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Validated All-in-One™ qPCR Primer for PAX8(NM_003466.3) Search again
Product ID:
HQP018794
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
PAX-8
Gene Description:
paired box 8
Target Gene Accession:
NM_003466.3(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 paired box (PAX) family of transcription factors. Members of this gene family typically encode proteins that contain a paired box domain, an octapeptide, and a paired-type homeodomain. This nuclear protein is involved in thyroid follicular cell development and expression of thyroid-specific genes. Mutations in this gene have been associated with thyroid dysgenesis, thyroid follicular carcinomas and atypical follicular thyroid adenomas. Alternateively spliced transcript variants encoding different isoforms have been described. [provided by RefSeq].
Gene References into function
- TTF-1 and Pax 8 cooperatively activate their target genes and their synergistic activity requires the cross-talk between enhancer and gene promoter
- Expression of PAX8-PPAR gamma 1 rearrangements in both follicular thyroid carcinomas and adenomas.
- directly interacts with TTF-1 and synergistically activates transcription
- Detection of the PAX8-PPAR gamma fusion oncogene in both follicular thyroid carcinomas and adenomas.
- transcription factor Pax-8 could be involved in the upregulation of D2 expression in the thyroid of Graves' patients
- results suggest that conventional follicular thyroid carcinomas develop through at least two distinct molecular pathways initiated by either RAS point mutation or PAX8-peroxisome proliferator-activated receptor gamma rearrangement
- lack of the PAX8/PPAR gamma rearrangement in the anaplastic thyroid carcinoma group suggests that the tumorigenic pathway in these tumors is likely to be independent of this fusion
- Pax8 regulates the transcriptional activity of Hex promoter; several Pax8 binding sites in the Hex promoter are present
- HNF1beta partially rescues Pax8/lim1-induced kidney malformations.
- the PAX8-PPARgamma1 translocation characterizes a subset of thyroid follicular carcinomas
- A novel and unique PAX8 mutation provides evidence for a crucial role of the p300 coactivator in mediating the functional synergism between PAX8 and TTF-1 in thyroid-specific gene expression.
- in JAR cells, hCG activates a cAMP-dependent pathway that can up-regulate WT1 expression through PAX8
- Pax8 may have a role in re-differentiation of thyroid cancer cells
- PAX8-PPARgamma disrupts normal transcriptional regulation by stimulating some genes and inhibiting others, the net effect of which may mediate follicular thyroid cell growth and loss of differentiation.
- In follicular variant of papillary thyroid carcinoma, the PAX8-PPARgamma rearrangement was significantly associated with multifocality and vascular invasion
- Suppression of NORE1A, a known Ras effector, in PAX8-PPARgamma fusion-carrying follicular thyroid cancer.
- Oligomerization chain reaction (OCR) strategy allows identification of Foxe1, TTF-1, and thyroid oxidase 2 as new direct targets of Pax8.
- Results showed no direct involvement of PAX-2 genes in Wilms tumor pathogenesis.
- PAX8 is expressed in ovarian cancer but not in the precursor ovarian surface epithelia of healthy individuals. PAX8 is expressed in the non-ciliated, secretory cells of healthy fallopian tube mucosal linings but not in the adjacent ciliated epithelia.
- PAX8 mutations in congenital hypothyroidism due to dysgenetic or orthotopic thyroid glands are rare. PAX8-T225M is probably a rare variant.
- identification of a novel PAX8 mutation in a particular variant of non-congenital early-onset hypothyroidism indicates a key function of PAX8 in the postnatal growth and functional maintenance of the thyroid gland
- PAX8PPARgamma increases thyroid cell viability and has opposite effects on thyroid-specific gene expression, suggesting that the presence of this rearrangement may contribute to the malignant transformation of thyroid follicular cells.
- Pax8 is a useful marker for the diagnosis of anaplastic carcinomas.
- PAX8 binds directly to the hTERT and hTR promoters, up-regulating hTERT and hTR mRNA, as well as telomerase activity
- PAX8 is an additional marker for identifying nephrogenic adenoma
- Pax8 is a useful marker in the differential diagnosis of ovarian and breast carcinomas.
- Results suggest that PARP1 behaves as an important negative co-factor involved in the regulation of Pax8-dependent gene expression.
- Pax-8 activity is regulated via a redox-based mechanism centered on the glutathionylation of specific cysteines in the N-terminal region (Cys45 and Cys57).
- Data show that Pax8 is targeted in the SUMO nuclear bodies, and that the steady-state protein level of Pax8 is controlled by sumoylation.
- Clinical analysis revealed distinct hormonal patterns in thyroid hypoplasia when compared with other variants of thyroid dysgenesis, with genetic abnormalities identified only in few cases in the TSH-R, PAX8, and NKX2.5 genes.