|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for PIK3CA(NM_006218.3) Search again
Product ID:
HQP104554
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CCM4, CLAPO, CLOVE, CWS5, MCAP, MCM, MCMTC, PI3K, PI3K-alpha, p110-alpha
Gene Description:
phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha
Target Gene Accession:
NM_006218.3(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.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
Phosphatidylinositol 3-kinase is composed of an 85 kDa regulatory subunit and a 110 kDa catalytic subunit. The protein encoded by this gene represents the catalytic subunit, which uses ATP to phosphorylate PtdIns, PtdIns4P and PtdIns(4,5)P2. This gene has been found to be oncogenic and has been implicated in cervical cancers. [provided by RefSeq].
Gene References into function
- This paper reports the first purification of a phosphoinositide 3-kinase and shows that the protein is a heterodimer of an 85 kd regulatory subunit that mediates binding to phosphorylated proteins and a 110 kd catalytic subunit.
- In squamous cell carcinomas the negative effect of p53 induction on cell survival involves transcriptional inhibition of PIK3CA that is independent of PTEN activity, as PTEN is not expressed in the primary tumors
- agonist binding to Gq-coupled receptors blocks Akt activation via the release of active Galphaq subunits that inhibit PI3K via an inhibitory interaction between Galphaq and p110alpha PI3K.
- data suggest that mutant PIK3CA is likely to function as an oncogene in human cancers; PIK3CA may prove useful for diagnostic and therapeutic purposes
- Missense Mutation in PIK3CA is associated with breast cancers
- Mutations of PIK3CA is associated with anaplastic oligodendrogliomas, high-grade astrocytomas, and medulloblastomas
- oncogenic mutations in human cancers
- Genetic alterations of class IA PI3K subunit genes can occasionally play a role in human glioblastoma by activating the PI3K-AKT signaling pathway independently of PTEN mutation.
- Data show that glucose is a crucial regulator of V-ATPase in renal epithelial cells and that the effect of glucose is mediated by phosphatidylinositol 3-kinase (PI3K).
- determined the growth-regulatory and signaling properties of the three most frequently observed PIK3CA mutations: E542K, E545K, and H1047R
- PIK3CA mutations in exons 9 & 20 were directly sequenced. A novel silent mutation was found. PIK3CA mutation may be an early event in ovarian carcinogenesis.
- Activation of the PI3K signalling pathway in gastric cancer may be achieved through up-regulation or mutation of PIK3CA, in which the latter may be a consequence of mismatch repair deficiency.
- Mutation of PIK3CA is frequent, occurs early in carcinoma development, and has prognostic and therapeutic implications for breast cancer.
- Data indicate that mutations of PIK3CA play an oncogenic role in substantial fractions of ovarian and breast carcinomas.
- mutation of the PIK3CA gene is not common, but its amplification is relatively common and may be a novel mechanism in activating the PI3K/Akt pathway in some thyroid tumors
- Colon cancer-associated PIK3CA mutations are functionally active so that they are likely to be involved in carcinogenesis.
- Amino acid substitutions in PIK3CA from human colorectal cancer cell lines constitutively activate the AKT pathway, and consequently, promote tumor cell growth and invasion.
- PI-3 kinase p110alpha subunit expression and recombinant heparin-binding epidermal growth factor-like growth factor (HB-EGF) synergistically decrease inducible nitric oxide synthase expression and nitric oxide production in intestinal epithelial cells
- copy number gains, instead of mutation, may be a common mechanism for activation of PIK3CA in tumorigenesis of primary nasopharyngeal carcinoma
- an important role of PIK3CA gene aberrations in the molecular pathogenesis of primary glioblastomas
- this study has shown that the mutations detected in the helical and kinase domains of PIK3CA do not seem to affect the PI3-K pathway characteristics of the eight cell lines studied
- The frequent and clustered mutations within PIK3CA make it an attractive molecular marker for early detection and a promising therapeutic target in breast cancer.
- analysis of PIK3CA mutations in ovarian cancer [letter]
- increased activation state of AKT kinase appears to be present in cervical carcinogenesis, and may be accounted for by PIK3CA amplification, whereas PTEN mutation seems to be of little importance
- Mutant PIK3CA is likely to function as an oncogene in anaplastic thyroid cancer and less frequently well-differentiated thyroid carcinomas.
- PIK3CA mutations are associated with breast cancer
- Data show that alpha6 and alpha3 integrin subunits interact with laminin 5 to increase expression of E-cadherin, and suggest that phosphoinositide 3-kinase (PI 3-kinase) activation plays a key role in this cross-talk.
- although introduction of activating mutations from p110alpha at the corresponding sites in p110beta failed to render the enzyme oncogenic in human cells, the possibility remains that other mutations might activate the beta isoform
- cancer-specific mutations in PIK3CA have made p110alpha an ideal drug target [Review]
- A mutation status profile of the PIK3Ca gene in the National Cancer Institute (NCI)-60 panel of human cancer cell lines provides insights into the role of mutant PIK3Ca in oncogenic signaling
- study extends previous observations in other tumor types by demonstrating presence of somatic PIK3CA mutations in both SCC and adenocarcinoma of the esophagus, thus implicating the PI3K pathway in the initiation and/or progression of esophageal cancers
- These results indicate that PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and EGF, and that insulin-stimulated, but not EGF-stimulated, ERK1/2 and Akt signalings diverge at PI3K.
- AT(1) receptor-mediated activation of PI 3-K/Akt cascades occurs at least partially via the transactivation of EGF receptor, which is under a negative control by AT(2) receptor in hypertrophic scar fibroblasts.
- PIK3CA mutations are associated with head and neck squamous cell carcinoma
- Although a key factor in TRAF6-dependent activation of PI 3-kinase, ectopic expression of Src was insufficient for NF-kappaB activation and, in contrast to NF-kappaB, was not inhibited by IRAK2.
- Mutation of PIK3CA is associated with breast cancer
- Somatic mutations of PIK3CA, encoding p110alpha catalytic subunit of Class IA PI3Ks, have been found in various cancers.
- inhibition of PI 3-kinase activity reduced hypoxic HIF-1alpha protein levels to a similar extent as serum deprivation
- PI3K-IA activity is necessary for both high NaCl- and ionizing radiation-induced activation of ATM and (ii) high NaCl activates PI3K-IA, which, in turn, contributes to full activation of TonEBP/OREBP via ATM.
- Various mutations in a variety of cancers, including a pseudogene and polymorphisms.
- p110alpha play an important role in tumor growth by inducing angiogenesis and by increasing HIF-1alpha and VEGF expression. This work provides a better understanding of the molecular mechanism of human cancer induced by the activation of PI3K signaling.
- First report of PIK3CA mutation in pancreatic cancer, providing evidence of its oncogenic properties.
- Increased expression for PIK3CA mrna is associated with regional lymph node metastasis in esophageal squamous cell carcinoma
- Acidic pH exposure protects HEMEC through induction of Hsps and activation of MAPK and PI3 kinase pathway.
- PIK3CA amplification is uncommon and appears to be late event in the development of ethmoid sinus adenocarcinoma.
- TGF-beta1 regulates COX-2 expression in human mesangial cells through the activation of ERK1/2, p38 MAPK, and PI3K.
- Pik3ca, Ras family, and Braf activating mutations occur rarely in human neuroblastomas or in a murine model driven by neural-restricted MYCN overexpression.
- These studies demonstrate that induction of fibulin 5 gene expression in lung fibroblasts is mediated via canonical TGF-beta/Smad signaling and requires the PI3-kinase/Akt pathway.
- The expression of p110alpha siRNA significantly decreased cell migration, invasion and proliferation.
- Outside-in signaling via P2Y12 and both PI3Kbeta and PI3Kgamma isoforms is required for maintenance of a platelet aggregate.
- PIK3CA mutations were strongly associated with FGFR3 mutations in superficial papillary bladder tumors.
- PIK3CA mutation incidence was significantly lower in lung adenocarcinoma than in lung squamous cell carcinoma; among eight patients with a PIK3CA mutation, three patients also harbored an EGFR somatic mutation.
- results confirm that PIK3CA mutations are frequent in endometrial carcinoma and support the hypothesis that PIK3CA mutations may have an additive effect to PTEN monoallelic inactivation in endometrial carcinoma
- PI3K is an important intracellular regulator of epidermal homeostasis and repair.
- It has recently been shown that Akt activation is associated with a worse outcome among endocrine treated breast cancer patients and that it also inhibits the progesterone receptor (PR) expression via the PI3K/Akt pathway in breast cancer cells.
- This is the first study showing PIK3CA mutations in pediatric glioblastomas, thus providing a molecular target in this important pediatric malignancy.
- Mutations of the PIK3CA gene is associated with the development of oral squamous cell carcinoma
- Activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression.
- PIK3CA may serve as a marker of invasion in endometrial cancer.
- Results show that coculture with ECs enhances VSMC adhesion and spreading by up-regulating beta(1)-integrin expression and activating the PI3K/Akt pathway. Interaction between ECs and VSMCs serves a role in vascular homeostasis and remodeling.
- PIK3CA mutations might exert their effects through activation of the phosphatidylinositol 3-kinase/AKT/ER-alpha pathway
- Results indicate that stimulation of heme oxygenase-1 expression by hypericin-PDT is a cytoprotective mechanism governed by the p38(MAPK) and PI3K pathways.
- PIK3CA alterations in primary (de novo) and secondary glioblastomas.
- These results demonstrate that hypoxic condition-and high cell density-induced expression of Redd1 is mediated by coactivation of Sp1 and HIF-1alpha downstream of the PI3K/Akt signaling pathway.
- These results suggest that there is a fine distinction between the signaling activators and downstream effectors of the oncogenic PI3K and RAS pathways in breast epithelium and those in other tissues.
- The data suggest that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate.
- These data demonstrate that IGF-I induces COX-2 expression in human ovarian cancer cells, which is mediated by three parallel signaling cascades--PI3K, MAPK, and PKC pathways that differentially regulate COX-2 expression.
- studies show that mutant PIK3CA increases the capacity for proliferation and survival under environmental stresses, such as growth factor deprivation stress while also imparting greater dependency on the PI3K pathway for proliferation and survival
- p110alpha PI-3K appears to uniquely regulate important monocyte functions, where other PI-3K isoforms are uninvolved or unable to fully compensate.
- PIK3CA mutations may have a role in cancer
- PIK3CA amplification and Ki-67 index were strong predictors for an early tumor-associated death in ovarian cancer patients.
- data from a Chinese cohort provide further genetic evidence suggesting that dysregulated PI3K/Akt pathway plays a significant role in the pathogenesis of thyroid tumors
- TLR3, PI3K, and IRF3 are involved in the poly IC-induced galectin-9 expression in HUVECs
- PI3K/ILK/Akt/NF-kappaB axis is a promising target for therapeutic intervention in renal cell carcinoma.
- Data suggest that lipid rafts play critical roles in KSHV infection and gene expression, probably due to their roles in modulating KSHV-induced PI3-K, RhoA-GTPase, and Dia-2 molecules essential for postbinding and entry stages of infection.
- Data suggest that PIK3CA mutations contribute to the invasion step from intramucosal carcinoma to invasive carcinoma in colorectal carcinogenesis.
- PIK3CA copy number gain and amplification is associated with head and neck squamous cell carcinoma
- PIK3CA mutations and PTEN loss were not mutually exclusive events and associated with similar prognostic factors
- Whereas PI3K is downstream of MUC1 activation and negatively regulates TLR5 signaling, it is not responsible for MUC1-induced suppression of TLR5 signaling.
- PIK3CA mutation was significantly associated with shorter relapse-free survival in stage II/III patients, and shorter disease-specific survival in all patients.
- These results suggest an important role for cross talk among Smad, p38 MAPK, JNK, and PI3K pathways in mediating the augmented expression of hAT(1)R following TGF-beta1 treatment in human fetal pulmonary fibroblasts.
- Phosphoinositide 3-kinase-independent non-genomic signals transit from the androgen receptor to Akt1 in membrane raft microdomains
- PIK3CA mutations are mutually exclusive with PTEN loss in diffuse large B-cell lymphoma
- Coexistent mutations/epigenetic inactivations in PI3K/AKT pathway may be responsible for the unusually aggressive course of ACC.
- oncogenic PIK3CA mutations contribute to the pathogenesis of skin tumors lacking malignant potential
- There was significant difference in survival between the lung cancer patients with PIK3CA normal copy number and the patients with PIK3CA amplification
- PIK3CA has an important role in human lung carcinogenesis, possibly by promoting malignant transformation.
- IGF-1 plays a role in potentiating platelet aggregation by complementing G(i)- but not G(q)-signaling pathways via PI3-K p110alpha.
- plexin-B1 promotes endothelial cell motility through RhoA and ROK by regulating the integrin-dependent signaling networks that result in the activation of PI3K and Akt
- Data suggest that PI3K-C2beta and AKT are epistatic to intersectin, and show that ITSN, independent of its role in endocytosis, regulates a critical cellular signaling pathway necessary for cell survival.
- The three most common tumour-derived alleles of p110alpha were shown to potently activate phosphoinositide 3-kinase signalling in human epithelial cells.
- Engagement of NKG2D by itself is sufficient to stimulate the formation of the natural killer cells immunological synapse (NKIS), with recruitment of NKG2D to the center synapse.
- High levels of p-AKT expression occurred independently of the presence of PTEN or PIK3CA mutations in endometrial cancer.
- In trastuzumab-treated breast cancer patients combined analysis of PTEN and PIK3CA identified twice as many patients at increased risk for progression compared to PTEN alone.
- rotavirus-induced PI3K activation causes regulation of integrin expression in intestinal cells, leading to prolonged adherence of infected cells to collagen and increased virus production.
- exon 9 PIK3CA mutations are typical of infiltrating lobular carcinomas
- The C allele of rs361072 attenuates insulin resistance in superobese European children.
- The results presented here indicate that actin reorganization through FAK/PI3-K/Rac-1 activation operates in various human cancer cell systems supporting a functional role for FAK/PI-3K/Rac1/actin signaling in controlling cell motility.
- An impaired control of glycogen synthase kinase-3beta activity by insulin receptor-mediated signalling plays a role in the pathogenesis of AD, facilitating tau protein phosphorylation and neurofibrillary tangle formation.
- Using both direct genomic DNA sequencing and novel mutant-enriched sequencing methods developed specifically for the 3 hot-spot mutations (H1047R, E545K and E452K) of PIK3CA, we detected 5 mutations of PIK3CA in the 24 pharyngeal cancers (20.8%).
- A higher incidence of PIK3CA alterations and the possible synergistic effect of these alterations and BRAF mutations suggest their major role in Middle Eastern papillary thyroid neoplasms.
- Sexual dimorphisms and tissue specific factors might directly or indirectly influence the occurrence of PI3KCA cancer alleles.
- These data provide the first evidence that IL-18 and FN stimulate each other's expression
- Phosphatidylinositol 3-kinase-dependent membrane recruitment of Rac-1 and p47phox is critical for alpha-platelet-derived growth factor receptor-induced production of reactive oxygen species.
- different PIK3CA mutations differentially contribute to breast cancer transformation
- study reports a 3.0 angstrom resolution structure of a complex between p110alpha and a polypeptide containing the p110alpha-binding domains of p85alpha; results suggest specific mechanisms for the effect of oncogenic mutations in p110alpha and p85alpha
- PIK3CA mutations are associated with myometrial invasion and tumors with PIK3CA mutations in exon 20 are frequently high-grade, invasive endometrial carcinomas.
- PIK3CA mutations in HNSCC are likely to be oncogenic and may significantly contribute to HNSCC carcinogenesis and pave attractive target for therapeutic prevention.
- In this study, we were unable to find a clear association between PIK3CA mutations and gene amplifications, nor with tumor histological subtypes or staging
- somatic PIK3CA mutations contribute to the frequent activation of the PI3K/AKT pathway in carcinomas of the biliary tract and liver
- PIK3CA mutations are common in invasive ductal carcinomas of the breast and PIK3CA exon 20 mutation is an independent risk factor for poor prognosis in breast cancer patients.
- analysis of PIK3CA mutations in Saudi Arabian colorectal cancer patience
- Poliovirus simultaneously activates the phosphatidylinositol 3-kinase (PI3K)/Akt survival signaling pathway in these cells, limiting the extent of JNK activation and thereby cell death.
- genetic alterations of KRAS and PIK3CA may play equivalent roles in endometrial carcinogenesis
- Mutations in the PIK3CA is associated with colon cancers
- In exon 9, a somatic mutation was found in two patients (2.2%) and in two cell lines; mutations included three E545K (G1633A) mutations and one E545Q (G1633C) mutation, in exon 20, no mutation was observed in our esophageal cancer patients
- The demonstration that p53 binds directly to the PIK3CA promoter and inhibits its activity identifies a novel mechanism whereby these two mediators regulate cellular functions.
- PI3Kalpha and -beta present distinct activation requirements and kinetics in G(1) phase, with a selective action of PI3Kalpha at the G(0)/G(1) phase transition
- point mutations in the p110alpha subunit of class IA PI3K confer factor independence to hematopoietic cells in vitro and leukemogenic potential in vivo, but have lower transforming activity than a deregulated class III receptor tyrosine kinase.
- identified and characterized the PIK3CA 5' upstream transcriptional regulatory region and confirmed that PIK3CA is transcriptionally regulated through NF-kappaB pathway
- high frequency of mutations in the PIK3CA, HRAS and KRAS genes leads us to believe that dysregulation of the phosphatidylinositol 3-kinase or Ras pathway is significant for the development and progression of penile carcinoma.
- PIK3CA mutation was associated with a decreased rate of node-positive disease, particularly among ER-positive tumors.
- PIK3CA is rarely mutated in diffuse large B-cell lymphoma
- structure of the complex between the catalytic subunit of PI3Kalpha, p110alpha, & a portion of its regulatory subunit, p85alpha reveals the majority of the oncogenic mutations occur at the interfaces between p110 domains & between p110 & p85 domains
- results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis
- FGFR3 and PIK3CA germline mutations can be excluded as an underlying genetic basis, therefore alternative mechanisms have to contribute to familial Seborrheic Keratoses.
- PIK3CA mutation is significantly associated with key molecular events in colorectal cancer, and MGMT loss likely contributes to the development of PIK3CA G>A mutation
- Overexpression of PI3K and Akt is associated with malignant rhabdoid tumor
- KRAS mutations and PI3KCA/PTEN deregulation significantly correlate with resistance to cetuximab.
- PIK3CA mutations, in comparison with PTEN loss and AKT1 mutations, were associated with significantly less and inconsistent activation of AKT and of downstream PI3K/AKT signaling in tumors and cell lines
- Exon 20 PIK3CA mutations are relatively frequent in Her-2+ breast tumors and shorten survival, whereas neither exons 9 and 20 mutations seem related with "triple negative" breast carcinomas
- study identified a potential hotspot for resistance mutations (I800), a drug-sensitizing mutation (L814C), and a surprising lack of resistance mutations at the "gatekeeper" residue
- RNA interference-mediated knockdown of PIK3CA inhibited colony formation of cell lines with PIK3CA mutations or gains but was not effective in PIK3CA wild-type cells. PIK3CA mutations or gains are present in a subset of lung cancers
- BRAF, KRAS and PIK3CA mutations occur prior to malignant transformation demonstrating that these oncogenic alterations are primary genetic events in colorectal carcinogenesis
- Inhibitors that target exclusively the cancer-specific mutants of p110 alpha constitute an important goal and challenge for current drug development.
- Higher BRCA1 mRNA expression is significantly correlated with advanced disease and ERBB2 overexpression in breast cancers.
- In tumors with co-occurring mutations in multiple components of the PI3K pathway, selective inhibition of the alpha isoform of p110 is an attractive therapeutic strategy, especially for late-stage tumors.
- These data establish a new function for the NBS1 protein as a regulator of PI3K activity via SFK members.
- our data reveal a novel function of p110alpha in medulloblastoma growth and survival.
- ARF1 regulates epidermal growth factor-dependent breast cancer cell growth and invasion during cancer progression by controlling the activation of the phosphatidylinositol 3-kinase pathway
- JAK2, EGFR and PI3KCA hot spot mutations are uncommon in endocrine tumors
- data showed a higher incidence of PIK3CA mutations in Malaysian breast cancers compared to colorectal & nasopharyngeal tumor tissue; findings also indicate PIK3CA mutations play a pivotal role in activation of the PI3 K signaling pathway in breast cancer
- inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers
- a selective downregulation of the p110alpha catalytic isoform in pregnancy
- PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies.
- Compared with patients with PIK3CA wild-type tumors, those with PIK3CA-mutated tumors experienced an increase in colon cancer-specific mortality according to univariate analysis.