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Validated All-in-One™ qPCR Primer for PRKG1(NM_006258.3) Search again
Product ID:
HQP014844
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AAT8, PKG, PKG1, PRKG1B, PRKGR1B, cGK, cGK 1, cGK1, cGKI, cGKI-BETA, cGKI-alpha
Gene Description:
protein kinase cGMP-dependent 1
Target Gene Accession:
NM_006258.3(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:
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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
- Sp1 binding activity on the PKG-Ialpha promoter was detected ... and this binding was inhibited by NO and cyclic nucleotides; PKG-Ialpha gene expression is driven by an Sp1 transcription mechanism
- G-kinase I beta interacted specifically with TFII-I, an unusual transcriptional regulator that associates with multiple proteins to modulate both basal and signal-induced transcription
- inhibits serum-response element-dependent transcription by inhibiting rho activation and functions
- PKG appears to be solicited for P-selectin expression when cAMP levels are elevated which suggest a cAMP/PKG-dependent pathway of platelet activation.
- PKG was found to be a target for phorbol 12-myristate 13-acetate (PMA)-responsive protein kinase C (PKC)
- NPRA-PKG association may have a role in compartmentation of cGMP-mediated signaling and regulation of receptor sensitivity
- dimerization of cGMP-dependent protein kinase Ibeta is mediated by an extensive amino-terminal leucine zipper motif, and dimerization modulates enzyme function
- G-kinase regulates vasodilator-stimulated phosphoprotein activity
- cyclic GMP-dependent protein kinase I binds to FHOD1 in vascular smooth muscle cells
- PKG has a role in platelet secretion
- CD38 is stimulated by sequential activation of IL8 receptor, IP(3)-mediated Ca(2+) rise, and cGMP/protein kinase G and plays an essential role in IL8-induced migration of LAK cells
- Rap 1-GTP levels in platelets were reduced by NO-donors and activators of NO-sensitive soluble guanylyl cyclase
- high-resolution structure of the coiled-coil domain of cGMP-dependent protein kinase Ialpha
- cGMP-dependent protein kinase Ibeta binds to TFII-I and IRAG through a common interaction motif
- Nitric oxide affects dendritic cell migration through the activation of cGMP kinase.
- Data suggest an important role of PKG in the PMA-induced inhibition of TRPC channels in native endothelial cells.
- regulatory domains of cGMP-dependent protein kinase Ialpha and Ibeta retain dimerization and native cGMP-binding properties and undergo isoform-specific conformational changes
- cGMP-dependent protein kinase expression is regulated by Rho and Kruppel-like transcription factor-4
- PKGI interacts with tripartite motif (TRIM) protein TRIM39R. TRIM proteins, through diverse molecular pathways, are often observed to regulate important aspects of cellular homeostasis.
- the leucine-zipper motif of PKG binds to that of MYPT1 to form a heterodimer; when the leucine-zipper motif of MYPT1 is absent, the PKG leucine-zipper motif binds to the coiled coil region and upstream segments of MYPT1 via formation of a heterotetramer
- Presence of cGKI alpha and beta provides further evidence for a significant role of these enzymes in the control of smooth muscle function in human penile erectile tissue.
- Activation of protein kinase G Increases the expression of p21CIP1, p27KIP1, and histidine triad protein 1 through Sp1.
- These results strongly suggest that TRPC6 channels can be negatively regulated by the nitric oxide-cyclic GMP-protein kinase G pathway, probably via T69 phosphorylation of the N-terminal.
- PDE5 inhibition can differentially impact selected cellular functions of platelets, and perhaps of other cell types
- analysis of the interaction between the coiled coil leucine zipper of cGMP-dependent protein kinase Ialpha and the C terminus of the myosin binding subunit of the myosin light chain phosphatase
- 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.
- resulting in a dose- and time-dependent increase in phospho-VASP
- PKG phosphorylates the N2-B and N2-A domains of titin.