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Validated All-in-One™ qPCR Primer for PKD2(NM_000297.3) Search again
Product ID:
HQP013180
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
APKD2, PC2, PKD4, Pc-2, TRPP2
Gene Description:
polycystin 2, transient receptor potential cation channel
Target Gene Accession:
NM_000297.3(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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Summary
This gene encodes a member of the polycystin protein family. The encoded protein contains multiple transmembrane domains, and cytoplasmic N- and C-termini. The protein may be an integral membrane protein involved in cell-cell/matrix interactions. The encoded protein may function in renal tubular development, morphology, and function, and may modulate intracellular calcium homoeostasis and other signal transduction pathways. This protein interacts with polycystin 1 to produce cation-permeable currents. Mutations in this gene have been associated with autosomal dominant polycystic kidney disease.
Gene References into function
- review of reported mutations
- functions as a calcium-activated intracellular calcium release channel in vivo, and polycystic kidney disease results from the loss of a regulated intracellular calcium release signalling mechanism
- found profound differences in the spatiotemporal expression of PKD1 and PKD2 during nephrogenesis, PKD2 being expressed earlier and more diffusely than PKD1
- identification, characterization, and localization of a complex with polycystin 1
- role in mediating cation channel activity
- Several independent lines of evidence reveal that the carboxyl terminal domain (D682-V968) of polycystin 2 interacts with cardiac and skeletal isoforms of troponin I.
- identified and demonstrated that the intracellular C terminus of PC2 associates with a core regulatory protein of the actin cytoskeleton system, tropomyosin-1
- that the location of PKD2 mutations did not influence the age of onset of ESRD, however, patients with splice site mutations appeared to have milder renal disease compared with patients with other mutation types
- REVIEW: Role in renal tubulogenesis
- An at-least weak hot spot in exon 1 of the PKD2 gene was found in autosomal dominant polycystic kidney disease patients in the Czech Republic.
- In PKD2- B-lymphoblastoid cells, transfection of a PKD2 full-length cDNA causes an increase in intracellular Ca2+ levels & cell proliferation. PC2 functions in a Ca2+ signaling context, which in turn modulates gene expression.
- Results show that mDia1 and PKD2 interact in native and in transfected cells, and binding is mediated by the cytoplasmic C terminus of PKD2 binding to the mDia1 N terminus.
- PC2 channel function may be essential in renal cell function and kidney development--REVIEW
- the intracellular location of polycystin-2 is regulated by PIGEA-14
- Data show that gene diagnosis can be done for PKD2 mutation carriers prior to cytogenesis.
- The PKD2 gene product, polycystin-2, is an integral membrane protein with molecular characteristics of a calcium-permeant cation channel.
- Structure and function of this gene shows how mutation at this locus results in the spectrum of changes seen in autosomal-dominant polycystic kidney disease. (review)
- Our findings indicate that physical forces exerted on cells regulate polycystin-2 channel activity by a sensory mechanism involving the actin cytoskeleton.
- The polycystin multiprotein complex is embedded in a cholesterol-containing signalling microdomain specified by flotillin-2, which is distinct from classical light-buoyant-density, detergent-resistant domains.
- A splice form of polycystin-2, lacking exon 7, does not interact with polycystin-1.
- Data suggested that the autosomal dominant polycystic kidney disease is not linked to PKD1 but to PKD2.
- PC2 and IP3R functionally interact and modulate intracellular Ca2+ signaling
- polycystin-2 is necessary for the proper growth and differentiation of kidney epithelial cells and suggest a possible mechanism for the cyst formation seen in ADPKD2
- PKD2 regulates the cell cycle through direct interaction with Id2; Id2 expression suppresses the induction of a cdk inhibitor, p21, by either PKD1 or PDK2. The PDK2-Id2 interaction is regulated by PDK1-dependent phosphorylation of PDK2.
- News: regulates the cell cycle by preventing nuclear localization of ID2
- A new phosphorylation site for polycystin-2 within its N-terminal domain (serine-76) is functionally significant for maintenance of normal glomerular and tubular morphology.
- kinesin-2 is a linker between polycystin-2(PC2) and fibrocystin and mediates the regulation of PC2 channel function by fibrocystin
- data are the first to provide a direct demonstration of a microtubular interaction with PC2 in the human syncytiotrophoblast
- Polycystin-2, or TRPP2 according to the TRP nomenclature, is encoded by PKD2, a gene mutated in patients with autosomal-dominant polycystic kidney disease--{REVIEW}
- These findings suggest that FPC and polycystins share, at least in part, a common mechanotransduction pathway.
- TRPP2 has been suggested to function as a mechanosensitive channel that detects fluid flow in the renal tubule lumen, supporting the proposed role of the primary cilium as the unifying pathogenic concept for cystic kidney disease.
- overexpression of human PKD2 leads to anomalies in tubular function, probably due to abnormalities in tubule morphogenesis.
- Angiotensin Ii stimulation increases expression of PC2 on the cell surface of glomerular mesangium cells.
- identify Kim1 as an endogenous ciliary protein
- Reactive oxygen species inhibit polycystin-2 (TRPP2) cation channel activity in term human syncytiotrophoblast.
- TNF-alpha, an inflammatory cytokine, disrupts the localization of polycystin-2 to the plasma membrane and primary cilia through a scaffold protein, FIP2, which is induced by TNF-alpha
- PC2, but not pathogenic mutants E837X and R872X, represses cell proliferation through promoting the phosphorylation of eukaryotic translation initiation factor eIF2alpha by pancreatic ER-resident eIF2alpha kinase (PERK).
- PC2-CC is involved in PC2 oligomerization, and PC2-EF is a Ca2+-sensitive switch
- characterization of an N-terminal oligomerization domain for polycystin-2
- Mutant PKD2 downregulates p57KIP2, upregulates CDK2, and increases rat & human kidney epithelial cell proliferation, independent of STAT-1/p21.
- Results suggest that polycystin-2 plays a role in centrosome duplication.
- These data suggest that channel regulation in human syncytiotrophoblasts is effected by a functional interface linking changes in actin filamental dynamics and changes in membrane structure.
- This minireview covers current knowledge about cytoskeletal interactions with TRPP2, and suggests that mutations in proteins of the TRPP2-cytoskeleton complex may be implicated in the pathogenesis of autosomal dominant polycystic kidney disease[review]
- To identify the gene regulated by PKD2 and c-Myc, we performed gene expression profiling in PKD2 and c-Myc overexpressing cells. NCAM is an important molecule in the cystogenesis induced by PKD2 overexpression.
- polycystin-1, polycystin-2, and fibrocystin are shed in membrane particles in the urine, and these particles interact with primary cilia