain of the p85 regulatory subumit is responsible for p110 regulatory contacts, and its disruption leads to constitutive p110 activity
- In conclusion, erythropoietin may attenuate high glucose-induced endothelial cell apoptosis via PI-3 kinase pathway.
- The protein phosphorylation activity of PIK3 plays an essential role in beta-adrenergic receptor internalization and identify non-muscle tropomyosin as a cellular substrate.
- In human islets, activation of PPAR-gamma inhibits h-IAPP-induced islet cell apoptosis, and this action is at least in part mediated through activation of the phosphatidylinositol 3'-kinase-Akt cascade.
- The TGFbeta(1)-induced destabilisation of E-cadherin-mediated cell-cell adhesion involves phosphorylation of beta-catenin, which is regulated by E-cadherin adhesion complex-associated PI3-kinase and PTEN.
- as tumorigenesis progresses the addiction of cancers to their initiating oncogene is reduced to, at least in the case of Ras, the PI3K/AKT pathway.
- this specific PI 3-kinase isoform is involved in both proliferation and the apoptosis resistance associated with chronic myeloid leukemia
- These results suggest that the cytoprotective effect of deprenyl is, in part, dependent on Nrf2-mediated induction of antioxidative proteins, suggesting that activation of the PI3K-Nrf2 system may be a useful therapeutic strategy for PD.
- Results showed that inhibition of PI-3 kinase with wortmannin was accompanied by a considerably reduced expression of beta-catenin.
- analysis of a nuclear matrix attachment region like sequence in the last intron of PI3Kgamma
- p110beta, -gamma, and -delta isoforms of class I phosphoinositide 3-kinase have roles in oncogenic transformation
- Cellular responsiveness to Notch signals depends on the activity of the PI3K-Akt pathway in cells as diverse as CHO cells, primary T-cells and hippocampal neurons.
- It is concluded that PI3-kinase induces or modulates the activity of recombinant TRPV2 channels; in contrast to the previously proposed mechanism, activation of TRPV2 channels by PI3-kinase is not due to channel translocation to the plasma membrane.
- The phosphatidylinositol 3-kinase (PI3K) pathway promotes cancer cell proliferation and survival.
- These studies have revealed a novel mechanism of Trichostatin A action through derecruitment of a repressor from the Luteinizing hormone receptor gene promoter in a PI3K/PKCzeta-induced Sp1 phosphorylation-dependent manner.
- The acid-unfolded state of the SH3 domain adopts a partly folded conformation through nonnative long-range contacts between the dynamically restricted residues at the amyloid-forming condition.
- vascular endothelial growth factor expression is induced through the glucocorticoid receptor-related phosphatidylinositol 3-kinase/Akt and beta-catenin/T-cell factor-dependent pathway in human endothelial cells
- These results demonstrate that estradiol positively regulates essential proteins of the IGF signalling pathway.
- PI3 kinase effectors PKB and PKC(zeta) are also activated by PI3 kinase in a CD14 dependent manner in lipopolysaccharides stimulated human peripheral blood mononuclear cells.
- PI3K and its product, PIP(3), facilitate bile acid-induced [Ca(2+)](i) responses in pancreatic acinar cells through inhibition of SERCA-dependent Ca(2+) reloading into the ER and that bile acid-induced trypsinogen activation is mediated by PI3K.
- We propose that PI(3)Kgamma regulates some aspects of neutrophil polarization that are relevant to movement, such as integrin-based adhesion and the accumulation of polymerized (F)-actin at the leading-edge.
- These data indicate that the aberrant expression of PTEN contributes to the activation of the PI3kinase/Akt pathway and its transcription factor mediators in glioma.
- PI 3-K signaling pathway suppresses phorbol 12-myristate 13-acetate-induced expression of p21WAF1/Cip1 in human leukemia cells, and that this effect is partly mediated by PKC zeta.
- This review describes the second-messenger PI3K gamma signalling pathways that are involved in immune responses relevant to the pathogenesis of rheumatoid arthritis and other inflammatory diseases.
- PI3K is not overexpressed in melanocytic lesions.
- PAR1 couples to G(i/o) in human platelets and activates phosphoinositide-3 kinase (PI3K).
- Elevated and highly expressed levels in both laarge B-cell lymphoma and Hodgkin lymphoma.
- SCF-enhanced proliferation and invasion of KIT-positive colorectal cancer cells is achieved mainly through the PI3K/Akt pathway.
- phosphatidylinositol 3-kinase/Akt signaling and induces apoptosis is inhibited by energy depletion via AMP-activated protein kinase-dependent phosphorylation of IRS-1 at Ser-794
- Evidence is presented that PI3K is involved in basic fibroblast growth factor-stimulated fibroblast-collagen matrix contraction.
- Phosphorylated PIK3 was documented in 15/17 cytokeratin-positive breast cancer samples.
- Results suggest that aberrant activation of PI3K-Akt pathway may contribute to increased cell invasiveness and facilitate prostate cancer progression.
- Ep-CAM cross signaling with N-cadherin involves Pi3K, resulting in the abrogation of the cadherin adhesion complexes in epithelial cells.
- These results suggest that PLEK2 is involved in actin rearrangement in a PI 3-kinase dependent manner.
- In macrophages, uPA was found to activate MAP-kinase through PI3 kinase (PI3K)
- These results suggested that PKB enhanced DNMT1 stability and maintained DNA methylation and chromatin structure, which might contribute to cancer cell growth.
- mTOR inhibition increases eIF4E phosphorylation through a PI3K-dependent and Mnk-mediated mechanism.
- These data identify a novel, PI-3K-dependent pathway by which CSF-1 directs delayed caspase activation in monocytes and thereby modulates DC differentiation.
- Phosphatidylinositol 3-kinase inhibition by LY294002 also enhanced TRAIL-induced apoptosis.
- phosphoinositide 3-kinase/Akt/eNOS, but not mitogen-activated protein kinase/ERK, signal transduction pathway may be involved in SDF-1alpha mediated migration of endothelial progenitor cells
- Migratory response of freshly isolated T cells is dependent on PI3K signals provided predominantly by PI3Kgamma.t he role of PI3K in cell migration is context-dependent and diminishes during ex vivo maintenance.
- VEGF regulates angiopoietin-Tie2 signaling by inducing proteolytic cleavage and shedding of Tie2 via a novel PI3K/Akt-dependent pathway.
- IFNalpha-induced apoptosis requires activation of ERK1/2, PKCdelta, and JNK downstream of PI3K and mTOR, and it can occur in a nucleus-independent manner, thus demonstrating that IFNalpha induces apoptosis in the absence of de novo transcription.
- human betaARs undergo a process of intracellular sequestration that is dynamically reversed after LVAD support. Importantly, mechanical unloading leads to complete reversal in PI3Kgamma and betaARK1-associated PI3K activation.
- Cyclin G2 expression is modulated by HER2 signaling through multiple pathways including phosphoinositide 3-kinase, c-jun NH(2)-terminal kinase, and mTOR signaling.
- These data suggest that the PI3K/Akt and mTOR/p70S6K signaling pathways are essential for adipogenesis of human mesenchymal stem cells.
- Signal transduction pathways underlying the enhanced cell migration reveal that the IGF-I-IGFBP-VN complex stimulates a transient activation of the ERK/MAPK signaling pathway and a sustained activation of the phosphatidylinositide 3-kinase/AKT pathway.
- although PI3K can enhance early responses to the bacterial chemoattractant fMLP, it is not required for migration towards this chemoattractant
- These results suggest that caffeine has a cytoprotective effect due to the activation of the PI3K/Akt pathways in SH-SY5Y cells.
- Association of a functional missense polymorphismwith colon cancer risk in a population-based case-control study. [review]
- TNF-alpha overrides the G2/M checkpoint in keratinocytes and allows for some cells containing unrepaired cyclobutane pyrimidine dimers to enter the cell cycle. TNF-alpha seems to be dependent on PI3K-Akt activation.
- These data show that Hsp27 antagonizes Bax-mediated mitochondrial injury and apoptosis by promoting Akt activation via a PI3-kinase-dependent mechanism.
- Data show that in airway smooth muscle cells from asthmatics, the presence of a strong proliferative stimulus (10% FBS) reduces ERK activation resulting in a shift to the PI 3-kinase pathway.
- Results identify a molecular mechanism by which activated FGFR2 recruits Cbl in raft micro-domains to trigger PI3K ubiquitination and proteasome degradation, and reveal a role for PI3K/Akt in the control of osteoblast survival by FGFR2 signaling.
- The PI3K/Akt/mTOR signaling pathway is implicated in the development of cervical cancer.
- Cav-1 increases the basal and TGF-beta1-induced expression of type I procollagen by regulating two opposite signaling pathways: inhibiting TGF-beta1/smad signaling and activating a PI-3 kinase/Akt/mTOR-dependent pathway in human dermal fibroblasts.
- This study provides a direct link between the growth factor signaling pathways regulated by PI3 kinase/Akt and MAP kinases with Myc-mediated transcription.
- Transforming growth factor beta induces apoptosis through repressing the phosphoinositide 3-kinase/AKT/survivin pathway in colon cancer cells.
- The interplay between cancer cell-derived clusterin and IGF-1 may dictate the outcome of cell growth and dormancy during tumorigenic progression.
- tau interactions with Src homology 3 domains of phosphatidylinositol 3-kinase, phospholipase Cgamma1, Grb2, and Src family kinases are regulated by phosphorylation
- High NG2/MPG expression correlated with multidrug resistance mediated by increased activation of alpha3beta1 integrin/PI3K signaling and their downstream targets, promoting cell survival
- 7-ketocholesterol-induced apoptosis has a role in phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway
- GILZ is a mediator of glucocorticoid killing, and is regulated by PI3-kinase/AKT.
- The role of PI3K pathway activation in thyroid cancer is discussed, with a focus on recent advances.
- Activation of the PI3K pathway mediated cytoplasmic retention of the Wilms tumor (WTI) protein, which strongly suppressed the hTERT promoter.
- Interleukin (IL) 1beta induction of IL-6 is mediated by a novel phosphatidylinositol 3-kinase-dependent AKT/IkappaB kinase alpha pathway targeting activator protein-1
- The p-EGFR:p-AKT ratio deserves further investigation as a predictive parameter for clinical response to erlotinib in NSCLC tumors expressing wild-type EGFR gene.
- Our results also indicated that the integrin alphaVbeta3 antibody (LM609) could block the Angptl3-induced protein kinase B phosphorylation.
- mediates intracellular signals to regulate a variety of cellular responses and its genomic mutations and alterations underlie cancer, viral and/or bacterial infections.[review]
- MCL-1 expression is activated by Triiodothyronine, which increases its promoter activity by a non-genomic mechanism using the PI3-K signal transduction pathway.
- required for sphingosine-1-phosphate -induced endothelial cell migration through activation of Rac1
- Activation of the PI3K pathway is significantly associated with adverse clinical outcome in renal cell carcinoma.
- Phosphoinositide 3-kinase/AKT signaling can promote AIB1 stability independently of GSK3 phosphorylation.
- Data show that M. bovis BCG-induced human beta-defensin mRNA expression in A549 cells is regulated at least in part through activation of signaling proteins of PKC, JNK and PI3K.
- None of the components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN influence the relation between IRS-1 genotype and prostate cancer risk. Ther is no association between carriage of the variant IRS-1 gene and prostate cancer risk.
- Datas show that transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab.
- PIK3IP1 is an important regulator of PI3K in vivo, and its dysregulation can contribute to liver carcinogenesis
- PI3K inhibition by Ly294002 alters gene expression in two breast cancer cell lines.
- ApoCIII activates PKCbeta, which inhibits the IRS-1/PI3K/Akt/eNOS pathway and induces endothelial dysfunction.
- Data show that IGF2 activates PI3K and TGFbeta signal pathways during proliferation and differentiation of chondrocytes.
- The role of PI3K/Akt activity and DNA-PKcs on XRCC1 expression/stabilization, was studied.
- DIDS-sensitive Cl- channels play a key role in the Low-density lipoprotein-induced cell proliferation of human aortic smooth muscle cells via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1.
- These results suggest that the BMP-2 acts through PI3K/Akt, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of beta1 integrin and contributing the migration of human chondrosarcoma cells.
- Endothelin signaling axis activates osteopontin expression through PI3 kinase pathway in A375 melanoma cells.
- A selective allosteric inhibitor of Akt kinase was used to interrogate a panel of breast cancer cell lines characterized for genetic lesions that activate PI3K/Akt signaling PI3K mutations.
- Gate control for cell polarization can explain how Rac can be employed for both PI3K-dependent and -independent signaling pathways coexisting in the same cell.
- These findings demonstrate that HAPO induces endothelial cell proliferation through the PI-3K/Akt pathway.
- Glycine-extended gastrin induced signalling involves a JAK2/PI3-kinase/Akt/NF-kappaB sequence leading to COX-2 transcription.
- These data show that, in addition to inactivation of 4E-BP1 via hyperphosphorylation, signaling through the PI3K pathway silences 4E-BP1 gene transcription.
- HuR is a direct transcription target of NF-kappaB; its activation in gastric cancer cell lines depends on phosphatidylinositol 3-kinase/AKT signaling. HuR activation by this pathway has proliferative and antiapoptotic effects on gastric cancer cells.
- These data demonstrate that integrin/EGFR cross-talk is required for expression of Egr-1 through a novel regulatory cascade involving the activation of the PI3K/Akt/Forkhead pathway.
- IFN-gamma exerted a delayed suppressive effect on K(+) channels by enhancing iNOS expression and an acute stimulatory effect, which was independent of either NO pathways or phosphorylation mediated by PKA, PKG, and PI3K in renal proximal tubule cells.
- PDGF-mediated protection also involved the inhibition of gp120-induced release of mitochondrial cytochrome C. Our findings thus underscore the roles of both PI3K/Akt and Bcl family pathways in PDGF-mediated neuroprotection.
- Altered insulin activation of the PI3K/Akt but not the MAPK pathway precedes and may contribute to development of whole-body insulin resistance and type 2 diabetes in men with low birth weight.
- NGF induces Mac-2BP expression via the PI3K/Akt/NF-kappaB pathway.
- These data demonstrated that cell adhesion-mediated PI3K/Akt activation could be one of the important mechanisms of resistance to genotoxin-induced cell death in differentiated epithelial cells.