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Validated All-in-One™ qPCR Primer for PIK3R1(NM_181523.2) Search again
Product ID:
HQP104560
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AGM7, GRB1, IMD36, p85, p85-ALPHA, p85alpha
Gene Description:
phosphoinositide-3-kinase regulatory subunit 1
Target Gene Accession:
NM_181523.2(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.
Validated result:
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| A | B |
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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. |
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Summary
Phosphatidylinositol 3-kinase phosphorylates the inositol ring of phosphatidylinositol at the 3-prime position. The enzyme comprises a 110 kD catalytic subunit and a regulatory subunit of either 85, 55, or 50 kD. This gene encodes the 85 kD regulatory subunit. Phosphatidylinositol 3-kinase plays an important role in the metabolic actions of insulin, and a mutation in this gene has been associated with insulin resistance. Alternative splicing of this gene results in three transcript variants encoding different isoforms. [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.
- Thus, the Met-326Ile variant of p85alpha is functional for intracellular signaling and adipocyte differentiation but has small alterations in protein expression and activity that could play a role in modifying insulin action.
- Expression of a mutated in a Hodgkin's lymphoma-derived cell line; the first detection in human hematopoietic cells further underlining a potential role of PI3-kinase/Akt signaling in human leukemogenesis
- The p85 subunit of PI 3-kinase mediates GPIb-related activation signals and activates Src independently of the enzymatic activity of PI 3- kinase.
- Gene expression of full-length p85alpha is increased in skeletal muscle from type 2 diabetics, this is not reflected by increased protein. Defects in PI 3-kinase activity are likely due to impaired activation of the enzyme.
- The isoleucine variant of codon 326 of the p85alpha subunit of PI3-K might be associated with decreased risk of Prostate Cancer.
- p55gamma binds to Rb and modification of this association can lead to cell cycle arrest
- protein whose expression is deregulated in the epidermis of the elderly.
- the role of p85-ALPHA in the survival of cancer cells that express wild-type PTEN
- a triple complex between AR, p85alpha, and Src is required for androgen-stimulated PI3K/Akt activation
- PI3K has a novel role as a bikunin target gene on uPA up-regulation and invasion
- These findings reveal key events of the phosphatidylinositol 3-kinase pathway that play distinct roles to maintain tissue polarity and that when disrupted are instrumental in the malignant breast tumor phenotype.
- coupling of Gab1 to PI3K is important for biological responses in RET-expressing cells
- Data suggest that SLP-76 may play a role in signaling pathways by interacting with the p85 subunit of phosphoinositide 3-kinase (PI3K).
- 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
- PI3K regulates cell cycle progression and cell proliferation in human gastric tumor cells via Rb-mediated pathway; effect mediated through direct association with Rb via N-terminal end of its p55 kDa regulatory subunits and modulating Rb-E2F interactions
- WAVE3-mediated migration in MDA-MB-231 cells via lamellipodia formation is activated downstream of PI3K and induced by PDGF
- calcium activates PLC-gamma1 via increased PIP3 formation mediated by c-src- and fyn-activated PI3K
- the nSH2 domain of the p85 regulatory subumit is responsible for p110 regulatory contacts, and its disruption leads to constitutive p110 activity
- Inhibitors may provide an alternative route to effective PI3K pathway inhibition for breast cancer treatment.
- the signals induced by integrin alpha6beta1 modulate at the level of PI3K and Cdc42 activity to allow platelets to actively form filopodia
- CD21 activation triggered Cbl tyrosine phosphorylation, which interacts with SH2 domains of p85 subunit, SH2 domains of Crk-L and with tyrosine phosphorylated Syk kinase. CD21 activation triggers dissociation of Cbl-Vav complex.
- SHP-2 recruitment to p85 is required for IGF-I-stimulated association of the p85/p110 complex with insulin receptor substrate-1 and for the subsequent activation of the PI-3 kinase pathway leading to increased cell migration
- the PI3-K pathway negatively regulates TGF-beta/Smad signaling in neuroblastoma cells
- increased expression of p85alpha may be one of the earliest molecular alterations in the mechanism of the insulin resistance associated with overfeeding
- MyD88 bridges TLR5 engagement to PI3K activation in response to flagellin
- Gab1 thus appears as a primary actor in coupling VEGFR-2 to PI3K/Akt, recruited through an amplification loop involving PtdIns(3,4,5)P3 and its PH domain
- Hsp90 inhibition transiently activates Src kinase and promotes Src-dependent p85 PI3K and Akt and Erk activation
- direct interactions between native Syk and PI3K proteins are differentially regulated during FcgammaR phagocytosis and endocytosis.
- 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.
- autotaxin induces uPA expression via the Gi-PI3K-Akt-NF-kappaB signaling pathway that might be critical for autotaxin-induced tumor cell invasion and metastasis
- Association of single nucleotide polymorphisms with serum leptin and body fat may reflect a diminished ability of this enzyme to signal in ersponse to leptin.
- constitutively active Stat5 mutant forms a complex with the p85 subunit of phosphatidylinositol 3-kinase and the scaffolding adapter Gab2 in leukemic bone marrow cells, resulting in the activation of Akt/PKB, a crucial downstream target of PI3-K
- hypothesized that variants in the SHP-2 gene PTPN11 and PI3K p85alpha subunit gene PIK3R1 may influence fasting levels of plasma apoB and/or LDL cholesterol
- the WASp/SNX9/p85/CD28 complex enables a unique interface of endocytic, actin polymerizing, and signal transduction pathways required for CD28-mediated T cell costimulation
- the recruitment of PI3K to the E-cadherin/beta-catenin/p120-catenin complex via beta-catenin at the plasma membrane is required for calcium-induced phospholipase C-gamma1 activation and, ultimately, keratinocyte differentiation
- PI3K is not overexpressed in melanocytic lesions.
- These results indicate that the phosphatidylinositol 3-kinase/Akt/FoxO1 pathway participates in Ang II suppression of hSR-BI/CLA-1 expression and suggests that the endothelial receptor for hSR-BI/CLA-1 is downregulated by the renin-angiotensin system.
- These results support a model in which phagosomal PI3K generates PI(3,4,5)P(3) necessary for later stages of phagocytosis, PTEN determines whether those late stages can occur, and SHIP-1 regulates when and where they occur.
- PKC alpha may be associated with regulation of cell proliferation/migration/invasion in human poorly differentiated hepatocellular carcinoma cells
- RhoG protects cells from apoptosis caused by the loss of anchorage through a PI3K-dependent mechanism, independent of its activation of Rac1
- IGF-1 activates the IGF receptor/IRS/PI3K/PKB pathway, and that PI3Kalpha is essential for the potentiatory effect of IGF-1 on platelet responses
- Endothelial cell PI 3-kinase activity and F-actin remodeling are required during lymphocyte diapedesis and identify a PI 3-kinase-dependent step following initial separation of the VE-cadherin barrier.
- 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
- PI3K is activated by toll-like receptor stimulation in primary human plasmacytoid predendritic cells (pDCs), and it is required for type I IFN production by pDCs, both at the transcriptional and protein levels
- Binding of CD95 Ligand to CD95 on glioblastoma cells recruit Yes and the p85 subunit of phosphatidylinositol 3-kinase to CD95, which signal invasion via the glycogen synthase kinase 3-beta pathway and subsequent expression of matrix metalloproteinases.
- p85alpha and p110beta are essential for androgen-stimulated AR transactivation, and their aberrant expression or activation might play an important role in prostate cancer progression
- 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
- the influenza A virus NS1 protein interacts with the p85beta, but not the p85alpha, subunit of phosphatidylinositol 3-kinase
- caspase 8 has a role as a modulator of p85alpha Rab5-GAP activity and endosomal trafficking
- 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