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Validated All-in-One™ qPCR Primer for AKT2(NM_001626.5) Search again
Product ID:
HQP004995
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HIHGHH, PKBB, PKBBETA, PRKBB, RAC-BETA
Gene Description:
AKT serine/threonine kinase 2
Target Gene Accession:
NM_001626.5(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
This gene is a putative oncogene encoding a protein belonging to a subfamily of serine/threonine kinases containing SH2-like (Src homology 2-like) domains. The gene was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors. Overexpression contributes to the malignant phenotype of a subset of human ductal pancreatic cancers. The encoded protein is a general protein kinase capable of phophorylating several known proteins. [provided by RefSeq].
Gene References into function
- evidence that Akt2 is transcriptionally regulated by MyoD and activates MyoD-myocyte enhancer binding factor-2 (MEF2) transactivation activity
- role in inhibiting JNK through activation of NF kappa B pathway in human epithelial cells
- In renal tubular epithelial cell, Akt phosphorylation is up-regulated in an effort to minimize cell death.
- Activation of AKT consequent to binding of albumin by CLL cells blocks chlorambucil- and radiation-induced apoptosis.
- a new mechanism for androgen-mediated prostate cancer cell survival and establish FKHR as nuclear target for both AKT-dependent and -independent survival signals in prostate cancer cells.
- Results describe the structure of an inactive and unliganded Akt2 kinase domain, and several features that distinguish it from other kinases.
- data indicate that AKT2 mediates PI3-K-dependent effects on adhesion, motility, invasion, and metastasis in vivo
- These results indicate that PI3k/Akt pathway is involved in the signaling cascade of glioma cells required to induce cell migration.
- results show that a defect in the ability of insulin to activate Akt-2 and -3 may explain the impaired insulin-stimulated glucose transport in insulin resistance
- AKT2 sensitizes A2780S and cisplatin-resistant A2780CP cells to cisplatin-induced apoptosis through regulation of the ASK1/JNK/p38 pathway.
- both p70S6K and Akt are activated in the majority of human papillary cancer cells.
- Akt regulates basic helix-loop-helix transcription factor-coactivator complex formation and activity during neuronal differentiation
- Akt2 phosphorylates MLK3, which results in the disassembly of the JNK complex bound to POSH and down-regulation of the JNK signaling pathway
- Akt2 may be an important regulator of both Xiap and p53 contents in ovarian cancer after CDDP challenge.
- Our data suggest that Akt is an endogenous inhibitor during TRAIL-mediated synovial cell apoptotic pathway.
- Findings suggest that Akt2 is a novel independent predictor for the development and progression of hepatocellular carcinoma .
- Lipid rafts(LR) may play important role in determining function of PI 3-K/Akt2 signaling, including stimulation of intestinal Na absorption. LR-associated Akt2 may be involved in enterocyte differentiation.
- data suggest that upstream perturbations of the PI3K/AKT pathway contribute to frequent activation of AKT2 in pancreatic cancer, which may contribute to the pathogenesis of this highly aggressive form of human malignancy
- Thus a physiological concentration of insulin stimulated Akt-1 & Akt-2 phosphorylation in human skeletal muscle in the absence of hyperglycemia, but Akt-2 expression is impaired in muscle of obese patients with atypical diabetes with severe hyperglycemia
- activated Akt and Akt2 have roles in progression of pancreatic ductal adenocarcinoma
- These results suggest that cross-talk between the PKB and caspase-8 pathways may regulate the balance between cell survival and cell death in ECV304.
- a mutation in AKT2 in a family showing autosomal dominant inheritance of severe insulin resistance and diabetes mellitus is described; the mutant kinase in cultured cells disrupted insulin signaling and inhibited the function of coexpressed, wild-type AK
- Akt2 is a critical kinase that regulates ezrin phosphorylation and activation
- AKT2 plays an important role in glioma cell motility and invasion
- Kinetic analysis of GST-AKT2 demonstrates that phosphorylation of Thr309 in the activation loop of the kinase is largely responsible for observed reduction in Km & for a subsequent 150-fold increase in the catalytic efficiency (k(cat)/Km) of the enzyme.
- in breast cancer patients, Akt activation is associated with tumour proliferation and poor prognosis, particularly in the subset of patients with ErbB2-overexpressing tumours
- In this study, we provide evidence for isoform-specific positive and negative roles for Akt1 and -2 in regulating growth factor-stimulated phenotypes in breast epithelial cells
- results suggest that AKT pathway may play an important role in the development and progression of gliomas
- These data show that specific interaction of the Akt2 isoform with p21 is key to its negative effect on normal cell cycle progression.
- Akt1 and Akt2 have opposing roles in Rac/Pak signaling and cell migration
- Akt1 induces CREB phosphorylation at Ser-133 and CREB target gene expression.
- Sequencing of the entire coding region and splice junctions of AKT2 and the relationship of genetic variations in the gene with multiple metabolic diseases is reported.
- Twist as a positive transcriptional regulator of AKT2 expression; Twist-AKT2 signaling is involved in promoting invasive ability and survival of breast cancer cells.
- Changes in tissue pressure during inflammation may regulate macrophage phagocytosis by activation of PI-3K, which activates Akt2, mTOR, and p70S6K.
- the PI3K/AKT/mTOR signaling pathway is involved in regulation of SphK1, with AKT2 playing a key role in PDGF-induced SphK1 expression
- Two variants in 5' regulatory region of Akt2 gene are associated and may modulate susceptibility to insulin resistance and related metabolic abnormalities.
- AKT2 up-regulation is characteristic of skin squamous cell carcinoma and coincident AKT2 activation through serine phosphorylation correlates with malignancy.
- Pressure did not stimulate translocation of AKT2 to the plasma membrane.
- PKB[alpha] and/or PKB[gamma] and not PKB[beta] alone are involved in gemcitabine resistance mechanisms.
- Akt2 is required for rapamycin-induced vascular smooth muscle cell differentiation, whereas Akt1 appears to oppose contractile protein expression.
- Akt1 and Akt2 mediate GPIb-IX signaling via the cGMP-dependent signaling pathway.
- a key regulatory role of the Akt/mTOR pathway in the generation of the effects of As(2)O(3)
- Functional convergence of Twist and AKT2 underscores the importance of this signaling pathway in tumor development and progression.
- Dlx5 can act as an oncogene by cooperating with Akt2 to promote lymphomagenesis
- Results suggest that Akt2 directly mediates EGF-induced chemotactic signaling pathways through PKCzeta and its expression is critical during the extravasation of circulating cancer cells.
- Akt2 down-regulation sensitizes ovarian cancer cells to paclitaxel-induced apoptosis, and inhibits survivin expression
- the consequence of PTEN loss and Akt2 overexpression function synergistically to promote metastasis