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Validated All-in-One™ qPCR Primer for PDPK1(NM_002613.4) Search again
Product ID:
HQP012979
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
PDK1, PDPK2, PDPK2P, PRO0461
Gene Description:
3-phosphoinositide dependent protein kinase 1
Target Gene Accession:
NM_002613.4(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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Gene References into function
- PDPK1 activity is regulated by reversible phosphorylation, possibly by a member of the Src kinase family.
- association of PDK1 with Hsp90 regulates its stability, solubility, and signaling
- Substitution of the autophosphorylation site Thr516 with a negatively charged residue confers constitutive activity to mouse 3-phosphoinositide-dependent protein kinase-1 in cells
- Data show that the translocation of 3-phosphoinositide-dependent protein kinase-1 from cytosol to the plasma membrane is critical for Akt and glycogen synthase kinase-3 activation.
- A point mutation in the substrate-binding region of PDK1 (L155E) rendered PDK1 incapable of phosphorylating PKB.
- 2.0 A crystal structure of the PDK1 kinase domain in complex with ATP
- 14-3-3 protein binds to PDK1 at Ser241 and negatively regulates PDK1 kinase activity.
- PDK1 has a role in activating atypical PKC and regulating the degradation of p21(WAF1)
- The in vivo role of the PIF-binding site of PDK1 is defined by knock-in mutation.
- peroxisomal targeting signal (PTS)-tagged CISK with deleted PX domain was able to direct 3-phosphoinositide-dependent protein kinase-1 (PDK-1) into peroxisomes
- Src- & ROS-dependent PDK1 activation leads to site-specific PAK1 phosphorylation. This is critically important for PDGF-induced VSMC migration, a process integral to the vascular response to injury that leads to vessel occlusion & plaque formation.
- role in metabolic actions of insulin
- the integrity of the alpha C-helix and HM-pocket in PDK1 is not regulated by T-loop phosphorylation
- PDK1 undergoes rapid and transient phosphorylation on S396, which was dependent upon plasma membrane localization; phosphorylation of S396 is necessary for nuclear shuttling of PDK1.
- PDK1 plays a critical role by nucleating the TCR-induced NF-kappaB activation pathway in T cells
- results indicate that 3-phosphoinositide-dependent protein kinase-1 is a critical regulator of cell survival by modulating the IkappaB kinase (IKK)/nuclear factor-kappaB pathway
- PDK-1 may promote oncogenesis in part through the activation of AKT and p7
- PDK1 mediates mammary epithelial cell growth and invasion in part by MT1-MMP induction, which in turn activates MMP-2 and modulates the ECM proteins decorin and collagen
- These data reveals for the first time that PDK1 and PKB may differentially activate NF-kappaB, and that TPCK may subserve a useful anti-inflammatory function by inhibiting IKKbeta.
- Ras is able to promote monocyte lineage selection via PKC and PDK1.
- Loss of PTEN expression in Jurkat T cells does not impact on the PDK-1/PKC pathway and that only a subset of kinases, such as PKB/Akt, are perturbed as a consequence PTEN loss.
- PDK-1/AKT pathway is activated in RMS and may play an important role in survival of RMS(rhabdomyosarcoma). PDK-1/AKT pathway may be an attractive therapeutic target for cancer intervention in RMS using OSU-03012.
- These data suggest that phosphorylation of PDK1 on Tyr(9), distinct from Tyr(373/376), is important for PDK1/Src complex formation, leading to PDK1 activation.